Protective role of sodium butyrate, a HDAC inhibitor on beta-cell proliferation, function and glucose homeostasis through modulation of p38/ERK MAPK and apoptotic pathways: Study in juvenile diabetic rat

Khan, Sabbir; Jena, Gopabandhu

doi:10.1016/j.cbi.2014.02.001

Cited by 141 publications

(93 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…24,28,29,31,38,49 Some studies have demonstrated that sodium butyrate, a SCFA, has beneficial effects on animal models of T1DM and T2DM. 31,36,39 In the present work, we demonstrated that butyrate alleviates the metabolic impairments induced by HF diet administration in mice, by inhibiting the development of an insulin resistance state, which was associated with improvement of insulin-secreting function of beta cells and strengthening of the TJ-mediated intestinal epithelial barrier.…”

Section: Discussionsupporting

confidence: 50%

“…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%

See 1 more Smart Citation

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)

105

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 50%

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)

105

View full text Add to dashboard Cite

show abstract

“…I] Sodium butyrate (NaB) [14] Sodium butyrate (NaB) is a short chain fatty acid having HDAC inhibitory activity.…”

Section: Hdaci Used In Diabetic Kidney Model Studymentioning

confidence: 99%

“…HDACI can improve the DN by inhibiting fibrosis [2], inhibiting transcription factors [2], may prevent Apoptosis [2] , anti-inflammatory [2], immunomodulation [2] correct renal metabolism. Improve Beta cell proliferation and function [14] and glucose homoeostasis. [14] However its long way to go and one say HDACI are still in initial stage in treatment of Diabetic Nephropathy.…”

Section: Figure From Sourcementioning

confidence: 99%

See 1 more Smart Citation

Embryonic Life of Hdac Inhibitors: – In Diabetic Nephropathy

Soni¹

2017

WJPPS

View full text Add to dashboard Cite

show abstract

Sodium Butyrate Ameliorates l‐Arginine‐Induced Pancreatitis and Associated Fibrosis in Wistar Rat: Role of Inflammation and Nitrosative Stress

Kanika

Khan

Jena

2015

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Several reports indicated that histone deacetylases (HDACs) play a crucial role in inflammation and fibrogenesis. Sodium butyrate (SB) is a short-chain fatty acid having HDAC inhibition potential. The present study aimed to evaluate the protective effect of SB against L-arginine (L-Arg)-induced pancreatic fibrosis in Wistar rats. Pancreatic fibrosis was induced by twice intraperitoneal (i.p.) injections of 20% L-Arg (250 mg/100 g) at 2-h interval on day 1, 4, 7, and 10, whereas SB (800 mg/kg/day) was administrated for 10 days. At the end of the study, biochemical estimations, histological alterations, DNA damage, and the expression of various proteins were evaluated. Posttreatment of SB decreased L-Arg-induced oxidative and nitrosative stress, DNA damage, histological alterations, and fibrosis. Interestingly, posttreatment of SB significantly decreased the expression of α-smooth muscle actin, interleukin-1β, inducible nitric oxide synthase, and 3-nitrotyrosine. The present study demonstrated that posttreatment of SB alleviates L-Arg-induced pancreatic damage and fibrosis in rat.

show abstract

Protective role of sodium butyrate, a HDAC inhibitor on beta-cell proliferation, function and glucose homeostasis through modulation of p38/ERK MAPK and apoptotic pathways: Study in juvenile diabetic rat

Cited by 141 publications

References 47 publications

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

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

Embryonic Life of Hdac Inhibitors: – In Diabetic Nephropathy

Sodium Butyrate Ameliorates l‐Arginine‐Induced Pancreatitis and Associated Fibrosis in Wistar Rat: Role of Inflammation and Nitrosative Stress

Contact Info

Product

Resources

About