Dataset Information

The mitigative effect of isorhamnetin against type 2 diabetes via gut microbiota regulation in mice.

ABSTRACT: In order to demonstrate the effects of isorhamnetin (IH) on the symptoms of type 2 diabetes mellitus (T2DM) and the role of gut microbiota in this process, an T2DM mouse model was established via a high-fat diet and streptozotocin. After 6 weeks of IH intervention and diabetes phenotype monitoring, the mice were dissected. We detected blood indicators and visceral pathology. Contents of the cecum were collected for 16S rRNA sequencing and short chain fatty acid (SCFAs) detection. The results showed that after IH intervention, the body weight of type 2 diabetic mice was gradually stabilized, fasting blood glucose was significantly decreased, and food intake was reduced (P < 0.05). Isorhamnetin significantly increased the level of SCFAs and decreased the levels of blood lipids and inflammatory factors in mice (P < 0.05). 16S rRNA sequencing results showed that Lactobacillus were significantly decreased and Bacteroidales S24-7 group_norank were significantly increased (P < 0.05). Interestingly, gut microbiota was significantly correlated with inflammatory factors, blood lipids, and SCFAs (P < 0.05). Taken together, our data demonstrated that isorhamnetin could improve the diabetic effects in T2DM mice, which might be mediated by gut microbiota.

SUBMITTER: Li J

PROVIDER: S-EPMC9815710 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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The mitigative effect of isorhamnetin against type 2 diabetes <i>via</i> gut microbiota regulation in mice.

Li Jinjun J Yuan Huimin H Zhao Zhiqi Z Li Li L Li Xiaoqiong X Zhu Liying L Wang Xin X Sun Ping P Xiao Yinping Y

Frontiers in nutrition 20221222

In order to demonstrate the effects of isorhamnetin (IH) on the symptoms of type 2 diabetes mellitus (T2DM) and the role of gut microbiota in this process, an T2DM mouse model was established <i>via</i> a high-fat diet and streptozotocin. After 6 weeks of IH intervention and diabetes phenotype monitoring, the mice were dissected. We detected blood indicators and visceral pathology. Contents of the cecum were collected for 16S rRNA sequencing and short chain fatty acid (SCFAs) detection. The resu ...[more]

PMID: 36618710

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Project description:This study aims to explore the molecular mechanisms of Lycium barbarum polysaccharide (LBP) in alleviating type 2 diabetes through intestinal flora modulation. A high-fat diet (HFD) combined with streptozotocin (STZ) was applied to create a diabetic model. The results indicated that LBP effectively alleviated the symptoms of hyperglycemia, hyperlipidemia, and insulin resistance in diabetic mice. A high dosage of LBP exerted better hypoglycemic effects than low and medium dosages. In diabetic mice, LBP significantly boosted the activities of CAT, SOD, and GSH-Px and reduced inflammation. The analysis of 16S rDNA disclosed that LBP notably improved the composition of intestinal flora, increasing the relative abundance of Bacteroides, Ruminococcaceae_UCG-014, Intestinimonas, Mucispirillum, Ruminococcaceae_UCG-009 and decreasing the relative abundance of Allobaculum, Dubosiella, Romboutsia. LBP significantly improved the production of short-chain fatty acids (SCFAs) in diabetic mice, which corresponded to the increase in the beneficial genus. According to Spearman's correlation analysis, Cetobacterium, Streptococcus, Ralstonia. Cetobacterium, Ruminiclostridium, and Bifidobacterium correlated positively with insulin, whereas Cetobacterium, Millionella, Clostridium_sensu_stricto_1, Streptococcus, and Ruminococcaceae_UCG_009 correlated negatively with HOMA-IR, HDL-C, ALT, AST, TC, and lipopolysaccharide (LPS). These findings suggested that the mentioned genus may be beneficial to diabetic mice's hypoglycemia and hypolipidemia. The up-regulation of peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and insulin were remarkably reversed by LBP in diabetic mice. The real-time PCR (RT-PCR) analysis illustrated that LBP distinctly regulated the glucose metabolism of diabetic mice by activating the IRS/PI3K/Akt signal pathway. These results indicated that LBP effectively alleviated the hyperglycemia and hyperlipidemia of diabetic mice by modulating intestinal flora.

Project description:Background/Objectives: Diabetes mellitus is often accompanied by mental health complications, including anxiety, depression, and cognitive decline. Recent research suggested that capsaicin, the active component of chili peppers, may influence mental health. This study aimed to determine the effect of dietary capsaicin on mental disorders in a type 1 diabetes (T1D) mouse model, while also exploring the potential involvement of the microbiota-gut-brain axis. Methods: We induced T1D in mice using streptozotocin (STZ) and administered a diet supplemented with 0.005% capsaicin for five weeks. Behavioral assessments, including the open field test (OFT), tail suspension test (TST), forced swimming test (FST), elevated plus maze (EPM) test, and Morris water maze (MWM) test, were conducted to evaluate depressive and anxiety-like behaviors as well as cognitive function. Targeted and untargeted metabolomics analyses were performed to assess neurotransmitter levels in the hippocampus and serum metabolites, while 16S rRNA sequencing was utilized to analyze gut microbiota composition. Intestinal barriers were determined using western blot detection of the tight junction proteins ZO-1 and occludin. Results: Dietary capsaicin exacerbated anxiety and depressive-like behaviors along with cognitive declines in T1D mice. Capsaicin reduced gut microbiota diversity and levels of beneficial bacteria, while broad-spectrum antibiotic treatment further intensified anxiety and depression behaviors. Metabolomic analysis indicated that capsaicin disrupted metabolic pathways related to tryptophan and phenylalanine, leading to decreased neuroprotective metabolites, such as kynurenic acid, hippurate, and butyric acid. Additionally, capsaicin diminished the expression of ZO-1 and occludin, indicating increased intestinal permeability. Conclusions: Dietary capsaicin aggravates gut microbiota and metabolic disturbances in diabetic mice, thereby worsening anxiety, depression, and cognitive decline.

Dataset Information

The mitigative effect of isorhamnetin against type 2 diabetes via gut microbiota regulation in mice.

Publications

The mitigative effect of isorhamnetin against type 2 diabetes <i>via</i> gut microbiota regulation in mice.

Similar Datasets

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