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Limosilactobacillus fermentum MG4295 Improves Hyperglycemia in High-Fat Diet-Induced Mice.

ABSTRACT: Hyperglycemia due to uncontrolled glucose regulation is widely known as cause of diabetes, non-alcoholic fatty liver disease (NAFLD), and other complications. NAFLD refers to a condition in which fat is excessively accumulated, whether inflamed or not, and has caused serious medical problems in recent years. The aim of this study was to explore the antihyperglycemia effects of Limosilactobacillus fermentum MG4295 (L. fermentum MG4295) in high-fat diet (HFD)-induced in vivo. We demonstrated the suitability of L. fermentum MG4295 as a probiotic by observing its stability, survivability, and proliferation under simulated gastrointestinal conditions, and safety, antibiotic susceptibility, hemolysis, and enzyme activity. The potential antihyperglycemic activity of L. fermentum MG4295 was investigated in an HFD and sugar-water-induced mouse model. Administration of this strain for 12 weeks showed an improved trend in glucose tolerance, insulin, alanine amino transferase, total cholesterol, low-density lipoprotein cholesterol, and glucagon-like peptide-1. Histopathological analysis revealed that L. fermentum MG4295 significantly reduced the histopathological scores of hepatic steatosis, inflammation, and hepatocellular hypertrophy in liver tissues and lipid content in adipose tissues. Administration of L. fermentum MG4295 upregulated IRS-1, AKT, and GLUT4 and downregulated G6Pc and PEPCK expression in liver and/or muscle tissues. Our results suggest that L. fermentum MG4295 can improve hyperglycemia. Furthermore, it can be used as a dietary functional supplement to manage blood glucose.

SUBMITTER: Kim JE

PROVIDER: S-EPMC8774940 | biostudies-literature |

REPOSITORIES: biostudies-literature

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<i>Limosilactobacillus fermentum</i> MG4294 and <i>Lactiplantibacillus plantarum</i> MG5289 Ameliorates Nonalcoholic Fatty Liver Disease in High-Fat Diet-Induced Mice.

Project description:Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease and the leading cause of liver-related deaths worldwide. It has been established that microorganisms are involved in the interaction between the intestinal lumen and the liver; therefore, studies on probiotics as potential candidates are increasing. This study evaluated the effects of Limosilactobacillus fermentum MG4294 and Lactiplantibacillus plantarum MG5289 on NAFLD. The MG4294 and MG5289 reduced lipid accumulation in FFA-induced HepG2 by suppressing the adipogenic proteins through the regulation of AMP-activated protein kinase (AMPK). The administration of these strains in the HFD-induced mice model lowered body weight, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and cholesterol levels. In particular, MG4294 and MG5289 restored liver TG and TC to normal levels by lowering lipid and cholesterol-related proteins via the modulation of AMPK in the liver tissue. In addition, the administration of MG4294 and MG5289 reduced pro-inflammatory cytokines (tumor necrosis factor (TNF)-α and interleukin (IL)-1β-, and IL6) in the intestinal tissues of the HFD-induced mouse model. In conclusion, MG4294 and MG5289 can be presented as probiotics with the potential to prevent NAFLD.

| S-EPMC10143775 | biostudies-literature

Plantago asiatica L. Seed Extract Improves Lipid Accumulation and Hyperglycemia in High-Fat Diet-Induced Obese Mice.

Project description:Obesity and its common association with type 2 diabetes, dyslipidemia, and cardiovascular diseases are worldwide epidemics. Currently, to prevent or treat obesity and associated metabolic disorders, herbal dietary supplements or medicines have attracted more and more attention owing to their relative effectiveness with fewer significant side effects. We investigate the therapeutic effects and underlying mechanisms of Plantago asiatica L. seed extract (PSE) on obesity and associated metabolic disorders in high-fat (HF) diet-induced mice. Our results displayed that PSE did not modify food intake or body weight but decreased abdominal white adipose tissue ratio, white/brown adipocyte size, serum total cholesterol, triglyceride (TG), low density lipoprotein cholesterol, free fatty acid, and hepatic TG concentrations when compared with the HF group. The levels of fasting blood glucose and glucose tolerance were improved in the PSE group when compared with the HF group. Furthermore, PSE upregulated mRNA expressions of peroxisome proliferator activated receptors (PPARs) and target genes related to fatty acid metabolism and energy expenditure in liver and adipose tissue of obese mice when compared with the HF group. PSE treatment effectively improved lipid and glucose metabolism in HF diet-induced obese mice. These effects might be attributed to the upregulation of PPAR signaling.

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FKBP12.6-knockout mice display hyperinsulinemia and resistance to high-fat diet-induced hyperglycemia.

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Slowly Digestible Carbohydrate Diet Ameliorates Hyperglycemia and Hyperlipidemia in High-Fat Diet/Streptozocin-Induced Diabetic Mice.

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| S-EPMC9051025 | biostudies-literature

High phenolics Rutgers Scarlet Lettuce improves glucose metabolism in high fat diet-induced obese mice.

Project description:ScopeThe ability of high phenolic Rutgers Scarlet Lettuce (RSL) to attenuate metabolic syndrome and gut dysbiosis was studied in very high fat diet (VHFD)-fed mice. Phenolic absorption was assessed in vivo and in a gastrointestinal tract model.Methods and resultsMice were fed VHFD, VHFD supplemented with RSL (RSL-VHFD) or store-purchased green lettuce (GL-VHFD), or low-fat diet (LFD) for 13 weeks. Compared to VHFD or GL-VHFD-fed groups, RSL-VHFD group showed significantly improved oral glucose tolerance (p<0.05). Comparison of VHFD, RSL-VHFD, and GL-VHFD groups revealed no significant differences with respect to insulin tolerance, hepatic lipids, body weight gain, fat mass, plasma glucose, triglycerides, free fatty acid, and lipopolysaccharide levels, as well as relative abundances of major bacterial phyla from 16S rDNA amplicon data sequences (from fecal and cecal samples). However, RSL and GL-supplementation increased abundance of several taxa involved in plant polysaccharide degradation/fermentation. RSL phenolics chlorogenic acid, quercetin-3-glucoside, and quercetin-malonyl-glucoside were bioaccessible in the TIM-1 digestion model, but had relatively low recovery.ConclusionsRSL phenolics contributed to attenuation of post-prandial hyperglycemia. Changes in gut microbiota were likely due to microbiota accessible carbohydrates in RSL and GL rather than RSL phenolics, which may be metabolized, absorbed, or degraded before reaching the colon.

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Diphyllin Improves High-Fat Diet-Induced Obesity in Mice Through Brown and Beige Adipocytes.

Project description:Brown adipose tissue (BAT) and beige adipose tissue dissipate metabolic energy and mediate nonshivering thermogenesis, thereby boosting energy expenditure. Increasing the browning of BAT and beige adipose tissue is expected to be a promising strategy for combatting obesity. Through phenotype screening of C3H10-T1/2 mesenchymal stem cells, diphyllin was identified as a promising molecule in promoting brown adipocyte differentiation. In vitro studies revealed that diphyllin promoted C3H10-T1/2 cell and primary brown/beige preadipocyte differentiation and thermogenesis, which resulted increased energy consumption. We synthesized the compound and evaluated its effect on metabolism in vivo. Chronic experiments revealed that mice fed a high-fat diet (HFD) with 100 mg/kg diphyllin had ameliorated oral glucose tolerance and insulin sensitivity and decreased body weight and fat content ratio. Adaptive thermogenesis in HFD-fed mice under cold stimulation and whole-body energy expenditure were augmented after chronic diphyllin treatment. Diphyllin may be involved in regulating the development of brown and beige adipocytes by inhibiting V-ATPase and reducing intracellular autophagy. This study provides new clues for the discovery of anti-obesity molecules from natural products.

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Haploid insufficiency of suppressor enhancer Lin12 1-like (SEL1L) protein predisposes mice to high fat diet-induced hyperglycemia.

Project description:Increasing evidence suggests that endoplasmic reticulum (ER) stress plays an important role in the pathogenesis of type 2 diabetes mellitus. SEL1L is an ER membrane protein that is highly expressed in the pancreatic islet and acinar cells. We have recently reported that a deficiency of SEL1L causes systemic ER stress and leads to embryonic lethality in mice. Here we show that mice with one functional allele of Sel1l (Sel1l(+/-)) are more susceptible to high fat diet (HFD)-induced hyperglycemia. Sel1l(+/-) mice have a markedly reduced β-cell mass as a result of decreased β-cell proliferation. Consequently, Sel1l(+/-) mice are severely glucose-intolerant and exhibit significantly retarded glucose-stimulated insulin secretion. Pancreatic islets from Sel1l(+/-) mice stimulated with a high concentration of glucose in vitro express significantly higher levels of unfolded protein response genes than those from wild-type control mice. Furthermore, dominant-negative interference of SEL1L function in insulinoma cell lines severely impairs, whereas overexpression of SEL1L efficiently improves protein secretion. Taken together, our results indicate that haploid insufficiency of SEL1L predispose mice to high fat diet-induced hyperglycemia. Our findings highlight a critical and previously unknown function for SEL1L in regulating adult β-cell function and growth.

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Resistant dextrin improves high-fat-high-fructose diet induced insulin resistance.

Project description:Background:Insulin resistance is an important defect associated with obesity and type 2 diabetes mellitus. Many studies have been reported that dietary fiber exerts beneficial metabolic effects. Resistant dextrin is a soluble fiber. The aim of this study was to investigate the effects of resistant dextrin on high-fat-high-fructose diet induced obese mice and to explore the underlying mechanisms. Methods:Seventeen 4-week-old male C57BL/6?J mice were fed a normal diet (ND) or HFHFD for 22?weeks, and were gavaged with resistant dextrin (5?g/kg) for 10?weeks. Glucose tolerance test (GTT) and insulin tolerance test (ITT) were performed, serum fasting insulin (FINS) and serum biochemical parameters were determined, the contents of triglyceride (TG) and total cholesterol (TC) in liver tissues were determined by enzymatic method. The pathological changes in liver were detected by HE staining. Real time PCR and Western blot were used to detect the expression of insulin signaling pathway and the fatty acid ? oxidation pathway related genes and proteins respectively. The gut microbiota were analyzed via 16?s rRNA sequencing. Results:Resistant dextrin significantly decreased serum FINS, improved serum lipid profiles, reduced the contents of liver TG and TC. The insulin signaling pathway and the fatty acid ? oxidation pathway were promoted. The abundance of metabolically beneficial bacteria such as Prevotella and Akkermansia in the intestinal flora of the resistant dextrin group were increased. Conclusions:Resistant dextrin can significantly ameliorate liver insulin resistance, improve serum lipid levels, as well as reduce hepatic lipid deposition. The modulation of gut microbiota might be responsible for the beneficial effects of resistant dextrin.

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Allicin Improves Metabolism in High-Fat Diet-Induced Obese Mice by Modulating the Gut Microbiota.

Project description:Allicin, naturally present in the bulbs of the lily family, has anticancer, blood pressure lowering, blood fat lowering and diabetes improving effects. Recent studies have shown that allicin promotes the browning of white adipocytes and reduces the weight gain of mice induced by high-fat diet. While the gut microbiota has a strong relationship with obesity and energy metabolism, the effect of allicin on weight loss via gut microorganisms is still unclear. In this study, we treated obese mice induced by high-fat diet with allicin to determine its effects on fat deposition, blood metabolic parameters and intestinal morphology. Furthermore, we used high-throughput sequencing on a MiSeq Illumina platform to determine the gut microorganisms' species. We found that allicin significantly reduced the weight gain of obese mice by promoting lipolysis and thermogenesis, as well as blood metabolism and intestinal morphology, and suppressing hepatic lipid synthesis and transport. In addition, allicin changed the composition of the intestinal microbiota and increased the proportion of beneficial bacteria. In conclusion, our study showed that allicin improves metabolism in high-fat induced obese mice by modulating the gut microbiota. Our findings provide a theoretical basis for further elucidation of the weight loss mechanism of allicin.

| S-EPMC6949904 | biostudies-literature

Resveratrol improves high-fat diet-induced insulin resistance in mice by downregulating the lncRNA NONMMUT008655.2.

Project description:As essential players in the field of diabetes treatment, resveratrol (RSV) has received much attention in recent years. However, it is unclear whether it can improve insulin resistance by regulating the long-chain non-coding RNA (lncRNA). The objective of this study was to investigate whether RSV improves high-fat diet-induced insulin resistance in mice by regulating thelncRNANONMMUT008655.2 in vivo and in vitro. To this end, animal and cell insulin resistance models were developed. Specifically, C57BL/6J mice were fed a high-fat diet (HFD) and administered RSV for eight weeks. Additionally, mouse Hepa cells were treated with palmitic acid, transfected with siRNA NONMMUT008655.2, and treated with RSV. Treated mice and cells were then compared to normal controls that were not exposed to RSV. In the animal model, RSV was found to decrease the levels of fasting blood glucose, triglycerides, and low-density lipoprotein cholesterol, as well as the insulin index and area under the curve; while increasing the insulin sensitivity index. Besides, RSV decreased the expression levels of SOCS3, G6PC, and FOXO1 yet increased that of p-Akt and p-FOXO1 in mice. The same results were observed following knockdown of NONMMUT008655.2 in cells. Overall, our results suggest that RSV may improve hepatic insulin resistance and control blood glucose levels by downregulating lncRNA NONMMUT008655.2.

| S-EPMC7013227 | biostudies-literature

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