Resistant starch from high amylose maize (HAM-RS2) and Dietary butyrate reduce abdominal fat by a different apparent mechanism

Vidrine, Kirk; Ye, Jianping; Martin, Roy J.; McCutcheon, Kathleen L; Raggio, Anne M.; Pelkman, Christine; Durham, Holiday; Zhou, June; Senevirathne, Reshani; Williams, C. C.; Greenway, Frank L.; Finley, John W.; Gao, Zhan‐Guo; Goldsmith, Felicia; Keenan, Michael J.

doi:10.1002/oby.20501

Cited by 57 publications

(48 citation statements)

References 18 publications

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“…Longer term studies that measured postprandial SCFA did not make the picture clearer, as the effects of RS on both fasting and postprandial SCFA and hormone responses vary markedly among the studies (37–39). In summary, though animal research has shown consistent increases in gut hormones following RS fermentation (6,40,41), human data are inconsistent. More acute and chronic RS feeding studies are required to determine whether gut hormones are affected by colonic fermentation.…”

Section: Discussionmentioning

confidence: 95%

Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans

et al. 2016

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BackgroundColonic fermentation of dietary-fibre to short-chain-fatty-acids (SCFA) influences appetite hormone secretion in animals, but SCFA production is excessive in obese animals. This suggests there may be resistance to the effect of SCFA on appetite-hormones in obesity.Objectivesto determine the effects of inulin (IN) and resistant-starch (RS) on postprandial SCFA, and gut hormone (GLP-1, PYY, and ghrelin) responses in healthy overweight/obese (OWO) vs lean (LN) humans.MethodsOvernight fasted participants (13 OWO, 12 LN) consumed 300mL water containing 75g glucose (GLU) as Control, or 75g glucose plus 24g IN, or 28.2g RS using a randomized, single-blind, cross-over design. Blood for appetite-hormones and SCFA was collected at intervals over 6h. A standard lunch was served 4h after the test drink.ResultsRelative to GLU, IN, but not RS, significantly increased SCFA AUC from 4–6h (AUC4-6). Neither IN nor RS affected GLP-1 or PYY-AUC4-6. Although neither IN nor RS reduced ghrelin-AUC4-6 compared to GLU, ghrelin at 6h after IN was significantly lower than that after GLU (p<0.05). After IN, relative to GLU, the changes in SCFA-AUC4-6 were negatively related to the changes in ghrelin-AUC4-6 (p=0.017). SCFA and hormone responses did not differ significantly between LN and OWO.ConclusionsAcute increases in colonic SCFA do not affect GLP-1 or PYY responses in LN or OWO subjects, but may reduce ghrelin. The results do not support the hypothesis that SCFA acutely stimulate PYY and GLP-1 secretion; however, a longer adaptation to increased colonic fermentation or a larger sample size may yield different results.

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Section: Discussionmentioning

confidence: 95%

Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans

et al. 2016

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“…S. boulardii has been shown to modify the production of SCFAs, such as butyrate (23). Evidence suggests that butyrate may contribute to the regulation of several functions at the level of the gut barrier but also to energy homeostasis (47–49) and hepatic steatosis (50). Further investigation is required to understand whether the positive effects observed upon S. boulardii treatment are mediated through butyrate- or SCFA-dependent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Saccharomyces boulardii Administration Changes Gut Microbiota and Reduces Hepatic Steatosis, Low - Grade Inflammation, and Fat Mass in Obese and Type 2 Diabetic db / db Mice

Everard

Matamoros

Geurts

et al. 2014

mBio

237

160

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Growing evidence shows that gut microbes are key factors involved in the regulation of energy homeostasis, metabolic inflammation, lipid metabolism, and glucose metabolism. Therefore, gut microbiota modulations caused by selectively fermented oligosaccharides or probiotic bacteria constitute an interesting target in the physiopathology of obesity. However, to date, no probiotic yeast has been investigated in this context. Therefore, our study aimed to evaluate the impact of the most-studied probiotic yeast (i.e., Saccharomyces boulardii Biocodex) on obesity and associated metabolic features, such as fat mass development, hepatic steatosis, and low-grade inflammation, in obese mice. S. boulardii was administered daily by oral gavage to leptin-resistant obese and type 2 diabetic mice (db/db) for 4 weeks. We found that S. boulardii-treated mice exhibited reduced body weight, fat mass, hepatic steatosis, and inflammatory tone. Interestingly, these effects of S. boulardii on host metabolism were associated with local effects in the intestine. S. boulardii increased cecum weight and cecum tissue weight but also induced dramatic changes in the gut microbial composition at the phylum, family, and genus levels. These gut microbiota changes in response to S. boulardii may also be correlated with the host metabolism response. In conclusion, this study demonstrates for the first time that S. boulardii may act as a beneficial probiotic treatment in the context of obesity and type 2 diabetes.

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“…Butyrate supplementation has been shown to improve glucose metabolism, increase in energy expenditure and reduction in adiposity in animal models [38]. Also, propionate has been shown to increase satiety in animals and humans [39–41]. …”

Section: Candidate Mechanisms Underlying Gut Microbiota Induced Obesitymentioning

confidence: 99%

Gut Microbiome and Obesity: A Plausible Explanation for Obesity

2015

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Obesity is a multifactorial disorder that results in excessive accumulation of adipose tissue. Although obesity is caused by alterations in the energy consumption/expenditure balance, the factors promoting this disequilibrium are incompletely understood. The rapid development of new technologies and analysis strategies to decode the gut microbiota composition and metabolic pathways has opened a door into the complexity of the guest-host interactions between the gut microbiota and its human host in health and in disease. Pivotal studies have demonstrated that manipulation of the gut microbiota and its metabolic pathways can affect host’s adiposity and metabolism. These observations have paved the way for further assessment of the mechanisms underlying these changes. In this review we summarize the current evidence for possible mechanisms underlying gut microbiota induced obesity. The review addresses some well-known effects of the gut microbiota on energy harvesting and changes in metabolic machinery, on metabolic and immune interactions and on possible changes in brain function and behavior. Although there is limited understanding on the symbiotic relationship between us and our gut microbiome, and how disturbances of this relationship affects our health, there is compelling evidence for an important role of the gut microbiota in the development and perpetuation of obesity.

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Resistant starch from high amylose maize (HAM-RS2) and Dietary butyrate reduce abdominal fat by a different apparent mechanism

Cited by 57 publications

References 18 publications

Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans

Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans

Saccharomyces boulardii Administration Changes Gut Microbiota and Reduces Hepatic Steatosis, Low - Grade Inflammation, and Fat Mass in Obese and Type 2 Diabetic db / db Mice

Gut Microbiome and Obesity: A Plausible Explanation for Obesity

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