Gut microbiota is a factor of risk for obesity and type 2 diabetes

Demidova, T. Yu.; Ойноткинова, О Ш

doi:10.26442/00403660.2020.10.000778

Cited by 9 publications

(2 citation statements)

References 78 publications

(105 reference statements)

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“…The gut microbiota can influence the differentiation and apoptosis of intestinal epithelial cells and positive regulation of the gut microbiota is conducive to alleviating metabolic syndromes ( 34 – 36 ). Some short-chain fatty acids among the metabolites of gut microbiota are capable of improving diet-induced obesity and insulin resistance ( 37 ).…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic acid improves glucose tolerance, lipid metabolism, inflammation and microbiota composition in diabetic db/db mice

Yan¹,

Shen³

et al. 2022

Front. Endocrinol.

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IntroductionChronic and acute chlorogenic acid (CGA) can improve glucose tolerance (GT) and insulin sensitivity (IS). However, whether acute administration of CGA has beneficial effects on hepatic lipid metabolism and cecal microbiota composition remains unclear.MethodsIn the current study, diabetic db/db mice were administered CGA or metformin, and db/m mice were used as controls to explore the effects of CGA on hepatic lipid metabolism, including fatty acid oxidation and transportation and triglyceride (TG) lipolysis and synthesis. Moreover, alterations in the inflammatory response and oxidative stress in the liver and gut microbe composition were evaluated.ResultsThe results showed that CGA decreased body weight and improved glucose tolerance and insulin resistance, and these effects were similar to those of metformin. CGA decreased hepatic lipid content by increasing the expression of CPT1a (carnitine palmitoyltransferase 1a), ACOX1 (Acyl-CoA oxidase 1), ATGL (adipose triglyceride lipase), and HSL (hormone-sensitive lipase) and decreasing that of MGAT1 (monoacylglycerol O-acyltransferase 1), DGAT1 (diacylglycerol O-acyltransferase), DGAT2, CD36, and FATP4 (fatty acid transport protein 4). Additionally, CGA restored the expression of inflammatory genes, including TNF-α (tumor necrosis factor-alpha), IL-1β (interleukin-1beta), IL-6, and IL-10, and genes encoding antioxidant enzymes, including SOD1 (superoxide dismutases 1), SOD2 (superoxide dismutases 2), and GPX1 (glutathione peroxidase 1). Furthermore, CGA improved the bacterial alpha and beta diversity in the cecum. Moreover, CGA recovered the abundance of the phylum Bacteroidetes and the genera Lactobacillus, Blautia, and Enterococcus.DiscussionCGA can improve the antidiabetic effects, and microbes may critically mediate these beneficial effects.

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Section: Discussionmentioning

confidence: 99%

Chlorogenic acid improves glucose tolerance, lipid metabolism, inflammation and microbiota composition in diabetic db/db mice

Yan¹,

Shen³

et al. 2022

Front. Endocrinol.

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“…There is clear evidence that the gut microbiota is related to the incretin effect, the gut microbiota does affect the differentiation and apoptosis of intestinal epithelial cells ( Demidova et al, 2020 ). Adding prebiotics to the diet can increase the amount of bifidobacterial in the distal gut, increase the fermentation of dietary fiber, promote the differentiation of colonic L cells, and increase the secretion of GLP-1.…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic Acid Improves NAFLD by Regulating gut Microbiota and GLP-1

Shi

Zheng

et al. 2021

Front. Pharmacol.

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Our previous studies have shown that chlorogenic acid (CGA) could significantly improve acute and chronic liver injury through antioxidant and anti-inflammatory activities. However, its effect on non-alcoholic fatty liver disease (NAFLD) are not entirely clear. This study aims to explore the effect of CGA on NAFLD induced by high-fat diet (HFD) and whether it regulates the gut microbiota and Glucagon-like peptide-1 (GLP-1). NAFLD mice were established by HFD and treated with or without CGA. Serum transaminase, fasting blood glucose (FBG), blood lipids, insulin, GLP-1 and lipopolysaccharide (LPS) were detected. Liver histology was evaluated with Hematoxylin-eosin staining. Toll like receptor 4 (TLR4) signaling pathway was analyzed with western blot and inflammatory cytokines were detected with real-time PCR. The content of gut microbiota were determined with real-time PCR of the bacterial 16S rRNA gene. Expressions of intestine tight junctional protein were examined with immunohistochemistry. CGA could alleviate HFD-induced hepatic steatosis and inflammation, reduce serum transaminase, FBG and blood lipids, increase insulin sensitivity. CGA also could reverse HFD-induced activation of TLR4 signaling pathway and expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in liver. Meanwhile, CGA increased the content of Bifidobacterium and reduced the content of Escherichia coli in feces. Furthermore, CGA could increase the expression of tight junction proteins Occludin and zonula occludens-1 (ZO-1) in intestinal tissue. Moreover, CGA could the level of LPS and increased the level of GLP-1 in portal vein. These results indicated that CGA protected against HFD-induced hepatic steatosis and inflammation probably through its anti-inflammatory effects associated with regulation of gut microbiota and an increase of GLP-1 secretion and thus could be used as a potential drug for prevention and treatment of NAFLD.

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Evaluation of the impact of unhealthy nutrition on the intestinal microbiota, mitochondrial function and the formation of multiple organ metabolic syndrome, ways of correction

et al. 2023

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BACKGROUND: The problem of metabolic syndrome is considered a demographic catastrophe. According to WHO experts,«by 2025, the prevalence of metabolic syndrome (MS) in the world will amount to more than 300 million people, and in the next 25 years it is expected to increase by 50%.» The pathophysiological mechanisms of MS formation and the role of unhealthy diet on the development of intestinal dysbiosis, mitochondrial insufficiency remain unclear.AIM: To study the effect of unhealthy diet on the state of the intestinal microbiota and the development of metabolicmitochondrial insufficiency in the formation of a multi-organ metabolic syndrome, evaluation of ways of correction.MATERIALS AND METHODS: Clinical picture assessment, anthropometric data (body mass index), laboratory results (glucose, cholesterol and fractions) were carried out in patients with MS, triglycerides, aspartate aminotransferase, alanine aminotransferase, C-reactive protein, lipid peroxidation indicators: malondialdehyde, diene conjugates, schiff bases, hydroperoxides, catalase, superoxide dismutase, succinate dehydrogenase (ASDH), α-glycerophosphate dehydrogenase (α-AGFDH). Hemorheological parameters were evaluated by the apparent viscosity of blood, the yield strength, the aggregation coefficient of erythrocytes and platelets. The microbiota and microbiome of the intestine were evaluated by species, strain composition and the level of metabolites-propionic, butyric, acetic acid, lipopolysaccharides, peptidoglycans. A questionnaire was conducted to study the nature of nutrition.RESULTS: The study included 128 patients with MS and 25 healthy individuals. According to medical outpatient records from anamnesis, questioning of each patient, complaints and clinical picture, 26.2% of patients had type 2 diabetes, 3.74% of men had erectile dysfunction, 7.5% of women had polycystic ovaries, 15.1% had night apnea syndrome, 8.7% hyperuricemic syndrome, 96.5% of patients had metabolic fatty liver steatosis. According to the results of the survey, it was revealed that 99.8% of patients adhered to an unhealthy and unbalanced, high-calorie diet, 46.4% of patients had a low level of physical activity, 48.7% had an average. The revealed disorders of lipid, carbohydrate metabolism, microbiota and intestinal microbiome were associated with increased lipid peroxidation, decreased levels of antioxidant defense enzymes, indicators reflecting mitochondrial function against the background of hemorheological disorders.CONCLUSION: In multi-organ MS, unhealthy diet can be considered as a targeted risk factor triggering pathophysiological mechanisms at the level of the intestinal microbiota, followed by a cascade of metabolic disorders in the form of activation of lipid peroxidation with inhibition of antioxidant defense enzymes, the development of multi-organ mitochondrial insufficiency and the development of latent hemorheological syndrome. The revealed metabolic complex obviously constitutes a multiorgan morphological cluster underlying the development of multi-organ metabolic syndrome. Based on the identified disorders, pathogenetically justified correction of MS should include a balanced diet with mitochondrial protective therapy.

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Gut microbiota is a factor of risk for obesity and type 2 diabetes

Cited by 9 publications

References 78 publications

Chlorogenic acid improves glucose tolerance, lipid metabolism, inflammation and microbiota composition in diabetic db/db mice

Chlorogenic acid improves glucose tolerance, lipid metabolism, inflammation and microbiota composition in diabetic db/db mice

Chlorogenic Acid Improves NAFLD by Regulating gut Microbiota and GLP-1

Evaluation of the impact of unhealthy nutrition on the intestinal microbiota, mitochondrial function and the formation of multiple organ metabolic syndrome, ways of correction

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