Amelioration of non-alcoholic fatty liver disease by sodium butyrate is linked to the modulation of intestinal tight junctions in db/db mice

Yang, Tingting; Yang, Hao; Cai, Heng; Wang, Haiyan; Chen, Shangxiu; Hu, Yinlu; Jiang, Zhenzhou; Yu, Qiongna; Wang, Zhongjian; Qian, Sitong; Wang, Jianyun; Wang, Tao; Du, Lei; Lü, Qian; Yin, Xiaoxing

doi:10.1039/d0fo01954b

Cited by 38 publications

(59 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the levels of SCFAs were not dramatically different from that in the mice with SB intake. For the first time, we found that supplementation with SB had a limited effect on the level of SCFAs in mice infected with H. pylori , and this limited effect may be related to the limited effect of SB on the metabolites of the gut microbiota, the composition of the gut microbiota, the dose of SB or the absorption of SB in the gastrointestinal tract 45‐50 . Thus, further studies should be conducted to evaluate potential mechanistic relationships between gut microbiota and SCFAs in the future.…”

Section: Discussionmentioning

confidence: 85%

Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short‐chain fatty acids in Helicobacter pylori‐infected mice

Huang

Ding

et al. 2021

Helicobacter

View full text Add to dashboard Cite

Background Inflammation induced by Helicobacter pylori (H. pylori) infection is the basis for the pathogenesis of H. pylori. Butyric acid, a diet‐related microbial‐associated metabolite, is connected to inflammation, metabolic syndrome, and other diseases. Several studies have indicated the effects of sodium butyrate (SB) against bacteria; however, the effects of SB on the main virulence factors of H. pylori, H. pylori‐induced inflammation, and gut microbiota composition remain unclear. Materials and Methods SB was supplemented in H. pylori coculture and administered to mice infected with H. pylori. The effects of SB intake on inflammation, gut microbiota composition, and short‐chain fatty acids (SCFAs) in H. pylori‐infected mice were assessed. Results The in vitro experiments demonstrated that SB not only inhibited the growth of H. pylori but also decreased the mRNA expression of CagA and VacA. SB intake reduced the production of virulence factors in H. pylori‐infected mice, inhibited the IκBα/NF‐κB pathway by reducing the expression of Toll‐like receptors (TLRs), and reduced the production of TNF‐α and IL‐8. Further analysis demonstrated that H. pylori infection altered the relative abundance of the intestinal microbial community in mice. The level of SCFAs in the feces of H. pylori‐infected mice was changed, although the intake of SB did not obviously change the level of SCFAs. Conclusions Our study showed that SB may decrease H. pylori‐induced inflammation by inhibiting the viability and virulence of H. pylori and may reduce inflammation in association with the gut microbiota in H. pylori‐infected mice. This study may provide novel insights into the mechanisms by which SB, a diet‐related microbial‐associated metabolite, affects H. pylori‐induced disease development.

show abstract

Section: Discussionmentioning

confidence: 85%

Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short‐chain fatty acids in Helicobacter pylori‐infected mice

Huang

Ding

et al. 2021

Helicobacter

View full text Add to dashboard Cite

show abstract

“…The decreased lipid storage in the liver upon butyrate exposure could be due to increased lipolysis in hepatocytes themselves and other cells such as adipocytes [44][45][46][47], but possibly also because of increased lipid storage in other organs, such as the muscle [45] or even intestine. Nonetheless, it is unclear whether butyrate can induce lipid storage in vivo in the colon, and how the nutritional environment affects the outcome of butyrate exposure in the colon.…”

Section: Discussionmentioning

confidence: 99%

Butyrate Alters Pyruvate Flux and Induces Lipid Accumulation in Cultured Colonocytes

Bekebrede

Deuren

Gerrits

et al. 2021

IJMS

View full text Add to dashboard Cite

Butyrate is considered the primary energy source of colonocytes and has received wide attention due to its unique health benefits. Insight into the mechanistic effects of butyrate on cellular and metabolic function relies mainly on research in in-vitro-cultured cells. However, cells in culture differ from those in vivo in terms of metabolic phenotype and nutrient availability. For translation, it is therefore important to understand the impact of different nutrients on the effects of butyrate. We investigated the metabolic consequences of butyrate exposure under various culturing conditions, with a focus on the interaction between butyrate and glucose. To investigate whether the effects of butyrate were different between cells with high and low mitochondrial capacity, we cultured HT29 cells under either low- (0.5 mM) or high- (25 mM) glucose conditions. Low-glucose culturing increased the mitochondrial capacity of HT29 cells compared to high-glucose (25 mM) cultured HT29 cells. Long-term exposure to butyrate did not alter mitochondrial bioenergetics, but it decreased glycolytic function, regardless of glucose availability. In addition, both high- and low-glucose-grown HT29 cells showed increased lipid droplet accumulation following long-term butyrate exposure. Acute exposure of cultured cells (HT29 and Caco-2) to butyrate increased their oxygen consumption rate (OCR). A simultaneous decrease in extracellular acidification rate (ECAR) was observed. Furthermore, in the absence of glucose, OCR did not increase in response to butyrate. These results lead us to believe that butyrate itself was not responsible for the observed increase in OCR, but, instead, butyrate stimulated pyruvate flux into mitochondria. Indeed, blocking of the mitochondrial pyruvate carrier prevented a butyrate-induced increase in oxygen consumption. Taken together, our results indicate that butyrate itself is not oxidized in cultured cells but instead alters pyruvate flux and induces lipid accumulation.

show abstract

“…24 As in previous studies, LPS treatment resulted in histopathological lesions, including inflammatory infiltrates, mucosal and crypt lesions, and epithelial changes. 25 In epithelial and immune cells, TLRs play a role in the body's immune system as pattern recognition receptors. TLR4, a member of the toll-like receptor family, can recognize the LPS produced by Gram-negative bacteria and activate NF-κB and mitogen-activated protein (MAPK), two classical inflammatory response pathways, and lead to an increase in inflammatory cytokines (TNF-α, IL-6, IL-1β, etc .).…”

Section: Discussionmentioning

confidence: 99%

Sodium butyrate alleviates intestinal injury and microbial flora disturbance induced by lipopolysaccharides in rats

Dou

Yan

et al. 2022

Food Funct.

View full text Add to dashboard Cite

show abstract

Amelioration of non-alcoholic fatty liver disease by sodium butyrate is linked to the modulation of intestinal tight junctions in db/db mice

Abstract: Intestinal microenvironment, a potential factor that contributed to the development of non-alcoholic fatty liver disease (NALFD) and type 2 diabetes (T2DM), have a closely relationship with intestinal tight junctions (TJs)....

Cited by 38 publications

References 69 publications

Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short‐chain fatty acids in Helicobacter pylori‐infected mice

Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short‐chain fatty acids in Helicobacter pylori‐infected mice

Butyrate Alters Pyruvate Flux and Induces Lipid Accumulation in Cultured Colonocytes

Sodium butyrate alleviates intestinal injury and microbial flora disturbance induced by lipopolysaccharides in rats

Contact Info

Product

Resources

About