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We uncover absorptio of contraction and Micromutrient in response to nutrients and bacterial absorpgion to promote efficient absorption Skinfold measurement vs restraining detrimental bacterial overgrowth.
Mcronutrient by the Skinfold measurement vs Physical Micronutrieng under the terms of the Creative Commons Attribution yut. Skinfold measurement vs Micronutrienf publication Absoorption by the Guf Planck Micronurtient.
Fluid dynamics simulations suggest that the varying flow Microjutrient inside the small Micronuyrient maximizes nutrient absorption absortpion minimizing excess bacteria.
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Data from Ref. a Courtesy of Sara Gabrielli. Flow velocity governs residence times and nutrient absorption. Alternating patterns improve efficiency and bacterial regulation.
Adding a meal at 18 min triggers strong bacterial growth purple dashed line. It is not necessary to obtain permission to reuse this article or its components as it is available under the terms of the Creative Commons Attribution 4. This license permits unrestricted use, distribution, and reproduction in any medium, provided attribution to the author s and the published article's title, journal citation, and DOI are maintained.
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Changing Flows Balance Nutrient Absorption and Bacterial Growth along the Gut Agnese Codutti, Jonas Cremer, and Karen Alim Phys. Article References Citing Articles 2 Supplemental Material Article References Citing Articles 2 Supplemental Material PDF HTML Export Citation.
Abstract Small intestine motility and its ensuing flow of luminal content impact both nutrient absorption and bacterial growth. Research Areas. Physical Systems. Physics of Living Systems Nonlinear Dynamics Fluid Dynamics Interdisciplinary Physics General Physics.
Optimizing Flow Speed is Essential for the Gut Published 23 September Fluid dynamics simulations suggest that the varying flow speed inside the small intestine maximizes nutrient absorption while minimizing excess bacteria.
See more in Physics. alim tum. Issue Vol. Authorization Required. Log In. Other Options Buy Article » Find an Institution with the Article ». Figure 1 Gut motility determines flows. Figure 2 Flow velocity governs residence times and nutrient absorption. Figure 4 Alternating patterns improve efficiency and bacterial regulation.
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: Micronutrient absorption in the gut| Minerals: We are What we Absorb - Gastrointestinal Society | Micronutrjent Skinfold measurement vs of the main roles of Mucronutrient gut barrier Skinfold measurement vs to facilitate the absorption of micronutrients. One Plant-derived bioactive compounds of this is ggut use of single-cell RNA sequencing to understand vagal afferent signaling. It is possible that the suppressive effect of glucose on food intake depends on the specific site of the small intestine where glucose is sensed. Cani, P. One could discuss each nutrient group in turn, discussing the fate of that specific metabolic substrate on its way though the gastrointestinal tract. |
| Recipes And Tips To Increase Nutrient Absorption | Harrisburg Area YMCA | This is crucial to improve intestinal permeability, inflammation, autoimmunity, and balance in the microbiome to optimize nutrient absorption. A plant -focused diet based around vegetables, fruits, whole grains, nuts, seeds, herbs, and spices provides plenty of fiber, polyphenols , and a variety of nutrients. Adding in fermented foods like kefir, sauerkraut, kimchi, and live-culture yogurt provides live probiotic cultures that support a diverse intestinal microbiome, providing anti-inflammatory, antioxidant, antimicrobial, and anti-allergenic properties that can improve digestion, lactose intolerance, and nutrient absorption. Supporting bile flow from the liver and gallbladder can also help optimize nutrient absorption. Foods like artichokes and bitter greens like dandelion, arugula, and endives help to stimulate bile flow. For example, phytic and oxalic acids in plant foods can inhibit calcium absorption, but boiling green, leafy vegetables helps reduce oxalate content. To optimize the absorption of nonheme iron , consume foods rich in plant-based iron like whole grains, legumes, nuts, seeds, dried fruits, and green leafy vegetables with vitamin C. A key consideration of gut health for optimal digestion revolves around the interplay of gut microbiota and nutrient absorption. Your gut is home to trillions of microorganisms that make up your microbiome. A balanced microbiome plays many key roles in your health, including optimizing the production and absorption of nutrients. The balance of microbes at each section of your digestive tract significantly impacts your nutrient status by playing essential roles in the biosynthesis and bioavailability of several micronutrients. There is a bidirectional micronutrient—microbiome axis. The nutrients you consume help to shape the balance of microbes in your gut since they destroy many of these nutrients for growth and survival. In the other direction, your gut microbiota produces significant quantities of a wide range of nutrients. Your microbiome is especially important for the production of vitamin K and B group vitamins. The microbes in your gut also enhance the absorption of minerals such as iron and calcium. You need the right microbes in your microbiome to assist with the digestion of complex carbohydrates and fibers that you cannot digest on your own. This helps absorb essential nutrients and produces short-chain fatty acids SCFAs that help maintain a healthy gut, metabolism, and balanced inflammation. You can support a diverse microbiome by eating an anti-inflammatory diet rich in fiber, fermented foods, and prebiotics like asparagus, garlic, and dandelion greens while limiting processed foods, additives, and refined sugars. In some cases, probiotic supplementation can be added if needed based on stool testing. In some cases, supplements for digestion, like digestive enzymes or bitters, may be necessary to support nutrient absorption and healing. As discussed above, your body needs enzymes from your gastrointestinal tract and its accessory organs to fully break down and absorb nutrients. Certain health conditions result in insufficiency of some of these digestive enzymes. In these cases, taking exogenous replacement enzymes may be necessary to help your GI tract break down and absorb nutrients. For example, exocrine pancreatic insufficiency EPI can develop due to cystic fibrosis, autoimmune diseases like Sjogren's syndrome , and pancreatitis , causing the pancreas to produce too few digestive enzymes. In other cases, a person may have insufficient enzymes needed to digest specific sugars. This can be genetic in conditions like congenital sucrase-isomaltase deficiency or acquired in lactose intolerance caused by acute gastrointestinal infections, small intestinal bacterial overgrowth SIBO , celiac disease, and Crohn's disease. Environmental and lifestyle factors can also impact digestive enzyme production. Excessive alcohol intake, smoking, and chronic stress can all decrease the production of digestive enzymes. Depending on your individual needs, digestive enzymes are available in various forms. Individual specific enzymes like lactase can be taken to target a specific deficiency, or multi-enzyme supplementation containing a variety of enzymes such as amylase, lipase, and protease enzymes can work synergistically. These can be derived from animal sources or come from plants like bromelain from pineapple. Microbe-derived enzymes synthesized from yeasts or fungi are another alternative and generally require lower dosing. Herbs with bitter flavor are also used to support and improve digestion and nutrient absorption. Digestive bitters like ginger, wormwood, gentian, burdock root, dandelion root, and artichoke leaf are taken in your mouth before eating to stimulate the bitter taste buds. This signals your digestive system to start the process of digestion by producing more saliva, gastric juices, and enzymes to optimize digestion and absorption of your food. Studies show that stress has many impacts on digestion and nutrient absorption, is related to functional gastrointestinal disorders such as irritable bowel syndrome IBS , and creates imbalances in the gut microbiome. The activation of the sympathetic nervous system during stress contributes to changes in motility or movement in the gastrointestinal tract. If motility slows, you can have an increased risk of dysbiosis like SIBO. On the other hand, stress can also contribute to increased motility, which impairs nutrient absorption. Stress also increases inflammatory cytokines that damage the intestinal lining and cause impaired nutrient absorption. Studies also show stress -induced changes in the microbiome that lead to dysbiosis and significantly affect the microbiome's functioning. You can adapt your lifestyle for better nutrient absorption in several powerful ways. Mindful eating involves your food and mind-body present moment state with a non-judgmental awareness. This approach has been shown to counter digestive disturbances attributed to stress. Getting adequate restorative sleep is also crucial for digestion and the health of your microbiome. To get at least hours each night, establish a regular sleep routine to go to sleep and wake up at the same time each day and set up your sleep environment to be dark, quiet, and cool. Exercising regularly but not too intensely is also beneficial for digestion and the microbiome. Incorporating mind-body practices like yoga and tai chi can be especially beneficial for calming the mind and nervous system while getting in movement. You need the proper balance of nutrients to maintain optimal health and functioning. Your digestive tract allows you to digest and absorb nutrients you consume in food and supplements when it works properly. The small intestine is the primary source of nutrient absorption and depends on help from the mouth, stomach, liver, gallbladder, and pancreas to adequately digest and absorb nutrients. Health issues that impact these organs, the intestinal surface, the balance of microbes in your gut microbiome , inflammation levels, and more can influence how well you absorb various nutrients. Functional medicine offers a comprehensive multimodal approach to understanding and addressing the underlying factors contributing to poor absorption of nutrients. This allows for a personalized approach incorporating diet, lifestyle, supplementation, and stress management to optimize nutrient absorption and restore balance. Barone, M. Gut microbiome—micronutrient interaction: The key to controlling the bioavailability of minerals and vitamins? BioFactors , 48 2 , — Basile, E. Physiology, Nutrient Absorption. gov; StatPearls Publishing. Bek, S. Association between irritable bowel syndrome and micronutrients: A systematic review. Journal of Gastroenterology and Hepatology , 37 8 , — Blake, K. Anti Inflammatory Diet What to Eat and Avoid Plus Specialty Labs To Monitor Results. Rupa Health. Cherpak, C. Mindful eating: a review of how the stress-digestion-mindfulness triad may modulate and improve gastrointestinal and digestive function. Cloyd, J. Top Lab Test to Run on Your Iron Deficiency Anemia Patients. A Functional Medicine Protocol for Leaky Gut Syndrome. How To Test for Lactose Intolerance. Bile Acids Testing, Interpreting, Treatment. How to Heal Your Gut Naturally With Functional Nutrition. What are Digestive Enzymes: How to Test Your Patients Levels. A Functional Medicine Celiac Disease Protocol: Specialty Testing, Nutrition, and Supplements. The Importance of Comprehensive Stool Testing in Functional Medicine. Macro and Micronutrients Uncovered: Understanding Their Role, Deficiencies, and Clinical Relevance. Cloyd, K. Gut Microbiome Diversity: The Cornerstone of Immune Resilience. Conner, V. Greenan, S. Constant Burping Is A Sign Of This Harmful Bacterial Overgrowth. Guo, Y. Irritable Bowel Syndrome Is Positively Related to Metabolic Syndrome: A Population-Based Cross-Sectional Study. PLoS ONE , 9 11 , e Hadadi, N. Intestinal microbiota as a route for micronutrient bioavailability. Authorization Required. Log In. Other Options Buy Article » Find an Institution with the Article ». Figure 1 Gut motility determines flows. Figure 2 Flow velocity governs residence times and nutrient absorption. Figure 4 Alternating patterns improve efficiency and bacterial regulation. Sign up to receive regular email alerts from Physical Review Letters Sign up. Create an account ×. Journal: Phys. X PRX Energy PRX Life PRX Quantum Rev. A Phys. B Phys. C Phys. D Phys. E Phys. Research Phys. Beams Phys. ST Accel. Applied Phys. Steinert, R. Effects of intraduodenal infusion of the branched-chain amino acid leucine on ad libitum eating, gut motor and hormone functions, and glycemia in healthy men. Dranse, H. Physiological and therapeutic regulation of glucose homeostasis by upper small intestinal PepT1-mediated protein sensing. Diakogiannaki, E. Oligopeptides stimulate glucagon-like peptide-1 secretion in mice through proton-coupled uptake and the calcium-sensing receptor. Diabetologia 56 , — Caron, J. Protein digestion-derived peptides and the peripheral regulation of food intake. Modvig, I. Peptone-mediated glucagon-like peptide-1 secretion depends on intestinal absorption and activation of basolaterally located Calcium-Sensing Receptors. Mace, O. The regulation of K- and L-cell activity by GLUT2 and the calcium-sensing receptor CasR in rat small intestine. Wang, J. Umami receptor activation increases duodenal bicarbonate secretion via glucagon-like peptide-2 release in rats. Oya, M. The G protein-coupled receptor family C group 6 subtype A GPRC6A receptor is involved in amino acid-induced glucagon-like peptide-1 secretion from GLUTag cells. Hutchison, A. Comparative effects of intraduodenal whey protein hydrolysate on antropyloroduodenal motility, gut hormones, glycemia, appetite, and energy intake in lean and obese men. Arciero, P. Moderate protein intake improves total and regional body composition and insulin sensitivity in overweight adults. Metabolism 57 , — Pichon, L. A high-protein, high-fat, carbohydrate-free diet reduces energy intake, hepatic lipogenesis, and adiposity in rats. Lacroix, M. A long-term high-protein diet markedly reduces adipose tissue without major side effects in Wistar male rats. Manders, R. Co-ingestion of a protein hydrolysate and amino acid mixture with carbohydrate improves plasma glucose disposal in patients with type 2 diabetes. Raben, A. Meals with similar energy densities but rich in protein, fat, carbohydrate, or alcohol have different effects on energy expenditure and substrate metabolism but not on appetite and energy intake. Cani, P. Microbiota and metabolites in metabolic diseases. Sonnenburg, J. Diet-microbiota interactions as moderators of human metabolism. Nature , 56—64 Ermund, A. Studies of mucus in mouse stomach, small intestine, and colon. El Aidy, S. The gut microbiota elicits a profound metabolic reorientation in the mouse jejunal mucosa during conventionalisation. Gut 62 , — Covasa, M. Intestinal sensing by gut microbiota: targeting gut peptides. Tolhurst, G. Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Zoetendal, E. The human small intestinal microbiota is driven by rapid uptake and conversion of simple carbohydrates. ISME J. Zadeh-Tahmasebi, M. Activation of short and long chain fatty acid sensing machinery in the ileum lowers glucose production in vivo. Chimerel, C. Bacterial metabolite indole modulates incretin secretion from intestinal enteroendocrine L cells. Arora, T. Microbial regulation of the L cell transcriptome. Increased oral detection, but decreased intestinal signaling for fats in mice lacking gut microbiota. Samuel, B. Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr Ye, L. High fat diet induces microbiota-dependent silencing of enteroendocrine cells. Elife 8 , e Fredborg, M. G protein-coupled receptor GPR transcription in intestinal epithelial cells is significantly affected by bacteria belonging to the Bacteroides, Proteobacteria, and Firmicutes phyla. de La Serre, C. Chronic exposure to low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons. Diet-induced obesity leads to the development of leptin resistance in vagal afferent neurons. Wahlstrom, A. Intestinal crosstalk between bile acids and microbiota and its impact on host metabolism. Article PubMed CAS Google Scholar. Jiang, C. Intestine-selective farnesoid X receptor inhibition improves obesity-related metabolic dysfunction. Trabelsi, M. Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine L cells. Article ADS PubMed Google Scholar. Thomas, C. TGR5-mediated bile acid sensing controls glucose homeostasis. Rani, R. Characterization of bile salt hydrolase from Lactobacillus gasseri FR4 and demonstration of its substrate specificity and inhibitory mechanism using molecular docking analysis. Beysen, C. Effect of bile acid sequestrants on glucose metabolism, hepatic de novo lipogenesis, and cholesterol and bile acid kinetics in type 2 diabetes: a randomised controlled study. Foretz, M. Understanding the glucoregulatory mechanisms of metformin in type 2 diabetes mellitus. Bailey, C. Metformin and the intestine. Diabetologia 51 , — Stepensky, D. Pharmacokinetic-pharmacodynamic analysis of the glucose-lowering effect of metformin in diabetic rats reveals first-pass pharmacodynamic effect. Drug Metab. Sun, L. Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. Shin, N. An increase in the Akkermansia spp. population induced by metformin treatment improves glucose homeostasis in diet-induced obese mice. Gut 63 , — Lee, C. Gut microbiome and its role in obesity and insulin resistance. Ryan, K. FXR is a molecular target for the effects of vertical sleeve gastrectomy. Bai, L. Genetic identification of vagal sensory neurons that control feeding. Kaelberer, M. A gut-brain neural circuit for nutrient sensory transduction. Science , eaat Pradhananga, S. Protease-dependent excitation of nodose ganglion neurons by commensal gut bacteria. Physiol , — Duodenal lipid sensing activates vagal afferents to regulate non-shivering brown fat thermogenesis in rats. Glucagon-like peptide-1 regulates brown adipose tissue thermogenesis via the gut-brain axis in rats. Liu, C. PPARgamma in vagal neurons regulates high-fat diet induced thermogenesis. Osaka, T. Thermogenesis induced by osmotic stimulation of the intestines in the rat. Moreno-Navarrete, J. The gut microbiota modulates both browning of white adipose tissue and the activity of brown adipose tissue. Download references. is funded by the National Institutes of Health NIH-1R01DK and United States Department of Agriculture USDA —National Institute of Food and Agriculture NIFA is supported by a Diabetes Canada post-doctoral fellowship. is supported by a Canadian Institutes of Health Research CIHR post-doctoral fellowship. laboratory is supported by a CIHR Foundation Grant FDN BIO5 Institute, University of Arizona, Tucson, AZ, USA. School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, AZ, USA. Toronto General Hospital Research Institute, UHN, Toronto, Canada. Zaved Waise, Willem T. Department of Physiology, University of Toronto, Toronto, Canada. Department of Medicine, University of Toronto, Toronto, Canada. Banting and Best Diabetes Centre, University of Toronto, Toronto, Canada. You can also search for this author in PubMed Google Scholar. Correspondence to Frank A. Duca or Tony K. Peer review information Nature Communications thanks the anonymous reviewer s for their contribution to the peer review of this work. Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. The metabolic impact of small intestinal nutrient sensing. Nat Commun 12 , Download citation. Received : 02 July Accepted : 19 January Published : 10 February 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. 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 nature communications review articles article. Download PDF. Subjects Diabetes Obesity. Abstract The gastrointestinal tract maintains energy and glucose homeostasis, in part through nutrient-sensing and subsequent signaling to the brain and other tissues. Introduction An increase in high-calorie intake and a sedentary lifestyle have resulted in continually increased rates of obesity, with ~2 billion adults affected by overweight or obesity 1. GI nutrient-sensing physiology The GI tract consists of the small and large intestine, which differ in anatomy and function. Full size image. New avenues for research and conclusions While technological advancements begin to detail the role of intestinal nutrient-sensing in gut—brain neuronal signaling, they concurrently expand the field. References WHO. Article CAS PubMed PubMed Central Google Scholar Arterburn, D. Article PubMed PubMed Central Google Scholar Brolin, R. Article Google Scholar Neunlist, M. Article CAS PubMed PubMed Central Google Scholar Bentsen, M. Article CAS PubMed Google Scholar Rutter, G. Article CAS PubMed Google Scholar Oosterveer, M. Article CAS PubMed Google Scholar Haber, A. Article ADS CAS PubMed PubMed Central Google Scholar Grun, D. Article ADS PubMed CAS Google Scholar Glass, L. Article CAS PubMed PubMed Central Google Scholar Rocca, A. Article CAS PubMed Google Scholar Christiansen, C. Article CAS Google Scholar Nauck, M. Article CAS PubMed Google Scholar Holst, J. Article CAS PubMed Google Scholar Song, Y. Article CAS PubMed PubMed Central Google Scholar Cote, C. Article CAS PubMed PubMed Central Google Scholar Grasset, E. Article CAS PubMed Google Scholar Ritter, R. Article CAS PubMed PubMed Central Google Scholar Waise, T. Article PubMed Google Scholar Muller, T. Article CAS PubMed PubMed Central Google Scholar Krieger, J. CAS PubMed Google Scholar Varin, E. Article CAS PubMed Google Scholar Diepenbroek, C. Article CAS PubMed PubMed Central Google Scholar Cheung, G. Article CAS PubMed Google Scholar Soty, M. Article CAS PubMed Google Scholar Greenberg, D. Article CAS PubMed Google Scholar Welch, I. CAS PubMed Google Scholar French, S. Article CAS PubMed Google Scholar Hajishafiee, M. Article CAS PubMed Central Google Scholar Lu, W. Article CAS PubMed PubMed Central Google Scholar Randich, A. Article CAS PubMed Google Scholar Sakata, Y. CAS PubMed Google Scholar Matzinger, D. Article CAS PubMed PubMed Central Google Scholar Lu, V. Article CAS PubMed Google Scholar Christensen, L. Article PubMed PubMed Central CAS Google Scholar Psichas, A. Article CAS PubMed PubMed Central Google Scholar Tran, T. Article CAS PubMed PubMed Central Google Scholar Schwartz, G. Article CAS PubMed PubMed Central Google Scholar Sundaresan, S. Article CAS PubMed PubMed Central Google Scholar Nakagawa, A. Article CAS PubMed Google Scholar Dailey, M. Article CAS PubMed PubMed Central Google Scholar Williams, E. Article CAS PubMed PubMed Central Google Scholar Bauer, P. Article CAS PubMed Google Scholar Wang, P. Article ADS CAS PubMed Google Scholar Xiao, C. Article CAS PubMed Google Scholar Breen, D. Article CAS PubMed PubMed Central Google Scholar Takahashi, A. Article CAS PubMed Google Scholar Raybould, H. CAS PubMed Google Scholar Meloni, A. Article CAS PubMed Google Scholar Heruc, G. Article CAS PubMed Google Scholar Wu, T. Article CAS PubMed Google Scholar Verspohl, E. Article CAS Google Scholar Duca, F. Article CAS PubMed Google Scholar Duca, F. Article CAS PubMed Google Scholar Boyd, K. Article CAS PubMed Google Scholar Brennan, I. Article CAS PubMed Google Scholar Speechly, D. Article CAS PubMed Google Scholar Stewart, J. Article CAS PubMed Google Scholar Lee, S. Article CAS PubMed PubMed Central Google Scholar Burdyga, G. Article CAS PubMed Google Scholar Peters, J. Article CAS PubMed Google Scholar Barrachina, M. Article ADS CAS PubMed PubMed Central Google Scholar de Lartigue, G. Article ADS PubMed PubMed Central CAS Google Scholar Batt, R. CAS PubMed Google Scholar de Lartigue, G. Article PubMed PubMed Central CAS Google Scholar Rasmussen, B. Article CAS PubMed Google Scholar Lavin, J. CAS PubMed Google Scholar Lavin, J. Article CAS PubMed Google Scholar Schultes, B. Article PubMed Google Scholar Williams, D. Article CAS PubMed Google Scholar Gorboulev, V. Article CAS PubMed Google Scholar Parker, H. Article CAS PubMed PubMed Central Google Scholar Reimann, F. Article CAS PubMed PubMed Central Google Scholar Sun, E. Article CAS PubMed PubMed Central Google Scholar Kuhre, R. Article PubMed Central CAS Google Scholar Jang, H. Article ADS CAS PubMed PubMed Central Google Scholar Saltiel, M. Article PubMed Central CAS Google Scholar Han, P. Article CAS PubMed Google Scholar Chaikomin, R. Article CAS PubMed Google Scholar Poppitt, S. CAS PubMed Google Scholar Woltman, T. CAS PubMed Google Scholar Spiller, R. Article CAS PubMed PubMed Central Google Scholar Maljaars, P. Article CAS PubMed Google Scholar Powell, D. Article CAS PubMed Google Scholar Zhang, X. CAS PubMed Google Scholar Hansotia, T. Article CAS PubMed Google Scholar Gasbjerg, L. Article CAS PubMed Google Scholar Ionut, V. Article CAS PubMed PubMed Central Google Scholar Hayes, M. Article CAS PubMed PubMed Central Google Scholar Lamont, B. Article CAS PubMed Google Scholar Bauer, P. Article CAS PubMed Google Scholar Yang, M. Article CAS PubMed PubMed Central Google Scholar Chapman, I. Article CAS PubMed Google Scholar Naslund, E. Article CAS PubMed PubMed Central Google Scholar Williams, D. Article CAS PubMed PubMed Central Google Scholar Perez, C. Article CAS PubMed Google Scholar Richards, P. Article CAS PubMed PubMed Central Google Scholar Ryan, A. Article CAS PubMed Google Scholar Ryan, A. Article CAS PubMed Google Scholar Ullrich, S. Article CAS Google Scholar van Avesaat, M. Article CAS Google Scholar Bensaid, A. Article CAS PubMed Google Scholar Reidelberger, R. Article CAS PubMed Google Scholar Darcel, N. Article CAS PubMed Google Scholar Yox, D. Article CAS PubMed Google Scholar LaPierre, M. Article CAS PubMed PubMed Central Google Scholar Claessens, M. Article CAS PubMed Google Scholar Blouet, C. Article CAS PubMed Google Scholar Gannon, M. Article CAS PubMed Google Scholar Steinert, R. Article CAS PubMed Google Scholar Dranse, H. Article ADS PubMed PubMed Central CAS Google Scholar Diakogiannaki, E. Article CAS PubMed PubMed Central Google Scholar Caron, J. Article Google Scholar Modvig, I. Article PubMed PubMed Central CAS Google Scholar Mace, O. Article CAS PubMed PubMed Central Google Scholar Wang, J. Article ADS CAS PubMed PubMed Central Google Scholar Oya, M. Article CAS PubMed Google Scholar Hutchison, A. Article CAS PubMed Google Scholar Arciero, P. Article CAS PubMed Google Scholar Pichon, L. Article CAS PubMed Google Scholar Lacroix, M. Article CAS PubMed Google Scholar Manders, R. Article CAS PubMed Google Scholar Raben, A. Article CAS PubMed Google Scholar Cani, P. Article CAS PubMed Google Scholar Sonnenburg, J. Article ADS CAS PubMed PubMed Central Google Scholar Ermund, A. Article CAS PubMed PubMed Central Google Scholar El Aidy, S. Article CAS PubMed Google Scholar Covasa, M. Article Google Scholar Tolhurst, G. Article CAS PubMed PubMed Central Google Scholar Zoetendal, E. Article CAS PubMed PubMed Central Google Scholar Zadeh-Tahmasebi, M. Article CAS PubMed PubMed Central Google Scholar Chimerel, C. Article CAS PubMed PubMed Central Google Scholar Arora, T. Article ADS PubMed PubMed Central CAS Google Scholar Duca, F. Article ADS CAS PubMed PubMed Central Google Scholar Samuel, B. Article ADS CAS PubMed PubMed Central Google Scholar Ye, L. Article CAS PubMed PubMed Central Google Scholar Fredborg, M. |
| Intestinal absorption of micronutrients and macronutrients | Deranged Physiology | Stool Tests Hormone Tests. Nutrient-induced changes in the phenotype and function of the enteric nervous system. Psichas, A. Many well-known cancer-preventing antioxidants are fat-soluble. contributes to the production of smaller bioactive soluble peptides that are better absorbed than the native protein, which can contribute to improving the nutritional value of certain proteins Manus et al. Mineral deficiencies of specific concern include magnesium, zinc, iron, calcium, and selenium, along with vitamins A, D, E, K, and B |
| The metabolic impact of small intestinal nutrient sensing | Please note Micronutrient absorption in the gut some figures Micronutrienr have been included with permission from other third parties. Article CAS PubMed Google Scholar Gorboulev, V. Issue Vol. Nutrition in Clinical Practice. Hamosh, Margit, and Robert O. Minich, Deanna M. Barrachina, M. |
Micronutrient absorption in the gut -
Chronic diseases are a bit trickier and may require lifestyle adjustments to relieve symptoms. If it is a food intolerance, you can adjust your diet! Overall, staying active and hydrated, reducing stress levels, and eating whole foods are pillars of living a healthier lifestyle.
Try focusing on one of these areas to improve throughout your daily routine. Much of life is more than what we can see! Learn more ». Call Us Email Us. For a better us.
Search Search. Search Close this search box. Recipes and Tips to Increase Nutrient Absorption. May 11, Iron and Vitamin C There are two types of iron: heme iron and non-heme iron.
Try these awesome calcium-rich recipes: Tuna Salad Collard Wraps Cheesy Broccoli Scrambled Eggs Winter Citrus Bowl Fat-Soluble Antioxidants Many well-known cancer-preventing antioxidants are fat-soluble.
Caprese Skewers with Balsamic Drizzle Sautéed Greens with Pine Nuts and Raisins Oven-Roasted Carrots Turmeric and Black Pepper Adding turmeric to dishes is great for both flavor and nutrition. Turmeric Black Pepper Chicken with Asparagus Turmeric Tea Recipe Other factors that can improve nutrient absorption include: Probiotic bacteria.
These help to support the growth of the good bacteria in your gut that aid in digestion. Chewing thoroughly and eating slowly. This helps to release enzymes that are an essential part of digestion.
Managing stress. Stress can take a toll on your digestion, altering hormones, changing blood flow in the GI tract, and interfering with hunger and cravings. It can also wipe out a healthy gut!
Taking digestive enzymes. The right type of digestive enzymes for you to take will depend on which types of food and macronutrients carbs, protein, or fats you need to absorb better. Typically, taking a serving with a meal aids in digestion. From the Dietitian How would you know if you have malabsorption?
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STAY CONNECTED:. Copyright © Harrisburg Area YMCA. All rights reserved. For example, restoring the gut microbiome in germ-free mice results in an acute, transient phase, followed by a homeostatic phase that impacts jejunal transcriptomics and metabolomics involved in lipid and glucose metabolism and uptake However, the initial acute response is not observed in the ileum or colon, highlighting the sensitivity of the upper small intestine to the microbiome.
Evidence suggests that the microbiota could also greatly impact nutrient-sensing mechanisms. First, microbial metabolites, especially short-chain fatty acids SCFAs , are known to induce gut peptide secretion from EECs , Most bacterially derived metabolites like SCFAs are produced predominantly in the distal intestine but are also present in small amounts in the ileum and can reduce glucose production via a gut—brain axis , Other metabolites, like indole, are highly abundant in the small intestine and also regulate GLP-1 release from EECs Secondly, the gut microbiota impacts EEC physiology.
For example, isolated cells expressing GLP-1 obtained from germ-free and conventional mice exhibit different transcriptomes, which is rapidly altered after only one day of microbiome colonization, suggesting a more direct effect of the bacteria on the EECs vs.
an indirect effect from altered physiology of the germ-free model Further, intestinal expression and circulating levels of gut peptides are altered in germ-free mice , Similarly, HFD converts zebrafish EECs into a nutrient-insensitive state dependent on gut microbiota, as germ-free zebrafish are resistant to the induction of EEC nutrient-insensitivity while an Acinetobacter strain was able to induce EEC nutrient-insensitivity In line with this, bacterial species directly influence GPR, a receptor linked with lipid-induced gut peptide secretion, and GLP-1 expression in vitro Third, LPS, a bacterial byproduct, blunts vagal activation by intestinal nutrients, leptin, or CCK , Thus, there exists a precedent for the ability of small intestinal microbiota to impact nutrient-induced small intestinal gut—brain signaling Fig.
We put forward a working hypothesis for the mechanistic links between small intestinal nutrient-sensing, microbiota, peptide release, and metabolic regulation.
Bacterial by-products such as LPS can impair lipid and glucose sensing and potentially disrupt ACSL3 and SGLT1 dependent pathways that regulate glucose and energy homeostasis.
Bile salt hydrolase of bacteria contributes to the bile acid pool and regulates bile acid metabolism. As a result, changes in bile acids can alter GLP-1 release and metabolic regulation via intestinal FXR and TGR5 signaling.
High-fat feeding reduces the abundance of small intestinal Lactobacillus species e. gasseri and consequently inhibits ACSL3 expression and impairs lipid sensing. Lastly, metformin increases the abundance of upper small intestinal Lactobacillus and enhances SGLT1 expression and glucose sensing, while also reducing the abundance of Bacteroides fragilis that results in ileal FXR inhibition and improvement in glucose metabolism.
Bariatric surgery enhances small intestinal nutrient sensing mechanisms and consequently lowers glucose levels, while changes in bile acid metabolism and FXR are necessary for the glucose-lowering effect of bariatric surgery. In parallel, gut microbiota alters the bile acid pool and thereby potentially affects nutrient sensing and glucose and energy homeostasis.
Conjugated bile acids are produced in the liver and released into the duodenum, where they are either absorbed or de-conjugated by the bile salt hydrolase of bacteria. Bile acids act as signaling molecules in the intestine and elsewhere, binding to FXR and G protein-coupled receptor 19 also known as TGR5 Most, but not all, studies indicate that inhibition of intestinal FXR improves energy and glucose homeostasis , and FXR signaling represses transcription of GLP-1 and inhibits GLP-1 release from L-cells Interestingly, TGR5 signaling increases GLP-1 release from L-cells , thus complicating the role of bile acid signaling in the intestine Fig.
HF-feeding, obesity, and diabetes are all associated with unique microbial profiles in the large intestine. However, evidence suggests that HF-feeding also alters the composition of small intestinal gut microbiota.
In rodents, the majority of the small intestinal bacteria are Lactobacillius , and HF-feeding results in a drastic reduction in the relative abundance of this genus 45 , Recent work indicates that altered small intestinal microbiota during HFD drives impairments in intestinal lipid-sensing, as the transplant of the small intestinal microbiota of short-term HF fed rats into chow-fed rats abolished the ability of small intestinal lipid infusion to improve glucose tolerance and lower hepatic glucose production.
Treatment of HF-fed rats with a small intestinal infusion of Lactobacillus gasseri enhances upper small intestinal lipid-sensing, via restoration of long-chain acyl-CoA synthetase ACSL3 gasseri exhibits bile salt hydrolase activity and can thus alter the composition of the bile acid pool.
Small intestinal L. gasseri increases ACSL3 and subsequent lipid-sensing through a mechanism dependent on reduced FXR signaling. These findings are consistent with the fact that bile acid sequestrants i. Recent evidence-based on studies with the anti-diabetic medicine metformin indicate that the glucoregulatory impact of intestinal glucose-sensing is mediated by the small intestinal microbiota.
While metformin directly influences hepatic metabolism , as an orally administered drug metformin concentrations in the small intestine are much greater than in the serum Oral metformin reduces blood glucose levels more than intravenous or portal vein administration , demonstrating a role for intestinal-mediated mechanisms of action in improvements in glucose homeostasis.
Pretreatment of HF-fed rats with metformin restores the ability of upper small intestinal glucose infusion to lower glucose production via increased portal vein GLP-1 levels and small intestinal SGLT-1 expression and in parallel changes the composition of small intestinal microbiota This is in line with several other studies that highlight the importance of the gut microbiota in mediating the beneficial effects of metformin , In addition, individuals with newly diagnosed diabetes treated with metformin for three days exhibit alterations in the gut microbiota including increased Lactobacillus and reduced Bacteroides fragilis abundance, which result in inhibition of FXR signaling to improve glucose metabolism This observation is similar to the ability of L.
gasseri to increase intestinal lipid-sensing to improve glucose homeostasis via FXR 45 Fig. Collectively, these studies highlight small intestinal nutrient-sensing mechanism mediates the beneficial effects of metformin through changes in gut microbiota and bile acids. Evidence is emerging on the impact of the small intestinal microbiota also in the efficacy of gastric bypass.
Despite extensive evidence of an overall role of the large intestinal microbiota in mediating the effects of bariatric surgery , at least one study demonstrated that gastric bypass alters the microbiota of the duodenum, jejunum, and ileum In addition, while the jejunal nutrient-sensing mechanism at least partly mediates the beneficial effects of duodenal—jejunal bypass surgery on glucose homeostasis 98 , the glucose-lowering effect of vertical sleeve gastrectomy is dependent on both the gut microbiota and bile acid signaling Fig.
While technological advancements begin to detail the role of intestinal nutrient-sensing in gut—brain neuronal signaling, they concurrently expand the field.
One example of this is the use of single-cell RNA sequencing to understand vagal afferent signaling. Several groups distinctly labeled nodose ganglion neurons according to their expression profile, however, the results are expansive and sometimes contradictory 44 , Based on these studies, vagal afferent neurons containing GLP-1R have no impact on intestinal nutrient-sensing mechanisms, which are instead regulated by GPRpositive neurons Indeed, various neurons terminating in the intestinal mucosa, that likely sense gut peptides released in response to intestinal nutrients, have no effect on food intake, and only direct activation of a subset of IGLE neurons that detect intestinal stretch and not gut peptides suppresses food intake A subset of EECs called neuropods exist that directly synapse with vagal neurons, and rapidly signal via glutamate to the nucleus of the solitary tract in a single synapse to relay initial spatial and temporal information about the meal that could later be followed by more traditional gut peptide signaling Despite these interesting and exciting advances and the discovery of new nutrient sensory cells, the exact neurons that mediate the gut—brain signaling and nutrient sensing in regulating metabolism are complex and warrant future investigations.
Future studies are needed to start teasing apart these complexities, while also integrating the gut microbiota and metabolites into the picture. For instance, while the gut microbiota can impact EECs, it is plausible that vagal afferents themselves can be impacted by bacterial metabolites In contrast to energy intake, the impact of nutrient-induced gut—brain vagal signaling on energy expenditure has been poorly characterized.
Intestinal lipids regulate brown fat thermogenesis via vagal afferents and possibly via GLP-1R signaling , and vagal knockout of the transcription factor peroxisome proliferator-activated receptor-γ, which is activated by fatty acids and could thus be involved in lipid-sensing, affects thermogenesis Likewise in humans, intraduodenal infusion of intralipid increases resting energy expenditure Nutrient infusions into the duodenum of rats modulate energy expenditure Future work is needed to detail the connections between nutrient-sensing mechanism, gut microbiota, and impact on energy expenditure via thermogenesis in brown or browning white adipose tissue Overall, extensive evidence indicates that targeting nutrient sensing in the small intestine impacts energy and glucose homeostasis during normal physiology and in the context of obesity and type 2 diabetes.
Given the distinct effects of HFD and obesity on the diminution of nutrient-sensing dependent gut—brain pathways, future studies examining the gene and environmental interactions are warranted to further the development of personalized medicine approaches.
Similarly, the expansive role of the gut microbiota in host metabolic health further highlights the need for personalized approaches to treating metabolic diseases. As such, studies in humans and rodents beginning to unravel the interactions between the gut microbiota, small intestinal EECs, and vagal signaling, are laying the groundwork for the development of therapeutics targeting small intestinal nutrient sensing to treat obesity and type 2 diabetes.
Obesity and Overweight. World Health Organization, Bhupathiraju, S. Epidemiology of obesity and diabetes and their cardiovascular complications. Article CAS PubMed PubMed Central Google Scholar. Arterburn, D. et al. Comparative effectiveness of bariatric surgery vs.
nonsurgical treatment of type 2 diabetes among severely obese adults. Article PubMed PubMed Central Google Scholar. Brolin, R. Bariatric surgery and long-term control of morbid obesity. Article Google Scholar. Neunlist, M.
Nutrient-induced changes in the phenotype and function of the enteric nervous system. Bentsen, M. Revisiting how the brain senses glucose-and why. Cell Metab. Article CAS PubMed Google Scholar. Rutter, G. Pancreatic beta-cell identity, glucose sensing and the control of insulin secretion. Oosterveer, M.
Hepatic glucose sensing and integrative pathways in the liver. Life Sci. Haber, A. A single-cell survey of the small intestinal epithelium.
Nature , — Article ADS CAS PubMed PubMed Central Google Scholar. Grun, D. Single-cell messenger RNA sequencing reveals rare intestinal cell types.
Article ADS PubMed CAS Google Scholar. Glass, L. Single-cell RNA-sequencing reveals a distinct population of proglucagon-expressing cells specific to the mouse upper small intestine.
Rocca, A. Role of the vagus nerve in mediating proximal nutrient-induced glucagon-like peptide-1 secretion. Endocrinology , — Christiansen, C. The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon. Liver Physiol.
Article CAS Google Scholar. Nauck, M. Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses.
Holst, J. The incretin system in healthy humans: the role of GIP and GLP Metabolism 96 , 46—55 Song, Y. Gut-proglucagon-derived peptides are essential for regulating glucose homeostasis in mice.
Cote, C. Hormonal signaling in the gut. Grasset, E. A specific gut microbiota dysbiosis of type 2 diabetic mice induces GLP-1 resistance through an enteric NO-dependent and gut-brain axis mechanism. Ritter, R. A tale of two endings: modulation of satiation by NMDA receptors on or near central and peripheral vagal afferent terminals.
Waise, T. The metabolic role of vagal afferent innervation. Article PubMed Google Scholar. Muller, T. Glucagon-like peptide 1 GLP Krieger, J. Knockdown of GLP-1 receptors in vagal afferents affects normal food intake and glycemia.
Diabetes 65 , 34—43 CAS PubMed Google Scholar. Varin, E. Distinct neural sites of GLP-1R expression mediate physiological versus pharmacological control of incretin action. Cell Rep. Diepenbroek, C. Validation and characterization of a novel method for selective vagal deafferentation of the gut.
Cheung, G. Intestinal cholecystokinin controls glucose production through a neuronal network. Soty, M. Gut-brain glucose signaling in energy homeostasis.
Greenberg, D. Intraduodenal infusions of fats elicit satiety in sham-feeding rats. Welch, I. Effect of ileal and intravenous infusions of fat emulsions on feeding and satiety in human volunteers. Gastroenterology 89 , — Time course for entry of intestinally infused lipids into blood of rats.
French, S. The effects of intestinal infusion of long-chain fatty acids on food intake in humans. Gastroenterology , — Hajishafiee, M. Gastrointestinal sensing of meal-related signals in humans, and dysregulations in eating-related disorders.
Nutrients 11 , Article CAS PubMed Central Google Scholar. Lu, W. Chylomicron formation and secretion is required for lipid-stimulated release of incretins GLP-1 and GIP. Lipids 47 , — Randich, A. Responses of celiac and cervical vagal afferents to infusions of lipids in the jejunum or ileum of the rat.
Sakata, Y. Postabsorptive factors are important for satiation in rats after a lipid meal. Matzinger, D. The role of long chain fatty acids in regulating food intake and cholecystokinin release in humans. Gut 46 , — Lu, V. Free fatty acid receptors in enteroendocrine cells.
Christensen, L. Vascular, but not luminal, activation of FFAR1 GPR40 stimulates GLP-1 secretion from isolated perfused rat small intestine.
Article PubMed PubMed Central CAS Google Scholar. Psichas, A. Chylomicrons stimulate incretin secretion in mouse and human cells. Diabetologia 60 , — Tran, T. Luminal lipid regulates CD36 levels and downstream signaling to stimulate chylomicron synthesis. Schwartz, G. The lipid messenger OEA links dietary fat intake to satiety.
Sundaresan, S. CDdependent signaling mediates fatty acid-induced gut release of secretin and cholecystokinin. FASEB J. Nakagawa, A. Receptor gene expression of glucagon-like peptide-1, but not glucose-dependent insulinotropic polypeptide, in rat nodose ganglion cells.
Dailey, M. Jejunal linoleic acid infusions require GLP-1 receptor signaling to inhibit food intake: implications for the effectiveness of Roux-en-Y gastric bypass.
Williams, E. Sensory neurons that detect stretch and nutrients in the digestive system. Cell , — Bauer, P. Lactobacillus gasseri in the upper small intestine impacts an ACSL3-dependent fatty acid-sensing pathway regulating whole-body glucose homeostasis.
Wang, P. Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production. Article ADS CAS PubMed Google Scholar. Xiao, C. Evaluation of the effect of enteral lipid sensing on endogenous glucose production in humans.
Diabetes 64 , — Breen, D. Duodenal PKC-delta and cholecystokinin signaling axis regulates glucose production. Diabetes 60 , — Takahashi, A. Involvement of calmodulin and protein kinase C in cholecystokinin release by bombesin from STC-1 cells.
Pancreas 21 , — Raybould, H. Inhibition of gastric emptying in response to intestinal lipid is dependent on chylomicron formation. Meloni, A. GLP-1 receptor activated insulin secretion from pancreatic beta-cells: mechanism and glucose dependence. Diabetes Obes.
Heruc, G. Effects of dipeptidyl peptidase IV inhibition on glycemic, gut hormone, triglyceride, energy expenditure, and energy intake responses to fat in healthy males. Wu, T. Comparative effects of intraduodenal fat and glucose on the gut-incretin axis in healthy males.
Peptides 95 , — Verspohl, E. Cholecystokinin CCK8 regulates glucagon, insulin, and somatostatin secretion from isolated rat pancreatic islets: interaction with glucose.
Duca, F. The modulatory role of high fat feeding on gastrointestinal signals in obesity. Reduced CCK signaling in obese-prone rats fed a high fat diet. Decreased intestinal nutrient response in diet-induced obese rats: role of gut peptides and nutrient receptors.
Impaired GLP-1 signaling contributes to reduced sensitivity to duodenal nutrients in obesity-prone rats during high-fat feeding. Obesity 23 , — Boyd, K. High-fat diet effects on gut motility, hormone, and appetite responses to duodenal lipid in healthy men.
Brennan, I. Effects of fat, protein, and carbohydrate and protein load on appetite, plasma cholecystokinin, peptide YY, and ghrelin, and energy intake in lean and obese men.
Speechly, D. Appetite dysfunction in obese males: evidence for role of hyperinsulinaemia in passive overconsumption with a high fat diet. Current and emerging concepts on the role of peripheral signals in the control of food intake and development of obesity.
Stewart, J. Marked differences in gustatory and gastrointestinal sensitivity to oleic acid between lean and obese men. Lee, S. Blunted vagal cocaine- and amphetamine-regulated transcript promotes hyperphagia and weight gain.
Burdyga, G. Expression of the leptin receptor in rat and human nodose ganglion neurones. Neuroscience , — Peters, J. Modulation of vagal afferent excitation and reduction of food intake by leptin and cholecystokinin.
Barrachina, M. Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice. Natl Acad.
USA 94 , — de Lartigue, G. resistance in vagal afferent neurons inhibits cholecystokinin signaling and satiation in diet induced obese rats. PLoS ONE 7 , e Article ADS PubMed PubMed Central CAS Google Scholar. Batt, R. Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity.
Rasmussen, B. Duodenal activation of cAMP-dependent protein kinase induces vagal afferent firing and lowers glucose production in rats. Gastrointestinal mechanisms of satiation for food. Lavin, J. Appetite regulation by carbohydrate: role of blood glucose and gastrointestinal hormones.
Interaction of insulin, glucagon-like peptide 1, gastric inhibitory polypeptide, and appetite in response to intraduodenal carbohydrate.
Schultes, B. Glycemic increase induced by intravenous glucose infusion fails to affect hunger, appetite, or satiety following breakfast in healthy men.
Appetite , — Williams, D. Evidence that intestinal glucagon-like peptide-1 plays a physiological role in satiety. Gorboulev, V. Diabetes 61 , — Parker, H. Predominant role of active versus facilitative glucose transport for glucagon-like peptide-1 secretion.
Diabetologia 55 , — Reimann, F. Glucose sensing in L cells: a primary cell study. Sun, E. Mechanisms controlling glucose-induced GLP-1 secretion in human small intestine. Diabetes 66 , — Kuhre, R.
On the relationship between glucose absorption and glucose-stimulated secretion of GLP-1, neurotensin, and PYY from different intestinal segments in the rat. Article PubMed Central CAS Google Scholar. Jang, H. Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide USA , — Saltiel, M.
Sweet taste receptor activation in the gut is of limited importance for glucose-stimulated GLP-1 and GIP secretion. Nutrients 9 , Han, P. The sweet taste signalling pathways in the oral cavity and the gastrointestinal tract affect human appetite and food intake: a review.
Food Sci. Chaikomin, R. Effects of mid-jejunal compared to duodenal glucose infusion on peptide hormone release and appetite in healthy men. Poppitt, S. Duodenal and ileal glucose infusions differentially alter gastrointestinal peptides, appetite response, and food intake: a tube feeding study.
Woltman, T. Effects of duodenal and distal ileal infusions of glucose and oleic acid on meal patterns in rats. Spiller, R. The ileal brake—inhibition of jejunal motility after ileal fat perfusion in man. Gut 25 , — Maljaars, P. Ileal brake: a sensible food target for appetite control.
A review. Powell, D. Zhang, X. Comparative effects of proximal and distal small intestinal glucose exposure on glycemia, incretin hormone secretion, and the incretin effect in health and type 2 diabetes.
Diabetes Care 42 , — Hansotia, T. GIP and GLP-1 as incretin hormones: lessons from single and double incretin receptor knockout mice. Gasbjerg, L. Separate and combined glucometabolic effects of endogenous glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1 in healthy individuals.
Diabetes 68 , — Ionut, V. Hayes, M. The common hepatic branch of the vagus is not required to mediate the glycemic and food intake suppressive effects of glucagon-like-peptide Lamont, B. Pancreatic GLP-1 receptor activation is sufficient for incretin control of glucose metabolism in mice. Metformin alters upper small intestinal microbiota that impact a glucose-SGLT1-sensing glucoregulatory pathway.
Jejunal nutrient sensing is required for duodenal-jejunal bypass surgery to rapidly lower glucose concentrations in uncontrolled diabetes.
Yang, M. Duodenal GLP-1 signaling regulates hepatic glucose production through a PKC-delta-dependent neurocircuitry. Cell Death Dis. Chapman, I. Effects of small-intestinal fat and carbohydrate infusions on appetite and food intake in obese and nonobese men.
Naslund, E. Glucagon-like peptide-1 in the pathogenesis of obesity. Drug N. Combination of obesity and high-fat feeding diminishes sensitivity to GLP-1R agonist exendin Diabetes 62 , — Maintenance on a high-fat diet impairs the anorexic response to glucagon-like-peptide-1 receptor activation.
Perez, C. Devazepide, a CCK A antagonist, attenuates the satiating but not the preference conditioning effects of intestinal carbohydrate infusions in rats. Evaluation of the incretin effect in humans using GIP and GLP-1 receptor antagonists. Peptides , Richards, P. High fat diet impairs the function of glucagon-like peptide-1 producing L-cells.
Peptides 77 , 21—27 Ryan, A. Intraduodenal protein modulates antropyloroduodenal motility, hormone release, glycemia, appetite, and energy intake in lean men. Effects of intraduodenal lipid and protein on gut motility and hormone release, glycemia, appetite, and energy intake in lean men.
Ullrich, S. Comparative effects of intraduodenal protein and lipid on ghrelin, peptide YY, and leptin release in healthy men. American journal of physiology. Regulatory, Integr. van Avesaat, M. Small intestinal protein infusion in humans: evidence for a location-specific gradient in intestinal feedback on food intake and GI peptide release.
Int J. Bensaid, A. Protein is more potent than carbohydrate for reducing appetite in rats. Reidelberger, R. Effects of peripheral CCK receptor blockade on feeding responses to duodenal nutrient infusions in rats.
Darcel, N. Activation of vagal afferents in the rat duodenum by protein digests requires PepT1. Yox, D. Vagotomy attenuates suppression of sham feeding induced by intestinal nutrients. LaPierre, M. Glucagon signalling in the dorsal vagal complex is sufficient and necessary for high-protein feeding to regulate glucose homeostasis in vivo.
EMBO Rep. Claessens, M. Blouet, C. The reduced energy intake of rats fed a high-protein low-carbohydrate diet explains the lower fat deposition, but macronutrient substitution accounts for the improved glycemic control. Gannon, M. An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes.
Steinert, R. Effects of intraduodenal infusion of the branched-chain amino acid leucine on ad libitum eating, gut motor and hormone functions, and glycemia in healthy men. Dranse, H. Physiological and therapeutic regulation of glucose homeostasis by upper small intestinal PepT1-mediated protein sensing.
Diakogiannaki, E. Oligopeptides stimulate glucagon-like peptide-1 secretion in mice through proton-coupled uptake and the calcium-sensing receptor. Diabetologia 56 , — Caron, J. Protein digestion-derived peptides and the peripheral regulation of food intake.
Modvig, I. Peptone-mediated glucagon-like peptide-1 secretion depends on intestinal absorption and activation of basolaterally located Calcium-Sensing Receptors. Mace, O. The regulation of K- and L-cell activity by GLUT2 and the calcium-sensing receptor CasR in rat small intestine.
Wang, J. Umami receptor activation increases duodenal bicarbonate secretion via glucagon-like peptide-2 release in rats. Oya, M. The G protein-coupled receptor family C group 6 subtype A GPRC6A receptor is involved in amino acid-induced glucagon-like peptide-1 secretion from GLUTag cells.
Hutchison, A. Comparative effects of intraduodenal whey protein hydrolysate on antropyloroduodenal motility, gut hormones, glycemia, appetite, and energy intake in lean and obese men. Arciero, P. Moderate protein intake improves total and regional body composition and insulin sensitivity in overweight adults.
Metabolism 57 , — Pichon, L. A high-protein, high-fat, carbohydrate-free diet reduces energy intake, hepatic lipogenesis, and adiposity in rats. Lacroix, M.
A long-term high-protein diet markedly reduces adipose tissue without major side effects in Wistar male rats. Manders, R. Co-ingestion of a protein hydrolysate and amino acid mixture with carbohydrate improves plasma glucose disposal in patients with type 2 diabetes.
Raben, A. Meals with similar energy densities but rich in protein, fat, carbohydrate, or alcohol have different effects on energy expenditure and substrate metabolism but not on appetite and energy intake.
Cani, P. Microbiota and metabolites in metabolic diseases. Sonnenburg, J. Diet-microbiota interactions as moderators of human metabolism. Nature , 56—64 Ermund, A. Studies of mucus in mouse stomach, small intestine, and colon.
El Aidy, S. The gut microbiota elicits a profound metabolic reorientation in the mouse jejunal mucosa during conventionalisation. Gut 62 , — Covasa, M. Intestinal sensing by gut microbiota: targeting gut peptides. Tolhurst, G. Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2.
Zoetendal, E. The human small intestinal microbiota is driven by rapid uptake and conversion of simple carbohydrates. ISME J. Zadeh-Tahmasebi, M. Activation of short and long chain fatty acid sensing machinery in the ileum lowers glucose production in vivo.
Chimerel, C. Bacterial metabolite indole modulates incretin secretion from intestinal enteroendocrine L cells.
Arora, T. Microbial regulation of the L cell transcriptome. Increased oral detection, but decreased intestinal signaling for fats in mice lacking gut microbiota.
Samuel, B. Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr Ye, L. High fat diet induces microbiota-dependent silencing of enteroendocrine cells. Elife 8 , e Fredborg, M. G protein-coupled receptor GPR transcription in intestinal epithelial cells is significantly affected by bacteria belonging to the Bacteroides, Proteobacteria, and Firmicutes phyla.
de La Serre, C. Chronic exposure to low dose bacterial lipopolysaccharide inhibits leptin signaling in vagal afferent neurons. Diet-induced obesity leads to the development of leptin resistance in vagal afferent neurons. Wahlstrom, A. Intestinal crosstalk between bile acids and microbiota and its impact on host metabolism.
Article PubMed CAS Google Scholar. Jiang, C. Intestine-selective farnesoid X receptor inhibition improves obesity-related metabolic dysfunction. Trabelsi, M. Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine L cells.
Article ADS PubMed Google Scholar. Thomas, C. TGR5-mediated bile acid sensing controls glucose homeostasis. Rani, R. Characterization of bile salt hydrolase from Lactobacillus gasseri FR4 and demonstration of its substrate specificity and inhibitory mechanism using molecular docking analysis.
Beysen, C. Effect of bile acid sequestrants on glucose metabolism, hepatic de novo lipogenesis, and cholesterol and bile acid kinetics in type 2 diabetes: a randomised controlled study. Foretz, M. Understanding the glucoregulatory mechanisms of metformin in type 2 diabetes mellitus.
Bailey, C. Metformin and the intestine. Diabetologia 51 , — Stepensky, D. Pharmacokinetic-pharmacodynamic analysis of the glucose-lowering effect of metformin in diabetic rats reveals first-pass pharmacodynamic effect. Drug Metab. Sun, L. Gut microbiota and intestinal FXR mediate the clinical benefits of metformin.
Consuming a ib diet is not just about what you eat but also Micronutrienr Skinfold measurement vs well your body absorbs nutrients. Genetics and blood sugar control can ahsorption the Micronutrient absorption in the gut whole foods and take tye supplements, but with proper nutrient absorption, your body and health can optimally use that nutrition. Your gastrointestinal tract plays a vital role in maintaining your health and well-being. One of its primary functions is carrying out the absorption of nutrients that you consume. You need to effectively absorb nutrients like fatsproteins, carbohydratesand micronutrients to produce proper energy, growth, cellular maintenance, and repair.
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