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: Calcium and liver health| The Effect of Calcium on the Liver | X Facebook LinkedIn. This Issue. Share X Facebook Email LinkedIn. February Ann Gerhardt, MD ; Arthur Greenberg, MD ; James J. Reilly Jr, MD ; et al David H. Van Thiel, MD. Author Affiliations From the Division of Clinical Nutrition, Department of Internal Medicine, School of Medicine, University of California, Davis Dr Gerhardt and the Renal-Electrolyte Dr Greenberg and Gastroenterology Divisions Dr Van Thiel of the Department of Medicine and the Department of Surgery Dr Reilly , University of Pittsburgh School of Medicine. visual abstract icon Visual Abstract. Access through your institution. Add or change institution. Download PDF Full Text Cite This Citation Gerhardt A , Greenberg A , Reilly JJ , Van Thiel DH. This study aimed to evaluate the effect of four different dietary calcium and VitD 3 cholecalciferol levels on the development of high-fat, high-fructose HFHFr diet-induced nonalcoholic fatty liver disease and AMP-activated protein kinase AMPK phosphorylation. Thirty male Wistar rats were fed with normal or HFHFr diet containing low calcium 0. After 60 days, anthropometric, metabolic and hepatic parameters were evaluated. The effect of the experimental diets on liver AMPK phosphorylation was also investigated. Rats fed on high calcium plus VitD 3 diets, especially VHCD, demonstrated lower adiposity, serum liver enzymes, hepatic lipid accumulation and steatosis. The LCD diet also decreased hepatic lipid content and fatty changes. The results showed high calcium plus VitD 3 intakes considerably prevent biochemical and hepatic changes induced by HFHFr diet, probably via an insulin and AMPK-independent pathway. A low intake of these two nutrients was also linked with a significant decrease in HFHFr diet-induced hepatic steatosis. This is a preview of subscription content, log in via an institution to check access. Rent this article via DeepDyve. Institutional subscriptions. Lazo M, Clark JM The epidemiology of nonalcoholic fatty liver disease: a global perspective. Semin Liver Dis — Article Google Scholar. Fabbrini E, Sullivan S, Klein S Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology — Article CAS Google Scholar. Keast DR, Gallant KMH, Albertson AM, Gugger CK, Holschuh NM Associations between yogurt, dairy, calcium, and vitamin D intake and obesity among us children aged 8—18 years: NHANES, — Nutrients — Tidwell DK, Valliant MW Higher amounts of body fat are associated with inadequate intakes of calcium and vitamin D in African American women. Nutr Res — Samadi M, Sadrzadeh-Yeganeh H, Azadbakht L, Feizi A, Jafarian K, Sotoudeh G Dietary calcium intake and risk of obesity in school girls aged 8—10 years. J Res Med Sci Google Scholar. Ferreira TDS, Rocha TM, Klein MRST, Sanjuliani AF Vitamin D deficiency is associated with insulin resistance independent of intracellular calcium, dietary calcium and serum levels of parathormone, calcitriol and calcium in premenopausal women. Nutr Hosp — da Silva FerreiraT, Torres MRSG, Sanjuliani AF Dietary calcium intake is associated with adiposity, metabolic profile, inflammatory state and blood pressure, but not with erythrocyte intracellular calcium and endothelial function in healthy pre-menopausal women. Brit J Nutr — Moore-Schiltz L, Albert JM, Singer ME, Swain J, Nock NL Dietary intake of calcium and magnesium and the metabolic syndrome in the National Health and Nutrition Examination NHANES — data. Kim KJ, Kim YJ, Kim SH, An JH, Yoo HJ, Kim HY, Seo JA, Kim SG, Kim NH, Choi KM Vitamin D status and associated metabolic risk factors among North Korean refugees in South Korea: a cross-sectional study. BMJ Open. doi: Küçükazman M, Ata N, Dal K, Yeniova AÖ, Kefeli A, Basyigit S, Aktas B, Akin KO, Üre ÖS, Topal F The association of vitamin D deficiency with non-alcoholic fatty liver disease. Clinics — Lu Z, Pan X, Hu Y, Hao Y, Luo Y, Hu X, Ma X, Bao Y, Jia W Serum vitamin D levels are inversely related with non-alcoholic fatty liver disease independent of visceral obesity in Chinese postmenopausal women. Clin Exp Pharmacol — Sergeev IN, Song Q High vitamin D and calcium intakes reduce diet-induced obesity in mice by increasing adipose tissue apoptosis. Mol Nutr Food Res — Siddiqui SM, Chang E, Li J, Burlage C, Zou M, Buhman KK, Koser S, Donkin SS, Teegarden D Dietary intervention with vitamin D, calcium, and whey protein reduced fat mass and increased lean mass in rats. Yin Y, Yu Z, Xia M, Luo X, Lu X, Ling W Vitamin D attenuates high fat diet—induced hepatic steatosis in rats by modulating lipid metabolism. Eur J Clin Invest — Hidayat M, Prahastuti S, Tiono H, Dianawati D Effect of calcium against weight gain and improved histopathologic fatty liver on male Wistar rats that fed high fat food. Obes Res Clin Pract — Pittas AG, Lau J, Hu FB, Dawson-Hughes B The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab — Thomas AP, Dunn TN, Drayton JB, Oort PJ, Adams SH A dairy-based high calcium diet improves glucose homeostasis and reduces steatosis in the context of preexisting obesity. Obesity E—E Thomas AP, Dunn TN, Drayton JB, Oort PJ, Adams SH A high calcium diet containing nonfat dry milk reduces weight gain and associated adipose tissue inflammation in diet-induced obese mice when compared to high calcium alone. Nutr Metab Lond Voznesenskaya A, Tordoff MG Low-calcium diet prevents fructose-induced hyperinsulinemia and ameliorates the response to glucose load in rats. Liu X-J, Wang B-W, Zhang C, Xia M-Z, Chen Y-H, Hu C-Q, Wang H, Chen X, Xu D-X Vitamin D deficiency attenuates high-fat diet-induced hyperinsulinemia and hepatic lipid accumulation in male mice. Endocrinology — Shirwany NA, Zou M-H AMPK: a cellular metabolic and redox sensor. A minireview. Front Biosci Landmark Ed Oakhill J, Scott J, Kemp B Structure and function of AMP-activated protein kinase. Acta Physiol — He Y-H, Li S-T, Wang Y-Y, Wang G, He Y, Liao X-L, Sun C-H, Li Y Postweaning low-calcium diet promotes later-life obesity induced by a high-fat diet. J Nutr Biochem — Gao L, Cao J-T, Liang Y, Zhao Y-C, Lin X-H, Li X-C, Tan Y-J, Li J-Y, Zhou C-L, Xu H-Y Calcitriol attenuates cardiac remodeling and dysfunction in a murine model of polycystic ovary syndrome. Endocrine — Shojaei Zarghani S, Soraya H, Zarei L, Alizadeh M Comparison of three different diet-induced non alcoholic fatty liver disease protocols in rats: a pilot study. Pharm Sci — National Research Council Nutrient requirements of laboratory animals, 4th edn. The National Academy Press, Washington, p Fleet JC, Gliniak C Modeling human vitamin D status in experimental rodents [abstract]. FASEB J 21 6 :A Folch J, Lees M, Sloane-Stanley G A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem — CAS Google Scholar. In addition to keeping your bones and teeth strong, calcium plays an important role in nerve signal transmission, muscle contraction, blood vessel dilation and constriction, heartbeat regulation and hormone secretion. Liver disease can affect calcium levels. Because calcium interferes with the absorption of iron, which can accumulate in the liver, calcium indirectly affects the liver. Iron overload, medically known as hemochromatosis, occurs when iron accumulates in the organs, most commonly the liver. Hemochromatosis may also affect the heart and the pancreas. Symptoms of iron overload include fatigue, lack of energy and abdominal pain. If left untreated, the buildup of iron can cause an enlarged liver, the buildup of scar tissue known as cirrhosis and liver disease. When taken at the same time, calcium decreases the absorption of iron. For this reason, usually doctors suggest taking iron supplements either two hours before or two hours after taking calcium supplements. For someone at risk for hemochromatosis, such as those with a genetic predisposition, the effect of calcium on iron absorption may be beneficial to the liver. The liver produces the major plasma protein in the blood known as albumin. |
| The Effect of Calcium on the Liver | livestrong | The National Academy Press, Washington, p Fleet JC, Gliniak C Modeling human vitamin D status in experimental rodents [abstract]. FASEB J 21 6 :A Folch J, Lees M, Sloane-Stanley G A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem — CAS Google Scholar. Yousefi K, Soraya H, Fathiazad F, Khorrami A, Hamedeyazdan S, Maleki-Dizaji N, Garjani A Cardioprotective effect of methanolic extract of Marrubium vulgare L. on isoproterenol-induced acute myocardial infarction in rats. Indian J Exp Biol — Soraya H, Farajnia S, Khani S, Rameshrad M, Khorrami A, Banani A, Maleki-Dizaji N, Garjani A Short-term treatment with metformin suppresses toll like receptors TLRs activity in isoproterenol-induced myocardial infarction in rat: are AMPK and TLRs connected? Int Immunopharmacol — Fon Tacer K, Rozman D Nonalcoholic Fatty liver disease: focus on lipoprotein and lipid deregulation. J Lipids. Han H, Cui M, You X, Chen M, Piao X, Jin G A role of 1, 25 OH 2 D 3 supplementation in rats with nonalcoholic steatohepatitis induced by choline-deficient diet. Nutr Metab Cardiovasc Dis — Sun C, Wang L, Yan J, Liu S Calcium ameliorates obesity induced by high-fat diet and its potential correlation with p38 MAPK pathway. Mol Biol Rep — Parra P, Bruni G, Palou A, Serra F Dietary calcium attenuation of body fat gain during high-fat feeding in mice. Browning JD, Horton JD Molecular mediators of hepatic steatosis and liver injury. J Clin Invest — Kahn BB, Flier JS Obesity and insulin resistance. Gagnon C, Daly RM, Carpentier A, Lu ZX, Shore-Lorenti C, Sikaris K, Jean S, Ebeling PR Effects of combined calcium and vitamin D supplementation on insulin secretion, insulin sensitivity and β-cell function in multi-ethnic vitamin D-deficient adults at risk for type 2 diabetes: a pilot randomized, placebo-controlled trial. PLoS ONE. Ryu O-H, Chung W, Lee S, Hong K-S, Choi M-G, Yoo HJ The effect of high-dose vitamin D supplementation on insulin resistance and arterial stiffness in patients with type 2 diabetes. Korean J Intern Med — Alkharfy KM, Al-Daghri NM, Yakout SM, Hussain T, Mohammed AK, Krishnaswamy S Influence of vitamin D treatment on transcriptional regulation of insulin-sensitive genes. Metab Syndr Relat Disord — Geldenhuys S, Hart PH, Endersby R, Jacoby P, Feelisch M, Weller RB, Matthews V, Gorman S Ultraviolet radiation suppresses obesity and symptoms of metabolic syndrome independently of vitamin D in mice fed a high-fat diet. Diabetes — Brink EJ, Beynen AC, Dekker PR, Van Beresteijn E, van der Meer R Interaction of calcium and phosphate decreases ileal magnesium solubility and apparent magnesium absorption in rats. Hruby A, Ngwa JS, Renström F, Wojczynski MK, Ganna A, Hallmans G, Houston DK, Jacques PF, Kanoni S, Lehtimäki T Higher magnesium intake is associated with lower fasting glucose and insulin, with no evidence of interaction with select genetic loci, in a meta-analysis of 15 CHARGE Consortium Studies. Nutr — Jeddi S, Syedmoradi L, Bagheripour F, Ghasemi A The effects of vitamin D on insulin release from isolated islets of rats. Int J Endocrinol Metab. Peterson JM, Seldin MM, Wei Z, Aja S, Wong GW CTRP3 attenuates diet-induced hepatic steatosis by regulating triglyceride metabolism. Am J Physiol Gastrointest Liver Physiol G—G Mol Cell Biochem — Li X, Jiang L, Yang M, Y-w Wu, S-x Sun, J-z Sun Expression of CTRP3, a novel adipokine, in rats at different pathogenic stages of type 2 diabetes mellitus and the impacts of GLP-1 receptor agonist on it. J Diabetes Res. Eliades M, Spyrou E, Agrawal N, Lazo M, Brancati F, Potter J, Koteish A, Clark J, Guallar E, Hernaez R Meta-analysis: vitamin D and non-alcoholic fatty liver disease. Aliment Pharmacol Ther — Targher G, Bertolini L, Scala L, Cigolini M, Zenari L, Falezza G, Arcaro G Associations between serum hydroxyvitamin D 3 concentrations and liver histology in patients with non-alcoholic fatty liver disease. Black LJ, Jacoby P, She Ping-Delfos WC, Mori TA, Beilin LJ, Olynyk JK, Ayonrinde OT, Huang RC, Holt PG, Hart PH, Oddy WH, Adams LA Low serum hydroxyvitamin D concentrations are associated with non-alcoholic fatty liver disease in adolescents independent of adiposity. J Gastroenterol Hepatol — Bril F, Maximos M, Portillo-Sanchez P, Biernacki D, Lomonaco R, Subbarayan S, Correa M, Lo M, Suman A, Cusi K Relationship of vitamin D with insulin resistance and disease severity in non-alcoholic steatohepatitis. J Hepatol — Li L, Zhang L, Pan S, Wu X, Yin X No significant association between vitamin D and nonalcoholic fatty liver disease in a Chinese population. Dig Dis Sci — Roth CL, Elfers CT, Figlewicz DP, Melhorn SJ, Morton GJ, Hoofnagle A, Yeh MM, Nelson JE, Kowdley KV Vitamin D deficiency in obese rats exacerbates nonalcoholic fatty liver disease and increases hepatic resistin and toll-like receptor activation. Kong M, Zhu L, Bai L, Zhang X, Chen Y, Liu S, Zheng S, Pandol SJ, Han Y-P, Duan Z Vitamin D deficiency promotes nonalcoholic steatohepatitis through impaired enterohepatic circulation in animal model. Marotte C, Weisstaub A, Bryk G, Olguin MC, Posadas M, Lucero D, Schreier L, De Portela MLPM, Zeni SN Effect of dietary calcium Ca on body composition and Ca metabolism during growth in genetically obese β male rats. Eur J Nutr — Bhat M, Noolu B, Qadri SS, Ismail A Vitamin D deficiency decreases adiposity in rats and causes altered expression of uncoupling proteins and steroid receptor coactivator3. J Steroid Biochem Mol Biol — Winder W, Hardie D AMP-activated protein kinase, a metabolic master switch: possible roles in type 2 diabetes. Am J Physiol Endocrinol Metab E1—E Steinberg GR, Kemp BE AMPK in health and disease. Physiol Rev — Guo T, Woo S-L, Guo X, Li H, Zheng J, Botchlett R, Liu M, Pei Y, Xu H, Cai Y Berberine ameliorates hepatic steatosis and suppresses liver and adipose tissue inflammation in mice with diet-induced obesity. Sci Rep. Muse ED, Obici S, Bhanot S, Monia BP, McKay RA, Rajala MW, Scherer PE, Rossetti L Role of resistin in diet-induced hepatic insulin resistance. Matsumoto M, Hagio M, Inoue R, Mitani T, Yajima M, Hara H, Yajima T Long-term oral feeding of lutein-fortified milk increases voluntary running distance in rats. Download references. The authors would like to express their gratitude toward Dr. Amir Abbas Farshid and Dr. Ali Asghar Tehrani for conducting the pathological assessments. The authors would also like to thank the Pharma chemie and Daana Pharmaceutical Companies and Beyza 21 Feed Mill Company. Student Research Committee, Department of Nutrition, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. Cellular and Molecular Research Center, Department of Pharmacology, Faculty of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran. Department of Nutrition, Food and Beverages Safety Research Center, Faculty of Medicine, Urmia University of Medical Sciences, PO Box: , Urmia, Iran. You can also search for this author in PubMed Google Scholar. Correspondence to Mohammad Alizadeh. All animal protocols were approved by the Ethics Committee of Urmia Medical Sciences University ir. Reprints and permissions. Shojaei Zarghani, S. Calcium and vitamin D 3 combinations improve fatty liver disease through AMPK-independent mechanisms. Eur J Nutr 57 , — Download citation. Received : 15 August Accepted : 06 December Published : 17 December Issue Date : March 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. Abstract Purpose Some research findings suggest that calcium plus vitamin D VitD might have a preventive effect on nonalcoholic fatty liver disease development. Methods Thirty male Wistar rats were fed with normal or HFHFr diet containing low calcium 0. Results Rats fed on high calcium plus VitD 3 diets, especially VHCD, demonstrated lower adiposity, serum liver enzymes, hepatic lipid accumulation and steatosis. Conclusions The results showed high calcium plus VitD 3 intakes considerably prevent biochemical and hepatic changes induced by HFHFr diet, probably via an insulin and AMPK-independent pathway. Access this article Log in via an institution. References Lazo M, Clark JM The epidemiology of nonalcoholic fatty liver disease: a global perspective. Semin Liver Dis — Article Google Scholar Fabbrini E, Sullivan S, Klein S Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology — Article CAS Google Scholar Keast DR, Gallant KMH, Albertson AM, Gugger CK, Holschuh NM Associations between yogurt, dairy, calcium, and vitamin D intake and obesity among us children aged 8—18 years: NHANES, — Nutrients — Article CAS Google Scholar Tidwell DK, Valliant MW Higher amounts of body fat are associated with inadequate intakes of calcium and vitamin D in African American women. Nutr Res — Article CAS Google Scholar Samadi M, Sadrzadeh-Yeganeh H, Azadbakht L, Feizi A, Jafarian K, Sotoudeh G Dietary calcium intake and risk of obesity in school girls aged 8—10 years. J Res Med Sci Google Scholar Ferreira TDS, Rocha TM, Klein MRST, Sanjuliani AF Vitamin D deficiency is associated with insulin resistance independent of intracellular calcium, dietary calcium and serum levels of parathormone, calcitriol and calcium in premenopausal women. Nutr Hosp — Google Scholar da Silva FerreiraT, Torres MRSG, Sanjuliani AF Dietary calcium intake is associated with adiposity, metabolic profile, inflammatory state and blood pressure, but not with erythrocyte intracellular calcium and endothelial function in healthy pre-menopausal women. Brit J Nutr — Article Google Scholar Moore-Schiltz L, Albert JM, Singer ME, Swain J, Nock NL Dietary intake of calcium and magnesium and the metabolic syndrome in the National Health and Nutrition Examination NHANES — data. Brit J Nutr — Article CAS Google Scholar Kim KJ, Kim YJ, Kim SH, An JH, Yoo HJ, Kim HY, Seo JA, Kim SG, Kim NH, Choi KM Vitamin D status and associated metabolic risk factors among North Korean refugees in South Korea: a cross-sectional study. Clinics — Article Google Scholar Lu Z, Pan X, Hu Y, Hao Y, Luo Y, Hu X, Ma X, Bao Y, Jia W Serum vitamin D levels are inversely related with non-alcoholic fatty liver disease independent of visceral obesity in Chinese postmenopausal women. Clin Exp Pharmacol — Article CAS Google Scholar Sergeev IN, Song Q High vitamin D and calcium intakes reduce diet-induced obesity in mice by increasing adipose tissue apoptosis. Mol Nutr Food Res — Article CAS Google Scholar Siddiqui SM, Chang E, Li J, Burlage C, Zou M, Buhman KK, Koser S, Donkin SS, Teegarden D Dietary intervention with vitamin D, calcium, and whey protein reduced fat mass and increased lean mass in rats. Nutr Res — Article CAS Google Scholar Yin Y, Yu Z, Xia M, Luo X, Lu X, Ling W Vitamin D attenuates high fat diet—induced hepatic steatosis in rats by modulating lipid metabolism. Eur J Clin Invest — Article CAS Google Scholar Hidayat M, Prahastuti S, Tiono H, Dianawati D Effect of calcium against weight gain and improved histopathologic fatty liver on male Wistar rats that fed high fat food. Obes Res Clin Pract —16 Article Google Scholar Pittas AG, Lau J, Hu FB, Dawson-Hughes B The role of vitamin D and calcium in type 2 diabetes. J Clin Endocrinol Metab — Article CAS Google Scholar Thomas AP, Dunn TN, Drayton JB, Oort PJ, Adams SH A dairy-based high calcium diet improves glucose homeostasis and reduces steatosis in the context of preexisting obesity. Obesity E—E Article CAS Google Scholar Thomas AP, Dunn TN, Drayton JB, Oort PJ, Adams SH A high calcium diet containing nonfat dry milk reduces weight gain and associated adipose tissue inflammation in diet-induced obese mice when compared to high calcium alone. For someone at risk for hemochromatosis, such as those with a genetic predisposition, the effect of calcium on iron absorption may be beneficial to the liver. The liver produces the major plasma protein in the blood known as albumin. Albumin binds to water and cations, like calcium, to regulate the osmotic pressure in the blood. A diseased liver cannot produce enough albumin, which affects the pressure within the vascular system and allows fluid to leak out of the blood vessels. In addition, when albumin levels fall, less calcium can remain in the bloodstream, leading to a condition known as hypocalcemia. Hypocalcemia occurs when the amount of calcium in the blood drops below 8. It's most commonly caused by a malfunction in the parathyroid gland, which produces parathyroid hormone essential to regulating blood calcium levels. Hypocalcemia produces symptoms ranging from mild repetitive tremors known as tetany to serious conditions like seizures, dementia, low blood pressure and congestive heart failure. To avoid low blood calcium levels caused by liver disease, it is important you maintain a healthy liver. Approximately 75 percent of the blood entering the liver flows through the portal vein carrying the blood from the small intestine, stomach, pancreas and spleen, according to Colorado State University. Although this blood contains all the nutrients just absorbed through the small intestine, it also contains all the toxins you ingested. Drugs, including prescription, over-the-counter and illegal, all travel through the liver. The alcohol you consume also flows into the liver. As the first organ to encounter these toxins, the liver sustains the majority of the damage. To keep your liver healthy and maintain your blood calcium level, avoid excessive drug use and alcohol consumption. Nutrition Nutrition Basics Vitamins and Supplements. |
| Too Much of a Good Thing: The Dangers of Supplements | The increasing number of young men seeking medical care for symptoms of liver damage Calcium and liver health heatlh otherwise uealth is aClcium increasing scrutiny on supplements that claim to burn fat or build muscle at dramatic rates. Article CAS Google Scholar. Writing — original draft: MNA ILB JV. Pharmacology of store-operated calcium channels. Schneeberger M, Everard A, Gomez-Valades AG, Matamoros S, Ramirez S, Delzenne NM, et al. |
| Ethanol Disrupts Hormone-Induced Calcium Signaling in Liver | Function | Oxford Academic | Rent this article abd DeepDyve. Copy to Calcium and liver health. Nad finding has Calcium and liver health clinical significance as it Calcjum that calcium may protect against adverse progression Pancreatic insufficiency treatment in those individuals unable to achieve or maintain weight loss, as is the case in many, if not most, human patients [ 60 ]. Full content visible, double tap to read brief content. These results were consistent with taxa driving separation in principal components analysis. The present study also has some limitations. Google Preview. |
Calcium and liver health -
When applicable, minor movements of the liver tissue in the x , y direction were corrected using the StackReg plugin for ImageJ. Difference images were processed with a median filter and a minimum threshold intensity to reduce noise. Photobleaching was carried out by briefly focusing the laser onto a single hepatocyte and then acquiring full-field images.
A linear fit was used to calculate the initial rate of fluorescence recovery. Single-cell imaging experiments were performed in HBSS containing — μM sulfobromophthalein and 0. The cells were washed twice with HBSS and then transferred to a thermostatically regulated microscope chamber 37°C.
The fura-2 calibration parameters were determined in vitro using a Kd value of nM. Changes in PKCβII-EGFP distribution were monitored by taking the ratio of the GFP fluorescence intensity changes in the membrane versus cytosol. The resulting membrane:cytosol ratio was normalized to the baseline values prior to data analysis.
Cells were washed and mounted on the stage of an Axiovert Zeiss spinning disc confocal microscope. Photolysis of caged IP 3 was achieved by light pulses 1 ns duration with a wavelength of nm and 1. Data analysis was performed using ImageJ NIH. The CFP donor emission image recorded at nm was divided by the acceptor emission image recorded at nm to obtain the FRET emission ratio.
Data are presented as means ± SD for the number of livers, separate hepatocyte preparations, or cells as indicated in the figure legend. The white box shows the area displayed as an insert in panel b at higher resolution. The lobular location of the cells is depicted by the similarly colored arrows shown on the insert.
Confocal images µm × µm of fluo-3 fluorescence are displayed in a linear grayscale with increases in fluorescence intensity at each time point displayed as a red overlay. Time s after vasopressin A, — s or ethanol B, 15— s reach the liver are shown in the top left of each image.
Periportal PP zone and the boundary white line of a lobule are illustrated in the first image of Panel A. White scale bar denotes µm.
Data were acquired at higher magnification ×20 in a separate liver preparation. The images in Figure 2B show the effect of perfusing the same liver with 20 mM ethanol in the continuing presence of the vasopressin.
The concentrations and duration of vasopressin and ethanol perfusion are shown by the horizontal bars. The data are expressed as the fold-change for the indicated ethanol concentrations.
Symbols are the mean ± SD, or mean data for experiments with less than three livers see also Table 1. Fura-2 fluorescence images were deconvolved prior to calculating the ratio as described previously. Previous studies have demonstrated the ability to assess gap junction communication by monitoring the rates of FRAP in both isolated hepatocyte couplets 62 and hepatocytes within the perfused liver.
The FRAP assay was carried out before and then after perfusing the liver for 5—10 min with 20 mM ethanol in the same hepatic lobule, but using different hepatocytes for each assay to avoid laser-induced injury Figure 4B. The initial rates of fluorescent recovery were determined, and summary data are presented in Figure 4C.
The data indicate that ethanol perfusion markedly inhibits the rate of fluorescence recovery. Acute Ethanol Perfusion Suppresses Gap Junction Communication. Images show the laser-induced photobleaching and recovery of the cell highlighted by the arrowhead.
White scale bar denotes 20 µm. B and C Fluorescence recovery after photobleaching FRAP assays were carried out before and after perfusion with 20 mM ethanol.
B Traces are the normalized fluorescence intensity changes from two different cells within the same hepatic lobule. C Summary data showing the initial rates of fluorescence recovery in the absence or presence of 20 mM ethanol.
Data points are recovery rates from individual cells. In some experiments, hepatocytes were transfected with genetically encoded calcium indicators GECIs targeted to the cytosol or nucleus, and then maintained in primary culture overnight.
After 5—10 min, the cultures were acutely treated with 30 mM ethanol. In separate studies, hepatocytes were transfected with GCaMPf6 C and D or ratiometric-pericam-nu E and F and then maintained in primary culture overnight.
In the next series of experiments, we investigated the actions of ethanol on the translocation of conventional PKCβII to the membrane. Hepatocyte cultures were transduced overnight with adenoviruses encoding enhanced green fluorescent protein EGFP tagged PKCβII gift from R.
Live-cell confocal imaging was used to measure the distribution of GFP fluorescence in hepatocytes expressing PKCβII-EGFP before Figure 6A , left and after stimulating with 1 µM ATP Figure 6A , right. Image analysis revealed that purinergic stimulation induced a decrease in GFP fluorescence in the perinuclear region and accumulation of the probe in a plasma membrane domain.
A ratio was calculated between the reciprocal changes GFP fluorescence intensity in membrane versus the cytoplasm to evaluate the translocation of PKC. Effect of Ethanol on Hormone-Induced Translocation of PKCβII. A Representative confocal images showing translocation of PKCβII-EGFP induced by 1 µM ATP.
White scale bar denotes 15 µm. Translocation of PKCβII was monitored by taking the ratio of the GFP fluorescence intensity changes in the membrane versus cytosol. The PKCβII membrane:cytosol ratio was normalized to the initial ratio.
We calculated the peak vasopressin-induced increases in the fura-2 ratio and extent of PKC translocation, as well as the rates of rise, rates of fall, and AUC for both parameters, before and after ethanol treatment in the same cell.
Summary results are shown in Figure 6E and F and Table 2. Effect of Ethanol Treatment on Vasopressin-Induced Calcium Increases and PKC Translocation. Ethanol 30 mM was added 10—20 min after hormone stimulation. The data are the means ± SD for the peak increase in the fura-2 excitation ratio or PKC translocation, the rates of rise and fall in fura-2 ratio or PKC translocation, and the AUC for fura-2 ratio or PKC translocation.
ns, not significant. The main pathway for ethanol clearance in hepatocytes is the sequential oxidation by alcohol dehydrogenase ADH to produce acetaldehyde followed by the conversion of acetaldehyde into acetate in the mitochondrial matrix by aldehyde dehydrogenase ALDH.
This stimulates the production of reactive oxygen species ROS , 65 , 66 which can potentiate the opening of IP 3 receptors. Cyanamide is a prodrug that requires bioconversion into the active compound necessitating the preincubation step.
Pretreating hepatocytes with 4-methylpyrazole to block ADH prevented the ethanol-induced increase in NADH fluorescence, consistent with the inhibition of ethanol metabolism Figure 7C.
A—C Hepatocytes were pretreated for 30 min with µM 4-methylprazole 4-MP , µM cyanamide, or buffer prior to data acquisition. B Summary data showing the effects of increasing concentrations of ethanol 0.
The changes in frequency are expressed as a fold-change for each cell analyzed. C The increases in hepatic NAD P H fluorescence in response to ethanol mM were determined in the absence left or presence right of 4-MP.
We further investigated the role of ethanol metabolism by inhibiting the clearance of the ethanol metabolite acetaldehyde with cyanamide. DMTU has been shown previously to suppress ROS production and apoptosis in hepatocytes during acute ethanol intoxication, 70 , 71 while the addition of DPPD inhibits oxidant-induced increases in lipid peroxidation.
The addition of nM IP 3 released 2. These data suggest that these pharmacologically relevant concentrations of ethanol or its metabolite, acetaldehyde, do not alter the properties of IP 3 receptors.
Ethanol Treatment Does Not Affect IP 3 Receptor Sensitivity but Suppresses Hormone-Induced Production of IP 3. IP 3 was uncaged with 4 UV pulses from a nitrogen-charged UV laser in the absence or presence of 30 mM ethanol 5 min pretreatment. Traces are the averaged responses calculated from three IRIS-1 spikes before and after the addition of ethanol 30 mM.
Data were calculated from 2 to 4 IRIS-1 spikes before and after addition of ethanol in the same cell. We initially utilized biochemical assays to investigate the actions of ethanol on hormone-stimulated PLC activity in cultured hepatocytes. In order to increase the signal to noise of the IRIS-1 FRET ratio, IP 3 spike traces were averaged from 2 to 4 sequential oscillations aligned to the rising phase of the individual spikes.
This allowed quantitation of the IP 3 spike kinetics following hormone stimulation before Figure 8E , left and after Figure 8E , right the addition of 30 mM ethanol. Ethanol treatment decreased the amplitude of the vasopressin-stimulated IP 3 oscillations, slowed the rates of rise and fall of the individual IP 3 spikes and decreased the AUC Figure 8F and G ; Table 3.
Effect of Ethanol Treatment on Vasopressin-Induced Increases in IRIS-1 Emission Ratio. Ethanol 30 mM was added 10—20 min after vasopressin stimulation. The data are the means ± SD for the peak VP-induced increases the IRIS-1 emission ratio, the rates of rise and fall of the IRIS-1 increase, and the AUC for the IRIS-1 spike.
The natural progression of alcohol-related liver disease ALD follows a well-characterized pattern. We have proposed that enhanced receptor-coupled PI-PLC activity induced by long-term and repeated exposure to ethanol may be another mechanism contributing to hepatic injury 17 , 29 ; the inappropriate activation of PLC-linked signaling cascades could underlie some of the pleiotropic actions of ethanol on liver function.
Blood alcohol concentrations in excess of mM are not observed in healthy volunteers given ethanol, 23 , 89 however, there are reports of alcoholics presenting at emergency departments with plasma ethanol concentrations between and mM, 22 , 23 as well as a single report of an alcoholic who survived a blood alcohol level of mM.
Bearing in mind the range of blood alcohol levels normally encountered, the more relevant effects of ethanol described here are to suppress hormonal signaling. The effects of 10 mM ethanol and below were completely blocked by 4-methylpyrazole, and this compound also significantly reduced the inhibitory effects of ethanol up to mM Figure 7B.
Another important effect of ethanol observed in our ex vivo perfused rat liver studies was the marked reduction in cell-to-cell communication in the presence of ethanol. Moreover, the reduction in cell-cell communication will reduce integrated lobular signaling, which we recently reported plays a key role in generating the global response of the liver to glycogenic hormones.
This is consistent with previous work showing the inhibitory effects of ethanol on gap junctions, and significantly, this effect was also reported to require ethanol metabolism.
It should be noted that ethanol also reacts with long-chain fatty acids to produce fatty acid ethyl esters FAEEs through a nonoxidative pathway catalyzed by fatty acid ethyl ester synthase.
Nevertheless, it is possible that this mechanism could play a role in liver damage in chronic alcoholics. Acute ethanol intoxication has been reported to induce the formation of ROS in mitochondria. Notably, production of mitochondrial ROS and cell death induced by the reoxygenation of anoxic hepatocytes has been shown to be markedly suppressed by DPPD.
In the short term, the acute inhibitory effects of ethanol on receptor-coupled PLC will perturb the normal hormonal regulation of hepatic metabolism. However, after long-term ethanol exposure, the liver overcomes the acute inhibitory actions of ethanol on IP 3 production by increasing the efficacy of hormones to stimulate PLC activity.
We thank Dr. Mikoshiba RIKEN for the pIRIS-1 construct, Dr. Miyawaki RIKEN for pRatiometric-pericam-nu construct, Dr. Kim HHMI for pGP-CMV-GCaMP6f, and Dr. Rizzuto University of Padua for the PKCβII-EGFP adenovirus particles Ad-PKCβII-EGFP. We thank Kerri Anne Stellato, Shwetal Metha, and Mimi Shon for technical assistance in carrying out the hepatocyte imaging studies and Dr.
Sandip Patel for helpful discussions. Graphical abstract was created with BioRender. performed the intact perfused liver and single hepatocyte imaging studies.
carried out the flash photolysis of caged IP 3 experiments and analysis. designed the study. wrote the manuscript. reviewed and edited the article. This work was supported by National Institutes of Health Grants AA L.
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Reilly Jr, MD ; et al David H. Van Thiel, MD. Author Affiliations From the Division of Clinical Nutrition, Department of Internal Medicine, School of Medicine, University of California, Davis Dr Gerhardt and the Renal-Electrolyte Dr Greenberg and Gastroenterology Divisions Dr Van Thiel of the Department of Medicine and the Department of Surgery Dr Reilly , University of Pittsburgh School of Medicine.
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Liger conducted a case-control study healrh Calcium and liver health the Calclum Cohort in China, including cases and Calcium and liver health and Calfium controls. A U-shaped Smoking cessation strategies was found for blood Mg and NAFLD, with the highest OR of 1. Liver function or lipid metabolism parameters may modify their association, suggesting an individualized prevention strategy for NAFLD. This is a preview of subscription content, log in via an institution to check access. Rent this article via DeepDyve. Institutional subscriptions.
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