Sodium butyrate reduces insulin-resistance, fat accumulation and dyslipidemia in type-2 diabetic rat: A comparative study with metformin

Khan, Sabbir; Jena, Gopabandhu

doi:10.1016/j.cbi.2016.06.007

Cited by 142 publications

(125 citation statements)

References 44 publications

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“…We found that HDAC inhibition effectively prevented body weight gain, attenuated hyperinsulinemia, hyperglycemia, triglycerides, and attenuated whole body insulin resistance in the HFD mice, implying that HDAC inhibition exerts a robust protective effect against HFD‐induced metabolic dysfunction. The effect of attenuating glucose tolerance by HDAC inhibition is also supported by a recent observation in which glucose homeostasis was improved by sodium butyrate in juvenile diabetic rat [Khan and Jena, ]. It was reported that food intake was increased with sodium butyrate in different strain of mice.…”

Section: Discussionmentioning

confidence: 69%

Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice

et al. 2017

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Histone deacetylases are recently identified to act as key regulators for cardiac pathophysiology and metabolic disorders. However, the function of histone deacetylase (HDAC) in controlling cardiac performance in type II diabetes and obesity remains unknown. Here we determine whether HDAC inhibition attenuates high fat diet (HFD)-induced cardiac dysfunction and improves metabolic features. Adult mice were fed with either HFD or standard chow food for 24 weeks. Starting at 12 weeks, mice were divided into four groups randomly, in which sodium butyrate (1%), a potent HDAC inhibitor, was provided to chow and HFD-fed mice in drinking water, respectively. Glucose intolerance, metabolic parameters, cardiac function, and remodeling were assessed. Histological analysis and cellular signaling were examined at 24 weeks following euthanization of mice. HFD-fed mice demonstrated myocardial dysfunction and profound interstitial fibrosis, which were attenuated by HDAC inhibition. HFD-induced metabolic syndrome features insulin resistance, obesity, hyperinsulinemia, hyperglycemia, lipid accumulations, and cardiac hypertrophy, these effects were prevented by HDAC inhibition. Furthermore, HDAC inhibition attenuated myocyte apoptosis, reduced production of reactive oxygen species, and increased angiogenesis in the HFD-fed myocardium. Notably, HFD induced decreases in MKK3, p38, p38 regulated/activated protein kinase (PRAK) and Akt-1, but not p44/42 phosphorylation, which were prevented by HDAC inhibition. These results suggest that HDAC inhibition plays a critical role to preserve cardiac performance and mitigate metabolic disorders in obesity and diabetes, which is associated with MKK3/p38/PRAK pathway. The study holds promise in developing a new therapeutic strategy in the treatment of type II diabetic-induced heart failure and metabolic disorders.

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Section: Discussionmentioning

confidence: 69%

Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice

et al. 2017

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“…Butyrate is also considered to exert prebiotic effects elsewhere in the body due to its ability to pass through enterocytes and into the circulation . Previous studies have demonstrated that butyrate reduces fat accumulation and suppresses insulin resistance . Here, gut microbiota‐produced butyrate greatly improved insulin resistance, which is highly associated with its positive effect on serum blood lipid compositions, including a reduction in the circulation of triacylglycerols and the suppression of Sphs and ceramides synthesis.…”

Section: Discussionmentioning

confidence: 87%

Gut Microbiome‐Induced Shift of Acetate to Butyrate Positively Manages Dysbiosis in High Fat Diet

Shang

Zhou

et al. 2018

Molecular Nutrition Food Res

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“…34 Regarding its systemic effect, there has been recently suggested an anti-diabetogenic effect of this SCFA in animal models of T1DM and T2DM, which was related to its action as histone deacetylase (HDAC) inhibitor. 31,[35][36][37][38][39] Nevertheless, to the best of our knowledge, there is no study looking at the relationship between the effect of butyrate on the T2DM-associated metabolic, hepatic and pancreatic alterations and its action on the TJ-mediated intestinal epithelial barrier. Therefore, the aim of the present work was to investigate the effect of diet supplementation with sodium butyrate on metabolic parameters, adiposity, hepatic and pancreatic lipid accumulation, beta cell function/mass as well as on the structure and function of the intestinal epithelial barrier of obese and prediabetic mice.…”

Section: Introductionmentioning

confidence: 99%

Butyrate reduces high-fat diet-induced metabolic alterations, hepatic steatosis and pancreatic beta cell and intestinal barrier dysfunctions in prediabetic mice

Matheus

Monteiro

Oliveira

et al. 2017

Exp Biol Med (Maywood)

130

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Butyrate is a short-chain fatty acid produced by the intestinal microbiota through the fermentation of non-absorbable carbohydrates and proteins (e.g. fibers). Sodium butyrate incorporated into the diet displayed a protective action on metabolic, hepatic, pancreatic and intestinal alterations induced by high-fat diet in mice, resulting in significant inhibition of the development of a prediabetic state. Thus, our data suggest that butyrate may have a potential therapeutic use in the treatment of type 2 diabetes and related disorders. AbstractIn this study, we investigated the effect of diet supplementation with sodium butyrate (5% w/w), a short-chain fatty acid produced by the intestinal microbiota, on metabolic parameters, body adiposity, hepatic and pancreatic lipid accumulation, beta cell function/mass as well as on the structure and function of the tight junction-mediated intestinal epithelial barrier in both normal and obese/prediabetic C57 mice fed a regular (control) or high-fat diet for 60 days, respectively. Butyrate treatment significantly inhibited all the high-fat-induced metabolic dysfunctions evaluated, i.e. significantly reduced the weight gain and body adiposity as well as the insulin resistant state, hyperglycemia and hyperinsulinemia, without changing food intake. In addition, high-fat-fed mice treated with this short-chain fatty acid displayed no compensatory hyperplasia of pancreatic beta cells nor marked hepatic steatosis as seen in prediabetic mice after high-fat diet only. Isolated pancreatic islets from high-fat-fed mice treated with butyrate showed improvement of the insulin secretion, which was associated with a significant decrease in lipid accumulation within the pancreas. Butyrate enhanced the intestinal epithelial barrier, as revealed by the FITC-Dextran permeability assay, which was accompanied by a significant increase in the junctional content of the tight junction-associated claudin-1 in intestinal epithelia of jejunum, ileum, and colon of both control and high-fat mice. In conclusion, our results showed that diet supplementation with butyrate inhibits the deleterious effects of high-fat diet intake on metabolic parameters and structure/function of several tissues/ organs associated with type 2 diabetes mellitus in a mouse model, suggesting a potential use of this short-chain fatty acid in the treatment of this endocrine-metabolic disorder.

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Sodium butyrate reduces insulin-resistance, fat accumulation and dyslipidemia in type-2 diabetic rat: A comparative study with metformin

Cited by 142 publications

References 44 publications

Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice

Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice

Gut Microbiome‐Induced Shift of Acetate to Butyrate Positively Manages Dysbiosis in High Fat Diet

Butyrate reduces high-fat diet-induced metabolic alterations, hepatic steatosis and pancreatic beta cell and intestinal barrier dysfunctions in prediabetic mice

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Sodium butyrate reduces insulin-resistance, fat accumulation and dyslipidemia in type-2 diabetic rat: A comparative study with metformin

Cited by 142 publications

References 44 publications

Sodium Butyrate Protects ­Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice

Sodium Butyrate Protects ­Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice

Gut Microbiome‐Induced Shift of Acetate to Butyrate Positively Manages Dysbiosis in High Fat Diet

Butyrate reduces high-fat diet-induced metabolic alterations, hepatic steatosis and pancreatic beta cell and intestinal barrier dysfunctions in prediabetic mice

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Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice

Sodium Butyrate Protects Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice