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MiR8175 has an effect on glucose metabolism in obese mice

ABSTRACT: miR8175 has an effect on glucose metabolism in obese mice

PROVIDER: PRJNA1042864 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26882187_1.fastq.gz	Fastqsanger.gz
	SRR26882187_2.fastq.gz	Fastqsanger.gz
	SRR26882188_1.fastq.gz	Fastqsanger.gz
	SRR26882188_2.fastq.gz	Fastqsanger.gz
	SRR26882189_1.fastq.gz	Fastqsanger.gz

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miR8175 has an effect on glucose metabolism in obese mice

Project description:The incidence of type 2 diabetes (T2DM) induced by obesity is rapidly increasing. Although there are many drugs developed for type 2 diabetes, but the anti-diabetic effect of homology of medicine and food is also very popular with the majority of people. Burdock is one such food, but the molecular mechanism of anti-diabetic effect is unclear, limiting its further promotion. In recent years, studies have shown that plant mirnas can regulate host gene expression through dietary absorption, so plant miRNAs have become one of the main active ingredients in traditional Chinese medicine. Here, we report that miR8175, a plant miRNA from burdock root, has effective antidiabetic activity. miR8175 is highly enriched in burdock decoction. After administration of burdock decoction or synthetic miR8175 by gavage, significantly elevated levels of miR8175 in mouse serum and liver can be observed. Furthermore, both burdock decoction and miR8175 can significantly improve the impaired glucose metabolism of diabetic mice induced by a high-fat diet (HFD). Our results demonstrate that burdock decoction and miR8175 enhance the insulin sensitivity of the hepatic insulin signaling pathway by targeting PTPRF and PTP1B, which may be the reason for the improvement in metabolism.

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Global, neuronal, and beta-cell specific deletion of the insulin inhibitory receptor (inceptor) improves glucose homeostasis in diet-induced obese male mice

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Identification of the pharmacological effects of Chrysanthemum morifolium Ramat. leaves extracts on high-fat diet induced obese mice through lipid-, and glucose metabolism

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Whole transcriptome analysis of obese adipose tissue suggests u001kfc.1 as a potential regulator to glucose metabolism

Project description:LncRNAs are newly proposed key factors controlling brown adipogenesis and development, but their regulatory effect to white adipocyte is still merely understood. Deciphering the underlying mechanism could be a novel way to discovering potential targets of obesity. In the present study, the whole transcriptome of adipose tissues collected from obese individuals and control subjects were analyzed by HTA2.0. A stepwise network reconstruction strategy was proposed to explore lncRNA-related functional modules altered in obesity. A lncRNA named uc001kfc.1, which was recognized from the core network, was suggested to be down regulated in obesity group and might regulate glucose metabolism of adipocytes through PI3K/PTEN pathway. Our study highlighted the potential of lncRNA regulating glucose homeostasis in human adipose tissue from a global perspective, which would facilitate deeply understanding pathology of obesity as well as developing novel therapeutic targets.

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of obese and lean mice.

Project description:Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcrips with elusive functions in metabolism. Here we report that an unexpectedly high fraction of lncRNAs, but not protein-coding mRNAs, is repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation specifically induced lncRNAs in mouse liver. Similarly, lncRNAs were lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirmed that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in primary hepatocytes and in vivo elicited a fasting-like expression profile, improved glucose metabolism, derepressed lncRNAs and prevented mammalian target of rapamycin (mTOR)-driven protein translation. We found that obesity-repressed lincIRS2 is controlled by MAFG and observed that genetic and RNAi-mediated lincIRS2 loss causes hyperglycemia, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a novel MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease.

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A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of obese and lean mice.

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Mss51 deletion enhances muscle metabolism and glucose homeostasis in mice

Project description:Myostatin is a negative regulator of muscle growth and metabolism and its inhibition in mice improves insulin sensitivity, increases glucose uptake into skeletal muscle, and decreases total body fat. A recently described mammalian protein called Mss51 is significantly downregulated with myostatin inhibition. In vitro disruption of Mss51 results in increased levels of ATP, β-oxidation, glycolysis and oxidative phosphorylation. To determine the in vivo biological function of Mss51 in mice, we disrupted the Mss51 gene by CRISPR/Cas9 and found that Mss51 KO mice have normal muscle weights and fiber-type distribution but reduced fat pads. Myofibers isolated from Mss51 KO mice showed an increased oxygen consumption rate compared to WT controls, indicating an accelerated rate of skeletal muscle metabolism. The expression of genes related to oxidative phosphorylation and fatty acid β-oxidation were enhanced in skeletal muscle of Mss51 KO mice compared to that of WT mice. We found that mice lacking Mss51 and challenged with a high fat diet were resistant to diet-induced weight gain, had increased whole-body glucose turnover and glycolysis rate, and increased systemic insulin sensitivity and fatty acid β-oxidation. These findings demonstrate that Mss51 modulates skeletal muscle mitochondrial respiration and regulates whole-body glucose and fatty acid metabolism, making it a potential target for obesity and diabetes.

2019-12-31 | GSE134519 | GEO

Secreted Protein Acidic and Rich in Cysteine Improves Glucose Tolerance via AMP-activated Protein Kinase Activation

Project description:Metabolic dysfunction of skeletal muscle is often prevalent at an early stage in the development of several non-communicable diseases. Here, we investigated the effect of a myokine, secreted protein acidic and rich in cysteine (SPARC), on glucose tolerance in human and mouse skeletal muscles. SPARC knockout mice showed marked decreases in parameters for whole-body glucose metabolism, along with reduced phosphorylation of AMPK and Akt in skeletal muscle tissues compared with wild-type mice. Furthermore, mice injected with SPARC showed improved glucose tolerance concomitant with AMPK activation. Exogenous SPARC treatment accelerated glucose uptake in muscle tissues isolated from wild-type mice but not from AMPKγ3 knockout mice. In muscle cells, SPARC increased glucose uptake concomitant with AMPK activation, mediated by a calcium-dependent signal. Chronic treatment of SPARC restored metabolic functions in diet-induced obese mice. These findings suggest that SPARC improves glucose metabolism via AMPK activation in skeletal muscle, providing mechanistic insights on exercise-induced metabolic benefits and physical inactivity-induced glucose intolerance.

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