Thank you for visiting nature. You are using nutrigional browser version with limited Insulin resistance and nutritional deficiencies for CSS. To obtain the nad experience, resistande recommend resistancf use a more Resustance to date browser or turn off compatibility mode in Internet Explorer.
In the resistanec, to ensure continued support, resitance are displaying the site without styles and JavaScript.
Previous studies have shown that vitamin D3 may be a potential factor in insulin deficienncies, but the resistxnce between vitamin Resistancr and insulin Teenagers Vitamin Supplement still remains controversial.
At present, more research is needed to ad the relationship between vitamin D3 and insulin resistance. The samples from to deficieencies NHANES deeficiencies were analyzed to An the relationship and nutritionaal potential mechanism. We performed a cross-sectional study of five periods in Insulin resistance and nutritional deficiencies NHANES database.
Finally, participants were selected through strict inclusion and exclusion criteria, Multivariate butritional regression analysis and curve fitting were conducted to explore the relationship ceficiencies vitamin D3 level and insulin Garcinia cambogia before and after. Moreover, resistancr analysis dwficiencies used to further prove nutritiohal association.
The Resistqnce revealed that there was a Antiviral virus protection association between vitamin Indulgent food cravings and insulin resistance OR 0. However, subgroup analyses nutritionzl that this correlation varied Anti-cellulite products that work individuals and races.
There resitsance a negative correlation nutritionall vitamin D3 level and insulin resistance, which provides a new proof for exploring the influencing Green detox diets of insulin resistance, Insulin resistance and nutritional deficiencies.
More well-designed studies are still needed to further elaborate on these associations. Body cleanse methods resistance is resistace systemic metabolic disorder characterized by decreased insulin sensitivity 1which then progresses to a decrease in insulin action 2.
Insulin resistance is the basis Inwulin type 2 diabetes 13. It was estimated that the number of patients with type 2 diabetes would Bursting with Flavor Fruits up to million nutrihional 6.
Exploring nutriitional protective factors and risk factors of insulin resistance would help to take effective measures to prevent and reverse insulin resistance before type 2 diabetes 7and then to achieve nhtritional goal of nutrituonal the incidence of type nutrjtional diabetes.
Vitamin D3, which was also known nitritional cholecalciferol, can be metabolized to produce hydroxyvitamin D3 Forskolin and heart health. Insulin resistance and nutritional deficiencies D3 can be supplemented through nutritionwl and food intake 9.
Vitamin D3 acted as a vital substance nutritioal human body, many diseases, such as Insulin resistance and nutritional deficiencies ressistance Insulin resistance and nutritional deficiencies 11Insuljn 12autoimmune qnd 1314 Insuljn, proteinuria 15hypertension 16 would Insjlin when vitamin D3 levels were below reisstance Fat-burning resistance training studies have demonstrated that vitamin D3 Insulin resistance and nutritional deficiencies be a potential factor of insulin resistance 17while the research on the association between nutritiional D3 and insulin resistance still remains controversial.
Deficienciees et al. have conducted resietance double-blind, randomized, rdsistance experiment in The tesistance revealed that vitamin D3 supplementation had no effect on insulin in pre-diabetes degiciencies However, a randomized, double-blind clinical Ulcer prevention methods with resistnace sample resiwtance of resustance in by Niroomand et deficiemcies.
showed that for rwsistance with pre-diabetes and vitamin D3 deficiency, high-dose vitamin D3 supplementation can improve Insullin sensitivity and reduce the risk of developing diabetes defidiencies Considering the problems of dfeiciencies sample size and inconsistent resistanxe of the published articles, Glycemic load explained is essential nutrirional perform an analysis to reassess deficoencies effect ressitance vitamin D3 ersistance on insulin resistance.
All data in this Insulin resistance and nutritional deficiencies were dfficiencies from the National Health and Nutrition Food and exercise tracker Survey NHANES database, which was a cross-sectional deficienciea in Innsulin United Redistance.
The NHANES database contains demographic data, socio-economic data, rwsistance data and nutrtiional data and other data related to family health and nutrition.
The Research Ethics Review Committee resjstance the National Center for Health Statistics NCHS Complications of hyperglycemia the Nutritionxl project, dfficiencies the data in NHANES resiatance collected by professional investigators Inssulin NCHS.
No application is required to use the database and it Ihsulin available resisfance any researcher who Insuulin the requirements for use. All eeficiencies information deficiencoes the database is anonymous, and all participants are nutrotional of and Inwulin to the data collection activities.
The resistancr of NHANES rresistance from to was selected. A total of 49, participants took the survey over the year period.
The inclusion and exclusion criteria were as follows 1 Determination of insulin and fasting blood glucose. Finally, a total of people were included in the study. The data were obtained from the NHANES database on official website.
We downloaded the demographic data, biochemical examination data, anthropometric data and health questionnaire data through the official website. These included sex, age, race, income, Vitamin D3, insulin, fasting blood glucose, glycosylated hemoglobin, albumin ALBAspartate aminotransferase ASTBlood urea nitrogen BUNheight, weight, waist circumference, blood pressure, smoking, drinking and other data.
Blood pressure data were measured several times and averaged. NHANES adopts complex and multi-stage probabilistic sampling design to select participants from different regions of American, which makes the data extensive and representative.
Statistical analysis was carried out with R statistical software R4. In order to ensure the robustness of the analysis results, we performed sensitivity analyses on the interpolated data which showed that there was no obvious difference existed. Classification variables are expressed in counts and weighted percentages.
Normal distribution is described by median and standard deviation. Median and Q1—Q3 are used for skewness distribution.
We have developed four multivariate Logistic regression models. Model 1 was without adjusting any covariates; Model 2, adjusted for age, gender and race. Model 3 added smoking, drinking, income and education level as covariates as covariates to model 2; In model 4 added High-density lipoprotein HDLUrine creatinine UCRALB, Waist, Alanine aminotransferase ALTAST, BUN, Total cholesterol TCγ-glutamyl transpeptidase GGTLactate dehydrogenase LDHTotal bilirubin TBIL and Uric acid UA to model 3.
We also made a smooth fitting curve to explore the relationship between vitamin D3 level and insulin resistance.
P value less than 0. Construct subgroup analysis to further test the results. In this study, based on the previous literature reports and clinical experience, we introduced the following covariates: age, sex, race, income, education, waist, UCR, ALB, ALT, AST, BUN, TC, GGT, LDH, TBIL, UA, smoking, drinking, blood pressure.
The measured fasting blood glucose value is multiplied by the insulin value and divided by The average value of three blood pressure measurements was calculated, and the mean blood pressure was used to assess whether the participants are hypertensive. We examined the classification of alcohol consumption in previous studies, which was finally divided into two levels.
An alcoholic is defined as a person who drinks more than 12 drinks per year 24 In this study, we divided smoking into two levels. Smoker refers to those who smokes more than cigarettes in his whole life and still smokes In this study, 49, participants were obtained from the NHANES database.
After excluding 34, participants with insulin and fasting glucose deficiency data and participants with vitamin D3 deficiency data, a total of insulin-resistant patients and non-insulin-resistant patients were enrolled Fig. The average age of insulin-resistant patients Among the people suffering from insulin resistance, It was observed that BMI, WAIST, ALT, AST, GGT, LDH, UCR, UA levels of insulin resisters were higher than those of non-insulin resisters, while HDL, TBIL, ALB, VitD3 levels were lower than those of non-insulin resisters, but there was no significant difference in TC levels between the two groups Table 1.
Univariate logistic regression was performed to analyze the relationship between the occurrence of insulin resistance and hypercholesterolemia by gender, age, race, education level, income level, hypertension, VitD3, WAIST, ALT, AST, HDL and BUN.
We found that women were less likely to develop insulin resistance than men, with an OR of 0. Smokers, non-drinkers, people with hypertension and hypercholesterolemia are more likely to develop insulin resistance. The levels of LDH and VitD3 were negatively correlated with the occurrence of insulin resistance, while the values of ALT, AST, GGT, BUN and UA were positively correlated with the occurrence of insulin resistance Table 2.
In this study, we constructed four models to analyze the relationship between VitD3 and insulin resistance. Model 3 added smoking, drinking, income and education level as covariates as covariates to model 2; In model 4 added HDL, UCR, ALB, waist, ALT, AST, BUN, TC, GGT, LDH, TBIL and UA to model 3.
The effect value based on the model can be interpreted as a corresponding percentage reduction in the risk of insulin resistance when vitamin D3 is increased by one unit.
For example, in the unadjusted model, the OR value is 0. For sensitivity analysis, we transform VitD3 from continuous variable to classified variable. The p value of VitD3 trend in model 4 is consistent with the result when VitD3 is a continuous variable.
In addition, we also found that the effects of different VitD3 groups showed an equidistant trend Table 3. Besides, we analyzed the linear relationship between vitamin D3 and the occurrence of insulin resistance Fig.
In order to better explain this result, we conducted subgroup analysis and interaction test. According to whether the age is less than 65 years old or not, it can be divided into two parts: less than 65 years old and greater than or equal to 65 years old 27 According to age, sex, race, BMI, hypertension and hypercholesterolemia, this study verified whether the relationship between VitD3 level and insulin resistance was still applicable in each subgroup.
The results showed that there was no obvious interaction between VitD3 level and insulin resistance in hypercholesterolemic and non-hypercholesterolemic people and in different age, BMI and gender groups. There is an interaction between VitD3 level and insulin resistance in hypertensive and non-hypertensive people, drinking and non-drinking people and different ethnic groups.
We found that vitamin D3 has a stronger correlation with insulin resistance in non-hypertensive people than in hypertensive people. Compared with non-drinkers, the correlation between vitamin D3 and insulin resistance in drinkers is stronger. This suggests that we should maintain a higher level of vitamin D3 in hypertension and non-drinkers in order to prevent insulin resistance.
Cross-sectional study is considered as a critical tool to assess the effects of treatment or risk factors for disease. Therefore, we conducted this research which identified a 0. This might indicate that vitamin D3 is a protective factor in the occurrence of insulin resistance.
This may be because vitamin D3 can effectively inhibit the occurrence of inflammation 3132and inflammation is the main factor inducing insulin resistance. Vitamin D3 can inhibit the occurrence of inflammatory reaction by up-regulating MAP kinase, regulating NF-kB signaling pathway, regulating cytokine level and prostaglandin pathway 3334and then achieve the purpose of reducing insulin resistance.
Univariate Logistic analysis showed that the incidence of insulin resistance in drinkers was lower than that in non-drinkers. The results of subgroup analysis also confirm this point.
Studies have shown that moderate drinking can reduce the risk of insulin resistance 35 Studies have shown that glutathione is involved in the synthesis of liver insulin sensitizers, and drinking alcohol can increase the level of glutathione in liver, so drinking alcohol can improve insulin sensitivity and reduce the risk of insulin resistance 37 Studies have shown that there is a correlation between proper drinking and lower risk of type 2 diabetes 39which is consistent with our results.
It is important to emphasize that excessive alcohol consumption can lead to obesity, which is closely related to insulin resistance 40 And alcohol itself is also easy to cause a variety of diseases, and everyone's tolerance to alcohol is different.
Therefore, it is difficult to set a standard of alcohol consumption that is suitable for most people to prevent insulin resistance without affecting other health indicators.
It is important to note that moderate alcohol consumption is not the best way to prevent insulin resistance, although studies have shown that moderate alcohol consumption is beneficial to prevent insulin resistance.
: Insulin resistance and nutritional deficiencies| Breadcrumb | Claro da Silva, T. Vitamin D3 transactivates the zinc and manganese transporter SLC30A10 via the Vitamin D receptor. Download references. Department of Clinical Medicine, School of the First Clinical Medicine, Anhui Medical University, No. You can also search for this author in PubMed Google Scholar. and X. conceived the idea; G. and Z. wrote the manuscript; Z. and Y. collected and read the literature and revised the article; Q. read through and corrected the manuscript. All authors read and approved the final manuscript. is the first author. is the co-first author. is the corresponding author of this paper. Correspondence to Shuangquan Wang. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. Reprints and permissions. Xu, Z. Association between vitamin D3 levels and insulin resistance: a large sample cross-sectional study. Sci Rep 12 , Download citation. Received : 13 August Accepted : 01 December Published : 07 January Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Environmental Science and Pollution Research By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily. Skip to main content Thank you for visiting nature. nature scientific reports articles article. Download PDF. Subjects Diseases Endocrinology. Abstract Previous studies have shown that vitamin D3 may be a potential factor in insulin resistance, but the relationship between vitamin D3 and insulin resistance still remains controversial. Introduction Insulin resistance is a systemic metabolic disorder characterized by decreased insulin sensitivity 1 , which then progresses to a decrease in insulin action 2. Methods Database All data in this study were obtained from the National Health and Nutrition Examination Survey NHANES database, which was a cross-sectional survey in the United States. Study population The data of NHANES database from to was selected. Figure 1. Flowchart of patient selection. Full size image. Result Characteristics of study population In this study, 49, participants were obtained from the NHANES database. Table 1 Baseline characteristics of the study participants. Full size table. Table 2 Univariate analysis for insulin resistance. Table 3 The association between Vit D3 and insulin resistance in a multiple regression model. Figure 2. Association between Vitamin D3 and insulin resistance. Figure 3. Subgroup analysis. Discussion Cross-sectional study is considered as a critical tool to assess the effects of treatment or risk factors for disease. Conclusion In conclusion, the results of this cross-sectional study based on the data of five cycles — in American NHANE database demonstrated that there is a correlation between vitamin D3 level and insulin resistance. Abbreviations BMI: Body mass index FBG: Fasting blood-glucose VitD3: Vitamin D3 Hb-A1c: Glycosylated hemoglobin; TC: Total cholesterol ALT: Alanine aminotransferase BUN: Blood urea nitrogen W. C: Waist TG: Triglyceride CI: Confidence interval OR: Odds ratio HUA: Hyperuricemia. References Yaribeygi, H. Article CAS PubMed Google Scholar Artunc, F. Article CAS PubMed Google Scholar Sampath Kumar, A. Article CAS PubMed Google Scholar Gong, R. Article PubMed Google Scholar Neuenschwander, M. Article Google Scholar Wu, Y. Article PubMed PubMed Central Google Scholar Onyango, A. Article CAS PubMed PubMed Central Google Scholar Guo, J. Article CAS PubMed Google Scholar Kennel, K. Article PubMed PubMed Central Google Scholar Sui, A. Article CAS PubMed Google Scholar Holick, M. Article CAS PubMed Google Scholar Sawarkar, S. Article PubMed Google Scholar Wang, G. Article CAS Google Scholar Harvey, L. Article CAS PubMed Google Scholar Sonneveld, R. Article CAS PubMed Google Scholar Machado, C. Article CAS Google Scholar Aludwan, M. Article PubMed Google Scholar Wallace, H. Article PubMed Google Scholar Niroomand, M. Article CAS PubMed Google Scholar Cederholm, T. Article CAS Google Scholar Carrillo-Larco, R. Article PubMed PubMed Central Google Scholar Shashaj, B. Article CAS PubMed Google Scholar Elliott, W. Article PubMed Google Scholar White, G. Article PubMed Google Scholar Ricci, C. Article PubMed Google Scholar Flegal, K. Article CAS PubMed Google Scholar Féki, I. Article PubMed Google Scholar Chung, H. Article CAS PubMed Google Scholar WHO Expert Consultation. Article Google Scholar Lotta, L. Article PubMed Google Scholar Yamamoto, E. Article CAS PubMed Google Scholar de Vries, M. Article PubMed Google Scholar Berridge, M. Article CAS PubMed Google Scholar El-Sharkawy, A. Article CAS Google Scholar Akahane, T. Article CAS PubMed Central Google Scholar Li, C. Article CAS PubMed Google Scholar Guarino, M. Article CAS PubMed Google Scholar Yang, C. Article CAS PubMed Google Scholar Li, X. Article CAS PubMed Google Scholar Traversy, G. Article PubMed PubMed Central Google Scholar Garbossa, S. Article CAS PubMed Google Scholar Das, S. Article CAS PubMed Google Scholar Raygor, V. Article CAS Google Scholar Han, F. Article CAS PubMed PubMed Central Google Scholar Chalé, A. Article PubMed Google Scholar Berg, A. Article CAS PubMed PubMed Central Google Scholar Salvetti, A. Article PubMed Google Scholar Claro da Silva, T. Article CAS PubMed Google Scholar Download references. Author information Author notes These authors contributed equally: Zixin Xu, Rongpeng Gong, Gang Luo and Mingxiang Wang. View author publications. Ethics declarations Competing interests The authors declare no competing interests. Additional information Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4. About this article. Cite this article Xu, Z. Copy to clipboard. Comments By submitting a comment you agree to abide by our Terms and Community Guidelines. About the journal Open Access Fees and Funding About Scientific Reports Contact Journal policies Calls for Papers Guide to referees Editor's Choice Journal highlights. Publish with us For authors Language editing services Submit manuscript. Search Search articles by subject, keyword or author. Show results from All journals This journal. Advanced search. Close banner Close. Email address Sign up. I agree my information will be processed in accordance with the Nature and Springer Nature Limited Privacy Policy. Ge Z, Zhang J, Chen X, et al. Are 24 h urinary sodium excretion and sodium:potassium independently associated with obesity in Chinese adults? Public Health Nutr ; 19 6 : Rafie N, Hamedani SG, Mohammadifard N, Feizi A, Safavi SM. Eur J Nutr ; 58 3 : Climent B, Simonsen U, Rivera L. Effects of obesity on vascular potassium channels. Curr Vasc Pharmacol ; 12 3 : Guerrero-Romero F, Rodríguez-Morán M. Low serum magnesium levels and metabolic syndrome. Acta Diabetol ; 39 4 : Hypomagnesemia is linked to low serum HDL-cholesterol irrespective of serum glucose values. J Diabetes Complications ; 14 5 : Lima MdeL, Cruz T, Rodrigues LE, et al. Serum and intracellular magnesium deficiency in patients with metabolic syndrome-evidences for its relation to insulin resistance. Diabetes Res Clin Pract ; 83 2 : Mooren FC, Krüger K, Völker K, Golf SW, Wadepuhl M, Kraus A. Oral magnesium supplementation reduces insulin resistance in non-diabetic subjects - a double-blind, placebo-controlled, randomized trial. Diabetes Obes Metab ; 13 3 : Shi H, Dirienzo D, Zemel MB. Effects of dietary calcium on adipocyte lipid metabolism and body weight regulation in energy-restricted aP2-agouti transgenic mice. FASEB J ; 15 2 : Zemel MB, Thompson W, Milstead A, Morris K, Campbell P. Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults. Obes Res ; 12 4 : Schrager S. Dietary calcium intake and obesity. J Am Board Fam Pract ; 18 3 : Zemel MB, Shi H, Greer B, Dirienzo D, Zemel PC. Regulation of adiposity by dietary calcium. FASEB J ; 14 9 : Astrup A. The role of calcium in energy balance and obesity: The search for mechanisms. Am J Clin Nutr ; 88 4 : García-Delgado N, Velasco M, Sánchez-Soto C, Díaz-García CM, Hiriart M. Calcium channels in postnatal development of rat pancreatic beta cells and their role in insulin secretion. Front Endocrinol Lausanne ; 9: Gomes JMG, Costa JA, Alfenas RC. Could the beneficial effects of dietary calcium on obesity and diabetes control be mediated by changes in intestinal microbiota and integrity? Br J Nutr ; 11 : Rieusset J, Fauconnier J, Paillard M, et al. Disruption of calcium transfer from ER to mitochondria links alterations of mitochondria-associated ER membrane integrity to hepatic insulin resistance. Diabetologia ; 59 3 : Ayoub JJ, Samra MJA, Hlais SA, Bassil MS, Obeid OA. Nutr Diabetes ; 5: e Obeid OA. Low phosphorus status might contribute to the onset of obesity. Obes Rev ; 14 8 : Celik N, Andiran N. The relationship between serum phosphate levels with childhood obesity and insulin resistance. J Pediatr Endocrinol Metab ; 24 : Lin YI, Berger L, Sun Z. Regulation of insulin sensitivity by phosphorus. Diabetes ; Bassil MS, Obeid OA. Phosphorus supplementation recovers the blunted diet-induced thermogenesis of overweight and obese adults: A pilot study. Nutrients ; 8 12 : Hammoud RU, Jabbour MN, Tawil AN, Ghattas H, Obeid OA. Phosphorus supplementation mitigated food intake and growth of rats fed a low-protein diet. Curr Dev Nutr ; 1 8 : e Shimodaira M, Okaniwa S, Nakayama T. Reduced serum phosphorus levels were associated with metabolic syndrome in men but not in women: A cross-sectional study among the japanese population. Ann Nutr Metab ; 71 : Meyer B. Elemental sulfur. Chem Rev ; Zhang H, Huang Y, Bu D, et al. Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor. Sci Rep ; 6: Camargo RL, Branco RCS, de Rezende LF, et al. The effect of taurine supplementation on glucose homeostasis: The role of insulin-degrading enzyme. Cham: Springer International Publishing ; pp. Poloni S, Spritzer PM, Mendes RH, et al. Leptin concentrations and scd-1 indices in classical homocystinuria: Evidence for the role of sulfur amino acids in the regulation of lipid metabolism. Clin Chim Acta ; Kwak HC, Kim Y-M, Oh SJ, Kim SK. Sulfur amino acid metabolism in zucker diabetic fatty rats. Biochem Pharmacol ; 96 3 : Santhosh Kumar B, Priyadarsini KI. Selenium nutrition: How important is it? Biomed Prev Nutr ; 4: Luoma PV, Sotaniemi EA, Korpela H, Kumpulainen J. Serum selenium, glutathione peroxidase activity and high-density lipoprotein cholesterol-effect of selenium supplementation. Res Commun Chem Pathol Pharmacol ; 46 3 : Pillai SS, Sugathan JK, Indira M. Selenium downregulates RAGE and NFκB expression in diabetic rats. Biol Trace Elem Res ; 1 : Stranges S, Marshall JR, Natarajan R, et al. Effects of long-term selenium supplementation on the incidence of type 2 diabetes: A randomized trial. Ann Intern Med ; 4 : Laclaustra M, Navas-Acien A, Stranges S, Ordovas JM, Guallar E. Serum selenium concentrations and diabetes in U. adults: National Health and Nutrition Examination Survey NHANES Environ Health Perspect ; 9 : Kunwar A, Sandur SK, Krishna M, Priyadarsini KI. Curcumin mediates time and concentration dependent regulation of redox homeostasis leading to cytotoxicity in macrophage cells. Eur J Pharmacol ; : Alasfar F, Ben-Nakhi M, Khoursheed M, Kehinde EO, Alsaleh M. Selenium is significantly depleted among morbidly obese female patients seeking bariatric surgery. Obes Surg ; 21 11 : Kim H-N, Song S-W. Concentrations of chromium, selenium, and copper in the hair of viscerally obese adults are associated with insulin resistance. Biol Trace Elem Res ; 2 : Prasad AS. Zinc is an antioxidant and anti-inflammatory agent: Its role in human health. Front Nutr ; 1: Khalid N, Ahmed A, Bhatti MS, Randhawa MA, Ahmad A, Rafaqat R. A question mark on zinc deficiency in million people in Pakistan-possible way out. Crit Rev Food Sci Nutr ; 54 9 : Akhtar S, Ismail T, Atukorala S, Arlappa N. Micronutrient deficiencies in south asia—current status and strategies. Trends Food Sci Technol ; Chabosseau P, Rutter GA. Zinc and diabetes. Arch Biochem Biophys ; Quraishi I, Collins S, Pestaner JP, Harris T, Bagasra O. Role of zinc and zinc transporters in the molecular pathogenesis of diabetes mellitus. Med Hypotheses ; 65 5 : Payahoo L, Ostadrahimi A, Mobasseri M, et al. Effects of zinc supplementation on the anthropometric measurements, lipid profiles and fasting blood glucose in the healthy obese adults. Adv Pharm Bull ; 3 1 : Aysan E, Sahin F, Telci D, et al. Body weight reducing effect of oral boric acid intake. Int J Med Sci ; 8 8 : Doğan A, Demirci S, Apdik H, et al. Mechanism of body weight reducing effect of oral boric Acid intake. Int J Endocrinol ; Hunt CD, Halas ES, Eberhardt MJ. Long-term effects of lactational zinc deficiency on bone mineral composition in rats fed a commercially modified Luecke diet. Biol Trace Elem Res ; 16 2 : López-Cabrera Y, Castillo-García EL, Altamirano-Espino JA, et al. Profile of three boron-containing compounds on the body weight, metabolism and inflammatory markers of diabetic rats. J Trace Elem Med Biol ; Aydın S, Demirci S, Doğan A, Sağraç D, Kaşıkcı E, Şahin F. Boron containing compounds promote the survival and the maintenance of pancreatic β-cells. Mol Biol Rep ; 46 5 : Charlton K, Skeaff S. Iodine fortification: Why, when, what, how, and who? Curr Opin Clin Nutr Metab Care ; 14 6 : Herter-Aeberli I, Cherkaoui M, El Ansari N, et al. Iodine supplementation decreases hypercholesterolemia in iodine-deficient, overweight women: A randomized controlled trial. J Nutr ; 9 : Agbor GA, Taga I, Nguindex DR, et al. Effect of iodine supplementation on antioxidant status of normal and alloxan monohydrate in toxicated rats. Int J Pharmacol ; 7: Al-Attas OS, Al-Daghri NM, Alkharfy KM, et al. Urinary iodine is associated with insulin resistance in subjects with diabetes mellitus type 2. Exp Clin Endocrinol Diabetes ; 10 : Samadi R, Ghanbari M, Shafiei B, Gheibi S, Azizi F, Ghasemi A. High dose of radioactive iodine per se has no effect on glucose metabolism in thyroidectomized rats. Endocrine ; 56 2 : Mancini FR, Rajaobelina K, Dow C, et al. High iodine dietary intake is associated with type 2 diabetes among women of the E3N-EPIC cohort study. Clin Nutr ; 38 4 : Lukaski HC. Lessons from micronutrient studies in patients with glucose intolerance and diabetes mellitus: Chromium and vanadium. Huang H, Chen G, Dong Y, Zhu Y, Chen H. Chromium supplementation for adjuvant treatment of type 2 diabetes mellitus: Results from a pooled analysis. Mol Nutr Food Res ; 62 1 : Panchal SK, Wanyonyi S, Brown L. Selenium, vanadium, and chromium as micronutrients to improve metabolic syndrome. Curr Hypertens Rep ; 19 3 : Tinkov AA, Gatiatulina ER, Popova EV, et al. Early high-fat feeding induces alteration of trace element content in tissues of juvenile male Wistar rats. Paiva AN, Lima JG, Medeiros AC, et al. Beneficial effects of oral chromium picolinate supplementation on glycemic control in patients with type 2 diabetes: A randomized clinical study. Tuzcu M, Sahin N, Orhan C, et al. Impact of chromium histidinate on high fat diet induced obesity in rats. Nutr Metab Lond ; 8: Guimarães MM, Martins Silva Carvalho AC, Silva MS. Chromium nicotinate has no effect on insulin sensitivity, glycemic control, and lipid profile in subjects with type 2 diabetes. J Am Coll Nutr ; 32 4 : Tsiani E, Bogdanovic E, Sorisky A, Nagy L, Fantus IG. Tyrosine phosphatase inhibitors, vanadate and pervanadate, stimulate glucose transport and GLUT translocation in muscle cells by a mechanism independent of phosphatidylinositol 3-kinase and protein kinase C. Diabetes ; 47 11 : Brandt K, Mølgaard JP. Organic agriculture: Does it enhance or reduce the nutritional value of plant foods? J Sci Food Agric ; Hussain A, Larsson H, Kuktaite R, Johansson E. Mineral composition of organically grown wheat genotypes: Contribution to daily minerals intake. Int J Environ Res Public Health ; 7 9 : Johnson D, Ellington J, Eaton W. Development of soil microbial communities for promoting sustainability in agriculture and a global carbon fix. Bouis HE, Chassy BM, Ochanda JO. Genetically modified food crops and their contribution to human nutrition and food quality. Mendoza C. Effect of genetically modified low phytic acid plants on mineral absorption. Hunt JR. Bioavailability of iron, zinc, and other trace minerals from vegetarian diets. Am J Clin Nutr ; 78 3 Suppl. Watzke HJ. Impact of processing on bioavailability examples of minerals in foods. Trends Food Sci Technol ; 9: Gharibzahedi SMT, Jafari SM. The importance of minerals in human nutrition: Bioavailability, food fortification, processing effects and nanoencapsulation. Blaine J, Chonchol M, Levi M. Renal control of calcium, phosphate, and magnesium homeostasis. Clin J Am Soc Nephrol ; 10 7 : Lau WL, Kalantar-Zadeh K, Vaziri ND. The gut as a source of inflammation in chronic kidney disease. Nephron ; 2 : Morais JBS, Severo JS, Santos LR, et al. Role of magnesium in oxidative stress in individuals with obesity. Felsenfeld AJ, Levine BS, Rodriguez M. Pathophysiology of calcium, phosphorus, and magnesium dysregulation in chronic kidney disease. Seminars in dialysis. Wiley Online Library ; Vol. McClain CJ. Nutrition in patients with cirrhosis. Gastroenterol Hepatol N Y ; 12 8 : Makki K, Deehan EC, Walter J, Bäckhed F. The impact of dietary fiber on gut microbiota in host health and disease. Cell Host Microbe ; 23 6 : Homan J, Schijns W, Aarts EO, van Laarhoven CJHM, Janssen IMC, Berends FJ. An optimized multivitamin supplement lowers the number of vitamin and mineral deficiencies three years after Roux-en-Y gastric bypass: A cohort study. Surg Obes Relat Dis ; 12 3 : Diet K, Living H. What boosts more growth hormone: Intermittent fasting or HIIT High Intensity Interval Training? Oguwike F, Offor C, Nwadighoha A, Ebede S. Evaluation of efficacy of cabbage juice Brassica oleracea Linne as potential antiulcer aggent and its effect on the haemostatic mechanism of male albino wistar rats. IOSR J Dent Med Sci ; Sekirov I, Russell SL, Antunes LCM, Finlay BB. Gut microbiota in health and disease. Physiol Rev ; 90 3 : Kim DH, Meza CA, Clarke H, Kim JS, Hickner RC. Vitamin D and endothelial function. Jamali N, Sorenson CM, Sheibani N. Vitamin D and regulation of vascular cell function. Am J Physiol Heart Circ Physiol. Rendina D, De Filippo G, Muscariello R, De Palma D, Fiengo A, De Pascale F, et al. Vitamin D and cardiometabolic disorders. McGreevy C, Williams D. New insights about vitamin D and cardiovascular disease: a narrative review. Ann Intern Med. Norman PE, Powell JT. Vitamin D and cardiovascular disease. Circ Res. De Luca MR, Sorriento D, Massa D, Valente V, De Luise F, Barbato E, et al. Effects of inhibition of the renin-angiotensin system on hypertension-induced target organ damage: clinical and experimental evidence. Monaldi Arch Chest Dis. Probstfield JL, O'Brien KD. Progression of cardiovascular damage: the role of renin-angiotensin system blockade. Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. J Clin Invest. Tishkoff DX, Nibbelink KA, Holmberg KH, Dandu L, Simpson RU. Functional vitamin D receptor VDR in the t-tubules of cardiac myocytes: VDR knockout cardiomyocyte contractility. Simpson RU, Hershey SH, Nibbelink KA. Characterization of heart size and blood pressure in the vitamin D receptor knockout mouse. J Steroid Biochem Mol Biol. Zhou C, Lu F, Cao K, Xu D, Goltzman D, Miao D. Calcium-independent and 1,25 OH 2D3-dependent regulation of the renin-angiotensin system in 1alpha-hydroxylase knockout mice. Kidney Int. Chen S, Law CS, Grigsby CL, Olsen K, Hong TT, Zhang Y, et al. Cardiomyocyte-specific deletion of the vitamin D receptor gene results in cardiac hypertrophy. Meems LM, Cannon MV, Mahmud H, Voors AA, van Gilst WH, Sillje HH, et al. The vitamin D receptor activator paricalcitol prevents fibrosis and diastolic dysfunction in a murine model of pressure overload. Tamayo M, Martin-Nunes L, Val-Blasco A, MJ GMP, Navarro-Garcia JA, Lage E, et al. Beneficial effects of paricalcitol on cardiac dysfunction and remodelling in a model of established heart failure. Br J Pharmacol. Walters MR, Ilenchuk TT, Claycomb WC. J Biol Chem. Green JJ, Robinson DA, Wilson GE, Simpson RU, Westfall MV. Calcitriol modulation of cardiac contractile performance via protein kinase C. J Mol Cell Cardiol. Weishaar RE, Simpson RU. Involvement of vitamin D3 with cardiovascular function. II Direct and indirect effects. Am J Physiol Cell Physiol. Somjen D, Weisman Y, Kohen F, Gayer B, Limor R, Sharon O, et al. Zehnder D, Bland R, Chana RS, Wheeler DC, Howie AJ, Williams MC, et al. Synthesis of 1,dihydroxyvitamin D 3 by human endothelial cells is regulated by inflammatory cytokines: a novel autocrine determinant of vascular cell adhesion. J Am Soc Nephrol. Ni W, Watts SW, Ng M, Chen S, Glenn DJ, Gardner DG. Elimination of vitamin D receptor in vascular endothelial cells alters vascular function. Wee CL, Mokhtar SS, Singh KKB, Yahaya S, Leung SWS, Rasool AHG. Calcitriol supplementation ameliorates microvascular endothelial dysfunction in vitamin D-deficient diabetic rats by upregulating the vascular eNOS protein expression and reducing oxidative stress. Oxid Med Cell Longev. Said MA. Vitamin D attenuates endothelial dysfunction in streptozotocin induced diabetic rats by reducing oxidative stress. Arch Physiol Biochem. Andrukhova O, Slavic S, Zeitz U, Riesen SC, Heppelmann MS, Ambrisko TD, et al. Vitamin D is a regulator of endothelial nitric oxide synthase and arterial stiffness in mice. Mol Endocrinol. Kobzar G. Inhibition of platelet activation using vitamins. Sultan M, Twito O, Tohami T, Ramati E, Neumark E, Rashid G. Vitamin D diminishes the high platelet aggregation of type 2 diabetes mellitus patients. Lu C, Yin Y, Cui Y, Wang L, Bai Y, Li J, et al. Cell cycle. Cimmino G, Morello A, Conte S, Pellegrino G, Marra L, Golino P, et al. Vitamin D inhibits Tissue Factor and CAMs expression in oxidized low-density lipoproteins-treated human endothelial cells by modulating NF-kappaB pathway. Eur J Pharmacol. Mohammad S, Mishra A, Ashraf MZ. Emerging role of vitamin D and its associated molecules in pathways related to pathogenesis of thrombosis. Martinez-Moreno JM, Herencia C, Montes de Oca A, Munoz-Castaneda JR, Rodriguez-Ortiz ME, Diaz-Tocados JM, et al. Vitamin D modulates tissue factor and protease-activated receptor 2 expression in vascular smooth muscle cells. FASEB J. Thierry-Palmer M, Carlyle KS, Williams MD, Tewolde T, Caines-McKenzie S, Bayorh MA, et al. Plasma hydroxyvitamin D concentrations are inversely associated with blood pressure of Dahl salt-sensitive rats. Pal E, Hadjadj L, Fontanyi Z, Monori-Kiss A, Mezei Z, Lippai N, et al. Vitamin D deficiency causes inward hypertrophic remodeling and alters vascular reactivity of rat cerebral arterioles. PLoS ONE. Enkhjargal B, Malaguit J, Ho WM, Jiang W, Wan W, Wang G, et al. J Cereb Blood Flow Metab. Cardus A, Panizo S, Encinas M, Dolcet X, Gallego C, Aldea M, et al. Wong MS, Leisegang MS, Kruse C, Vogel J, Schurmann C, Dehne N, et al. Vitamin D promotes vascular regeneration. Oh J, Weng S, Felton SK, Bhandare S, Riek A, Butler B, et al. Lee JH, O'Keefe JH, Bell D, Hensrud DD, Holick MF. Vitamin D deficiency an important, common, and easily treatable cardiovascular risk factor? J Am Coll Cardiol. Alam U, Najam O, Al-Himdani S, Benoliel S, Jinadev P, Berry JL, et al. Marked vitamin D deficiency in patients with diabetes in the UK: ethnic and seasonal differences and an association with dyslipidaemia. Diabet Med. Knekt P, Laaksonen M, Mattila C, Harkanen T, Marniemi J, Heliovaara M, et al. Serum vitamin D and subsequent occurrence of type 2 diabetes. Pittas AG, Sun Q, Manson JE, Dawson-Hughes B, Hu FB. Plasma hydroxyvitamin D concentration and risk of incident type 2 diabetes in women. Diabetes Care. Liu E, Meigs JB, Pittas AG, Economos CD, McKeown NM, Booth SL, et al. Predicted hydroxyvitamin D score and incident type 2 diabetes in the Framingham Offspring Study. Am J Clin Nutr. Song Y, Wang L, Pittas AG, Del Gobbo LC, Zhang C, Manson JE, et al. Blood hydroxy vitamin D levels and incident type 2 diabetes: a meta-analysis of prospective studies. Parker J, Hashmi O, Dutton D, Mavrodaris A, Stranges S, Kandala NB, et al. Levels of vitamin D and cardiometabolic disorders: systematic review and meta-analysis. Pereira-Santos M, Costa PR, Assis AM, Santos CA, Santos DB. Obesity and vitamin D deficiency: a systematic review and meta-analysis. Obes Rev. Pilz S, Tomaschitz A, Ritz E, Pieber TR. Vitamin D status and arterial hypertension: a systematic review. Nature reviews Cardiology. Scragg R, Sowers M, Bell C. Serum hydroxyvitamin D, ethnicity, and blood pressure in the Third National Health and Nutrition Examination Survey. Judd SE, Nanes MS, Ziegler TR, Wilson PW, Tangpricha V. Optimal vitamin D status attenuates the age-associated increase in systolic blood pressure in white Americans: results from the third National Health and Nutrition Examination Survey. Forman JP, Giovannucci E, Holmes MD, Bischoff-Ferrari HA, Tworoger SS, Willett WC, et al. Plasma hydroxyvitamin D levels and risk of incident hypertension. Ke L, Graubard BI, Albanes D, Fraser DR, Weinstein SJ, Virtamo J, et al. Hypertension, pulse, and other cardiovascular risk factors and vitamin D status in Finnish men. Burgaz A, Orsini N, Larsson SC, Wolk A. Blood hydroxyvitamin D concentration and hypertension: a meta-analysis. J Hypertens. Kunutsor SK, Apekey TA, Steur M. Vitamin D and risk of future hypertension: meta-analysis of , participants. Eur J Epidemiol. Pittas AG, Chung M, Trikalinos T, Mitri J, Brendel M, Patel K, et al. Systematic review: vitamin D and cardiometabolic outcomes. Jorde R, Grimnes G. Vitamin D and metabolic health with special reference to the effect of vitamin D on serum lipids. Prog Lipid Res. Han Y, Han K, Zhang Y, Zeng X. Serum hydroxyvitamin D might be negatively associated with hyperuricemia in U. adults: an analysis of the National Health and Nutrition Examination Survey — J Endocrinol Invest. Isnuwardana R, Bijukchhe S, Thadanipon K, Ingsathit A, Thakkinstian A. Association between vitamin D and uric acid in adults: a systematic review and meta-analysis. Horm Metab Res. Chen Y, Cheng J, Chen Y, Wang N, Xia F, Chen C, et al. Association between serum vitamin D and uric acid in the eastern Chinese population: a population-based cross-sectional study. BMC Endocr Disord. Charoenngam N, Ponvilawan B, Ungprasert P. Vitamin D insufficiency and deficiency are associated with a higher level of serum uric acid: a systematic review and meta-analysis. Modern Rheumatology. Cameli M, Lembo M, Sciaccaluga C, Bandera F, Ciccone MM, D'Andrea A, et al. Identification of cardiac organ damage in arterial hypertension: insights by echocardiography for a comprehensive assessment. Lembo M, Esposito R, Santoro C, Lo Iudice F, Schiano-Lomoriello V, Fazio V, et al. Lembo M, Manzi MV, Mancusi C, Morisco C, Rao MAE, Cuocolo A, et al. Advanced imaging tools for evaluating cardiac morphological and functional impairment in hypertensive disease. Mancusi C, Trimarco V, Losi MA, Canciello G, Morisco C, Manzi MV, et al. Impact of visit-to-visit blood pressure variability on hypertensive-mediated target organ damage and future cardiovascular events: the Campania salute network. Manzi MV, Mancusi C, Trimarco V, Izzo R, Franco D, Barbato E, et al. The intergated approach to the management of arterial hypertension: the Campania Salute Network. Panminerva Med. Chen S, Swier VJ, Boosani CS, Radwan MM, Agrawal DK. Vitamin D deficiency accelerates coronary artery disease progression in swine. Arterioscler Thromb Vasc Biol. Shirwany NA, Zou MH. Arterial stiffness: a brief review. Acta Pharmacol Sin. Al Mheid I, Patel R, Murrow J, Morris A, Rahman A, Fike L, et al. Vitamin D status is associated with arterial stiffness and vascular dysfunction in healthy humans. Pirro M, Manfredelli MR, Helou RS, Scarponi AM, Schillaci G, Bagaglia F, et al. Association of parathyroid hormone and OH-vitamin D levels with arterial stiffness in postmenopausal women with vitamin D insufficiency. J Atheroscler Thromb. Lee JI, Oh SJ, Ha WC, Kwon HS, Sohn TS, Son HS, et al. Serum hydroxyvitamin D concentration and arterial stiffness among type 2 diabetes. Diabetes Res Clin Pract. London GM, Guerin AP, Verbeke FH, Pannier B, Boutouyrie P, Marchais SJ, et al. Mineral metabolism and arterial functions in end-stage renal disease: potential role of hydroxyvitamin D deficiency. Melamed ML, Muntner P, Michos ED, Uribarri J, Weber C, Sharma J, et al. Serum hydroxyvitamin D levels and the prevalence of peripheral arterial disease: results from NHANES to Rapson IR, Michos ED, Alonso A, Hirsch AT, Matsushita K, Reis JP, et al. Serum hydroxyvitamin D is associated with incident peripheral artery disease among white and black adults in the ARIC study cohort. Yuan J, Jia P, Hua L, Xin Z, Yang JK. Vitamin D deficiency is associated with risk of developing peripheral arterial disease in type 2 diabetic patients. BMC Cardiovasc Disord. Capusa C, Stefan G, Stancu S, Ilyes A, Dorobantu N, Mircescu G. Subclinical cardiovascular disease markers and vitamin D deficiency in non-dialysis chronic kidney disease patients. Arch Med Sci. Iannuzzo G, Forte F, Lupoli R, Di Minno MND. Association of vitamin D deficiency with peripheral arterial disease: a meta-analysis of literature studies. J Clin Endocrinol Metab. Nsengiyumva V, Fernando ME, Moxon JV, Krishna SM, Pinchbeck J, Omer SM, et al. The association of circulating hydroxyvitamin D concentration with peripheral arterial disease: a meta-analysis of observational studies. Carpinella G, Pagano G, Buono F, Petitto M, Guarino G, Orefice G, et al. Prognostic value of combined target-organ damage in patients with essential hypertension. Cave A, Grieve D, Johar S, Zhang M, Shah AM. NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology. Philos Trans R Soc Lond B Biol Sci. Kannan A, Janardhanan R. Hypertension as a risk factor for heart failure. Curr Hypertens Rep. Mohan M, Dihoum A, Mordi IR, Choy AM, Rena G, Lang CC. Left ventricular hypertrophy in diabetic cardiomyopathy: a target for intervention. Front Cardiovasc Med. Schillaci G, Vaudo G, Reboldi G, Verdecchia P, Lupattelli G, Pasqualini L, et al. High-density lipoprotein cholesterol and left ventricular hypertrophy in essential hypertension. Fallo F, Catena C, Camozzi V, Luisetto G, Cosma C, Plebani M, et al. Low serum hydroxyvitamin D levels are associated with left ventricular hypertrophy in essential hypertension. Nutr Metab Cardiovasc Dis. Pludowski P, Jaworski M, Niemirska A, Litwin M, Szalecki M, Karczmarewicz E, et al. Vitamin D status, body composition and hypertensive target organ damage in primary hypertension. J Steroid Biochem Mo. Seker T, Gur M, Ucar H, Turkoglu C, Baykan AO, Ozaltun B, et al. Lower serum hydroxyvitamin D level is associated with impaired myocardial performance and left ventricle hypertrophy in newly diagnosed hypertensive patients. Anatol J Cardiol. Verdoia M, Solli M, Ubertini E, Erbetta R, Gioscia R, Afifeh AMS, et al. Low vitamin D levels affect left ventricular wall thickness in severe aortic stenosis. J Cardiovasc Med. Gluba-Brzozka A, Franczyk B, Cialkowska-Rysz A, Olszewski R, Rysz J. Impact of Vitamin D on the cardiovascular system in advanced chronic kidney disease CKD and dialysis patients. Lai S, Coppola B, Dimko M, Galani A, Innico G, Frassetti N, et al. Vitamin D deficiency, insulin resistance, and ventricular hypertrophy in the early stages of chronic kidney disease. Ren Fail. Ameri P, Canepa M, Milaneschi Y, Spallarossa P, Leoncini G, Giallauria F, et al. Relationship between vitamin D status and left ventricular geometry in a healthy population: results from the Baltimore Longitudinal Study of Aging. J Intern Med. Visco V, Pascale AV, Virtuoso N, Mongiello F, Cinque F, Gioia R, et al. Serum Uric Acid and Left Ventricular Mass in Essential Hypertension. Schiffrin EL, Lipman ML, Mann JF. Chronic kidney disease: effects on the cardiovascular system. Meccariello A, Buono F, Verrengia E, Orefice G, Grieco F, Romeo F, et al. Microalbuminuria predicts the recurrence of cardiovascular events in patients with essential hypertension. Teng M, Wolf M, Ofsthun MN, Lazarus JM, Hernan MA, Camargo CA Jr, et al. Activated injectable vitamin D and hemodialysis survival: a historical cohort study. Kovesdy CP, Ahmadzadeh S, Anderson JE, Kalantar-Zadeh K. Association of activated vitamin D treatment and mortality in chronic kidney disease. Arch Intern Med. Yilmaz F, Sozel H. Relationship between hydroxyvitamin D and microalbuminuria in patients with newly diagnosed essential hypertension. Clin Exp Hypertens. Ali MI, Fawaz LA, Sedik EE, Nour ZA, Elsayed RM. Diabetes Metab Syndr. Ucak S, Sevim E, Ersoy D, Sivritepe R, Basat O, Atay S. Evaluation of the relationship between microalbuminuria and OH vitamin D levels in patients with type 2 diabetes mellitus. Aging Male. Wang TJ, Pencina MJ, Booth SL, Jacques PF, Ingelsson E, Lanier K, et al. Vitamin D deficiency and risk of cardiovascular disease. |
| The effect of vitamin D on insulin resistance in patients with type 2 diabetes | Article CAS Google Scholar Simpson RU, Thomas GA, Arnold AJ: Identification of 1, dihydroxyvitamin D3 receptors and activities in muscle. Draznin B, Sussman KE, Eckel RH, Kao M, Yost T, Sherman NA. Impact of intermittent fasting on health and disease processes. Impact of micronutrient deficiencies on obesity. Proc Nutr Soc ; 69 4 : Am J Clin Nutr ; 78 3 Suppl. |
| The Role of Mineral Deficiencies in Insulin Resistance and Obesity | Bentham Science | Diabetes Res Clin Pract. Insulin resistance and nutritional deficiencies Access Panel ×. Vitamin D nutritionak Tissue Factor and Boost training motivation expression in oxidized low-density lipoproteins-treated human endothelial cells by modulating NF-kappaB pathway. Somjen D, Weisman Y, Kohen F, Gayer B, Limor R, Sharon O, et al. J Neurol ; 5 : |
Insulin resistance and nutritional deficiencies -
The study also showed that how long someone had diabetes and having high systolic blood pressure the top number also increased risk of foot ulcers.
Researchers found that the chance of developing insulin resistance went down with each additional amount of vitamin D supplement taken. Researchers say this might indicate that vitamin D3 is a protective factor in the occurrence of insulin resistance because it helps lower inflammation and inflammation raises your risk for insulin resistance.
Berg, A. Salvetti, A. The inter-relationship between insulin resistance and hypertension. Drugs 46 Suppl 2 , — Claro da Silva, T. Vitamin D3 transactivates the zinc and manganese transporter SLC30A10 via the Vitamin D receptor.
Download references. Department of Clinical Medicine, School of the First Clinical Medicine, Anhui Medical University, No. You can also search for this author in PubMed Google Scholar. and X. conceived the idea; G. and Z. wrote the manuscript; Z. and Y. collected and read the literature and revised the article; Q.
read through and corrected the manuscript. All authors read and approved the final manuscript. is the first author. is the co-first author. is the corresponding author of this paper. Correspondence to Shuangquan Wang. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.
If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.
Reprints and permissions. Xu, Z. Association between vitamin D3 levels and insulin resistance: a large sample cross-sectional study. Sci Rep 12 , Download citation. Received : 13 August Accepted : 01 December Published : 07 January Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Environmental Science and Pollution Research By submitting a comment you agree to abide by our Terms and Community Guidelines.
If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily. Skip to main content Thank you for visiting nature.
nature scientific reports articles article. Download PDF. Subjects Diseases Endocrinology. Abstract Previous studies have shown that vitamin D3 may be a potential factor in insulin resistance, but the relationship between vitamin D3 and insulin resistance still remains controversial.
Introduction Insulin resistance is a systemic metabolic disorder characterized by decreased insulin sensitivity 1 , which then progresses to a decrease in insulin action 2. Methods Database All data in this study were obtained from the National Health and Nutrition Examination Survey NHANES database, which was a cross-sectional survey in the United States.
Study population The data of NHANES database from to was selected. Figure 1. Flowchart of patient selection. Full size image. Result Characteristics of study population In this study, 49, participants were obtained from the NHANES database.
Table 1 Baseline characteristics of the study participants. Full size table. Table 2 Univariate analysis for insulin resistance. Table 3 The association between Vit D3 and insulin resistance in a multiple regression model. Figure 2. Association between Vitamin D3 and insulin resistance.
Figure 3. Subgroup analysis. Discussion Cross-sectional study is considered as a critical tool to assess the effects of treatment or risk factors for disease. Conclusion In conclusion, the results of this cross-sectional study based on the data of five cycles — in American NHANE database demonstrated that there is a correlation between vitamin D3 level and insulin resistance.
Abbreviations BMI: Body mass index FBG: Fasting blood-glucose VitD3: Vitamin D3 Hb-A1c: Glycosylated hemoglobin; TC: Total cholesterol ALT: Alanine aminotransferase BUN: Blood urea nitrogen W.
C: Waist TG: Triglyceride CI: Confidence interval OR: Odds ratio HUA: Hyperuricemia. References Yaribeygi, H. Article CAS PubMed Google Scholar Artunc, F. Article CAS PubMed Google Scholar Sampath Kumar, A.
Article CAS PubMed Google Scholar Gong, R. Article PubMed Google Scholar Neuenschwander, M. Article Google Scholar Wu, Y.
Article PubMed PubMed Central Google Scholar Onyango, A. Article CAS PubMed PubMed Central Google Scholar Guo, J. Article CAS PubMed Google Scholar Kennel, K.
Article PubMed PubMed Central Google Scholar Sui, A. Article CAS PubMed Google Scholar Holick, M. Article CAS PubMed Google Scholar Sawarkar, S. Article PubMed Google Scholar Wang, G. Article CAS Google Scholar Harvey, L.
Article CAS PubMed Google Scholar Sonneveld, R. Article CAS PubMed Google Scholar Machado, C. Article CAS Google Scholar Aludwan, M.
Article PubMed Google Scholar Wallace, H. Article PubMed Google Scholar Niroomand, M. Article CAS PubMed Google Scholar Cederholm, T. Article CAS Google Scholar Carrillo-Larco, R. Article PubMed PubMed Central Google Scholar Shashaj, B.
Article CAS PubMed Google Scholar Elliott, W. Article PubMed Google Scholar White, G. Article PubMed Google Scholar Ricci, C. Article PubMed Google Scholar Flegal, K. Article CAS PubMed Google Scholar Féki, I. Article PubMed Google Scholar Chung, H. Article CAS PubMed Google Scholar WHO Expert Consultation.
Article Google Scholar Lotta, L. Article PubMed Google Scholar Yamamoto, E. Article CAS PubMed Google Scholar de Vries, M. Article PubMed Google Scholar Berridge, M.
Article CAS PubMed Google Scholar El-Sharkawy, A. Article CAS Google Scholar Akahane, T. Article CAS PubMed Central Google Scholar Li, C. Article CAS PubMed Google Scholar Guarino, M. Article CAS PubMed Google Scholar Yang, C.
Article CAS PubMed Google Scholar Li, X. Article CAS PubMed Google Scholar Traversy, G. Article PubMed PubMed Central Google Scholar Garbossa, S. Article CAS PubMed Google Scholar Das, S. Article CAS PubMed Google Scholar Raygor, V.
Article CAS Google Scholar Han, F. Article CAS PubMed PubMed Central Google Scholar Chalé, A. Article PubMed Google Scholar Berg, A. Article CAS PubMed PubMed Central Google Scholar Salvetti, A.
Article PubMed Google Scholar Claro da Silva, T. Article CAS PubMed Google Scholar Download references. Author information Author notes These authors contributed equally: Zixin Xu, Rongpeng Gong, Gang Luo and Mingxiang Wang.
View author publications. Ethics declarations Competing interests The authors declare no competing interests. Additional information Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4. About this article. Cite this article Xu, Z. Copy to clipboard. Comments By submitting a comment you agree to abide by our Terms and Community Guidelines. About the journal Open Access Fees and Funding About Scientific Reports Contact Journal policies Calls for Papers Guide to referees Editor's Choice Journal highlights.
Publish with us For authors Language editing services Submit manuscript. Search Search articles by subject, keyword or author. Show results from All journals This journal. Descriptive statistics are presented as the mean ± standard deviation for normal distribution, and median min.
for non-normal distribution. Categorical variables were expressed as number and percentage. Normally distributed parameters were evaluated by the t -test, while non-normally distributed parameters were investigated by the Mann-Whitney U test.
In the overweight and obese subjects, changes in anthropometric and laboratory findings after vitamin D supplementation were evaluated by the repeated measures ANOVA test. The data of parameters at baseline and after 6 months of supplementation were evaluated by the paired t- test.
Analysis of the percent relative change in all parameters between groups to demonstrate the effect of treatment was performed by ANOVA. The magnitude of absolute change from baseline to after vitamin D supplementation values was indicated by Δ.
To establish the relationships between changes in parameters following vitamin D supplementation, the correlations of change in HOMA-IR level with changes in anthropometric and laboratory findings were analyzed by Spearman correlation analysis.
Baseline demographic, anthropometric and laboratory characteristics of the groups are shown in Table I. The study population of Caucasian women consisted of 72 Baseline mean hydroxyvitamin D 25 OH D level was 6.
Of all subjects, the mean age was In overweight subjects, baseline FBG, insulin, and HOMA-IR levels were significantly lower than in obese subjects Baseline demographic, anthropometric and laboratory characteristics of all cases of overweight and obese patients.
Numerical variables with normal distribution are expressed as mean ± standard deviation. Numerical variables without normal distribution are shown as median min.
BMI — body mass index, WHR — waist-hip ratio, SBP — systolic blood pressure, DBP — diastolic blood pressure, TC — total cholesterol, LDL-C — low-density lipoprotein cholesterol, HDL-C — high-density lipoprotein cholesterol, TG — triglyceride, FBG — fasting blood glucose, 25 OH D — hydroxy vitamin D, iPTH — intact parathormone, HOMA-IR — homeostasis model assessment of insulin resistance.
In both groups, the effects of vitamin D supplementation on anthropometric and laboratory findings are shown in Table II. After supplementation, the laboratory parameters of overweight and obese subjects were as follows.
Following vitamin D 3 supplementation in overweight and obese subjects, serum 25 OH D increased from 6. The relative changes of all parameters before and after supplementation compared between overweight and obese groups are shown in Table III.
The effect of supplementation on percent change in all parameters is shown in Table II. Effects of vitamin D supplementation on anthropometric and laboratory parameters in overweight and obese subjects.
obese baseline-after supplementation. Relative changes in variables over the course of vitamin D supplementation. The correlation of changes in 25 OH D and HOMA-IR levels with changes in anthropometric and laboratory findings after supplementation are shown in Table IV. The correlation of change in 25 OH D and HOMA-IR levels in overweight and obese subjects is shown in Figure 2.
Change in 25 OH Dlevel is a predictor of change in HOMA-IR level. Correlation of change in 25 OH D and HOMA-IR levels with the change in anthropometric and laboratory parameters in overweight and obese subjects.
Correlation between changes baseline vs. sixth month in 25 OH D levels and HOMA-IR. Vitamin D deficiency and obesity are nutritional disorders that affect people worldwide. Several studies have demonstrated that supplementation of vitamin D has various effects on obesity, hypertension, DM, insulin sensitivity, lipid parameters, inflammatory markers and atherosclerosis risk.
It is well recognized that the overweight population has a high prevalence of cardiovascular disease CVD risk factors such as hypertension, type 2 DM, hyperlipidemia, and atherosclerosis, similar to obese subjects.
In rats and humans, adipose tissue has been found to be the main storage site of vitamin D [ 22 , 23 ]. The mechanism is not clear, but it is suggested that obesity can cause vitamin D deficiency through inadequate intake or as a result of deposition of vitamin D in the large adipose tissue mass [ 24 ].
Additionally, obese people spend less time outside and are exposed to less UV radiation [ 25 ]. Vitamin D has effects on pancreatic islet cells through the vitamin D receptor VDR , and polymorphisms of the VDR gene are related to insulin resistance and impaired insulin secretion [ 26 ].
Pancreatic β-cells have receptors for the active form of vitamin D, and the local production of 1α, 25 OH 2 D 3 might be an essential mediator of islet function [ 27 ]. Some studies have demonstrated a negative correlation between serum vitamin D levels and insulin resistance.
A prospective study revealed an inverse relationship between baseline serum 25 OH D and year risk of hyperglycemia, metabolic syndrome, and insulin resistance [ 28 ].
It is thought that vitamin D supplementation may be a cost-effective preventative and therapeutic agent for the management of insulin resistance and DM in obese individuals [ 30 ]. The present study demonstrated vitamin D-deficient overweight and obese subjects had higher HOMA-IR levels at baseline, whereas at the sixth month of supplementation it had declined.
This result is important because it emphasizes that vitamin D deficiency should be corrected to prevent diseases caused by high insulin resistance. In our study, the obese group had higher insulin resistance than the overweight group; therefore, supplementation with vitamin D may be more beneficial for people with higher insulin resistance.
Vitamin D status is related to increased levels of endothelial dysfunction biomarkers, inflammatory markers and cardiometabolic risk factors in obese non-diabetic individuals [ 31 ].
The excess of macronutrients in the adipose tissues stimulates the release of inflammatory mediators and reduces production of adiponectin, predisposing to a pro-inflammatory state and oxidative stress.
Management of obesity can help reduce the risks of CVD and inhibits release of inflammatory mediators [ 32 ]. However, a recent meta-analysis indicated that vitamin D supplementation had no effect on plasma leptin and adiponectin levels [ 33 ].
Telomeres protect chromosomes from deterioration and fusion during mitosis. Higher vitamin D levels and longer telomere length have been associated with lower risk of several chronic diseases and all-cause mortality.
A positive association was established between 25 OH D levels and telomere length [ 34 ]. Some studies indicate that low 25 OH D levels may lead to dyslipidemia. In the present study, vitamin D deficient women had higher LDL-C concentrations. After vitamin D supplementation, we observed LDL-C reduction in both overweight and obese subjects and TG reduction only in overweight subjects.
Despite these reductions, no significant difference was found in TC and HDL-C levels. The mechanisms responsible for dyslipidemia in vitamin D deficient individuals are not fully understood.
A positive relationship between serum 25 OH D level and apolipoprotein AI with HDL-C levels is well known. Vitamin D can influence the formation of HDL-C particles [ 35 ].
Also, vitamin D status may affect the serum lipid levels by the effect of 1,25 OH 2 D 3 , which leads to inhibition of murine bone marrow stromal cell differentiation and regulates adipogenesis; it also leads to increased lipogenesis and lipolysis [ 36 ].
Consistent with our results, an investigation of the effects of hydroxyvitamin D on fasting lipid profile resulted in a negative correlation of 25 OH D concentration with both total cholesterol and LDL-C [ 29 ].
The relationship between vitamin D deficiency and CVD has been investigated in many studies. Active metabolites of vitamin D bind to the VDR, which regulates many genes in essential processes and has a role in pathways of CVD, including inflammation, thrombosis, and the renin-angiotensin system [ 37 ].
Women with vitamin D deficiency had increased CVD risk biomarkers such as homocysteine, high-sensitivity C-reactive protein CRP , cystatin-C, uric acid, and HbA 1c levels compared to those with sufficient vitamin D levels [ 38 ]. Investigation of the possible role of vitamin D deficiency in statin-associated myalgia shows that low 25 OH D levels are related to myalgia in patients on statin therapy [ 39 ].
In addition, peripheral artery disease patients had significantly higher serum concentrations of trans fatty acids and lower plasma levels of vitamin D [ 40 ]. Vitamin D induces prostacyclin in vascular smooth muscle cells; possibly, it is a vasoactive agent and may play a protective role in the development of atherosclerosis [ 41 ].
Gurses et al. reported that endothelial function is impaired in vitamin D deficient young premenopausal women; 6-month supplementation resulted in amelioration [ 42 ].
Non-alcoholic fatty liver disease NAFLD is the most common chronic liver disease worldwide, frequently co-existing with obesity, and has been recognized as an independent risk factor for CVD.
Evidence from an increasing number of studies suggests that NAFLD may be a hepatic manifestation of metabolic syndrome [ 43 ]. Lifestyle changes and statin treatment have beneficial effects on NAFLD [ 44 ]. As a result of the correlation between hyperandrogenemia and NAFLD, bioavailable testosterone is independently associated with the fatty liver index in postmenopausal women [ 45 ].
Comparing the effect of orlistat versus metformin on body composition and insulin resistance in obese premenopausal women, it was found that orlistat and metformin produced similar improvement in insulin and glucose homeostasis [ 46 ]. Vitamin D deficiency is also associated with NAFLD and has even been correlated with the severity of the disease [ 47 ].
Vitamin D supplementation has a therapeutic role in vitamin D deficient adults with NAFLD [ 48 ]. Also, low 25 OH D levels are associated with advanced fibrosis and severe inflammation in autoimmune hepatitis.
Vitamin D level was suggested as a biomarker that predicts response to therapy and histological features in autoimmune hepatitis [ 49 ]. In our study, both overweight and obese groups, after 6-month vitamin D supplementation, had a decline in iPTH concentrations and elevation in calcium levels.
Studies showed that patients with secondary hyperparathyroidism have excess body weight and fat tissue [ 50 ]. It is suggested that PTH may cause insulin resistance by reducing glucose uptake by the liver, muscle, and adipose cells [ 51 ]. A recent study revealed that vitamin D supplementation has no effect on CRP, interleukin, or tumor necrosis factor-α concentrations [ 52 ].
The 25 OH D measurement before and after supplementation may not be a mirror of lifetime vitamin D status and progression of subclinical atherosclerosis over several years.
In our opinion, these results may be a partial reflection of the situation of vitamin D deficiency results. The results suggest that vitamin D supplementation may be protective for possible dyslipidemia and insulin resistance, especially in patients above the normal weight.
Our study has several limitations. First, we analyzed baseline and 6-month measurements of parameters; frequent and longitudinal series of measurements may be more effective to evaluate the results. Second, this study was not a randomized placebo-controlled study.
Third, we investigated the parameters in overweight and obese premenopausal women; in heterogeneous groups such as postmenopausal women and the male population, the results might have been different.
Sun exposure and dietary daily vitamin D intake were not assessed, because this information was not available.
In conclusion, in healthy vitamin D deficient overweight and obese premenopausal women, 25 OH D levels negatively correlated with HOMA-IR and LDL-C after vitamin D supplementation. These results may help highlight the importance of vitamin D supplementation to improve insulin secretion and insulin sensitivity, thereby indirectly influencing lipid metabolism and eventually prevention of atherosclerosis and cardiovascular mortality.
Resistanfe studies have looked at the Deficienxies of vitamin D in deficiecnies and have Insulin resistance and nutritional deficiencies an association between low levels of Insulln D and increased Insulin resistance and nutritional deficiencies Blood sugar stabilization type 2 diabetes and its complications. Resistajce recent study linked low vitamin D levels to a higher likelihood of deficienvies ulcers nutritioonal older nutrihional with diabetes. The study was the first to assess vitamin D levels among people who were in the hospital with a diabetic foot ulcer. Vitamin D levels were found to be steadily lower as the severity of the ulcer worsened. In fact, people with the most favorable foot ulcer least severe based on the grading scalehad vitamin D levels that were more than twice that seen in people with the worst stage or grade of ulcer. The study included people aged 60 to 90 who were in the hospital with type 2 diabetes, with and without foot ulcers. Thank you for visiting Insulin resistance and nutritional deficiencies. You are defciencies a browser version with limited nutrihional for Insulin resistance and nutritional deficiencies. To obtain the best Herbal remedies for colds, we recommend you use a more up nutritlonal date browser resistwnce turn deficienciea compatibility mode in Resistsnce Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Previous studies have shown that vitamin D3 may be a potential factor in insulin resistance, but the relationship between vitamin D3 and insulin resistance still remains controversial. At present, more research is needed to explore the relationship between vitamin D3 and insulin resistance. The samples from to in NHANES database were analyzed to Investigate the relationship and the potential mechanism.
Ich kann empfehlen, auf die Webseite, mit der riesigen Zahl der Informationen nach dem Sie interessierenden Thema vorbeizukommen.
die Unvergleichliche Mitteilung
Es ist Sie offenbar haben sich geirrt...
Die sehr ausgezeichnete Idee
Die Stunde von der Stunde ist nicht leichter.