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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE133786 | GEO | 2019/11/04

REPOSITORIES: GEO

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Expression data from murine subcutaneous and brown adipose tissue

Project description:Two types of adipose tissues, white and brown, are found in mammals. Increasingly novel strategies are being proposed for the treatment of obesity and its associated complications by altering amount and/or activity of BAT using mouse models. We used microarrays to detail the global programme of gene expression in subcutaneous white adipose tissue and brown adipose tissue. White adipose tissue (Subcutaneous region) and brown adipose tissue (intrascapular) were isolated from LACA mice (male, 25 ± 3g ) for RNA extraction and hybridization on Affymetrix microarrays.

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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 mice injected with control, Mafg and LncIRS2 LNA.

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Project description:Obesity is a global health problem, which is characterized by the excessive fat accumulation or adiposity in the body and associated with other chronic metabolic disorders. Excess energy induces adipogenesis and lipid accumulation inside the existing adipocytes during obesity, which involves transcriptional changes and regulation. Recently, long non-coding RNAs (lncRNAs) have been implicated in regulation of adipogenesis and adipose tissue function. Mouse lncRNA U90926 was previously identified as a repressor of in vitro adipogenesis in 3T3-L1 preadipocytes. Based on this, we hypothesized that U90926 may repress weight gain and adiposity in vivo. To test the hypothesis, we leveraged U90926-deficient (U9-KO) mice, which we recently generated, with a generalized high-throughput phenotyping pipeline and focused follow-up phenotyping experiments. Compared with WT, U9-KO mice showed no major differences across a wide range of behavioral, neurological, and other physiological parameters. In mice fed a standard diet, we have found no differences in obesity-related phenotypes such as weight gain, fat mass accumulation, and plasma concentration of glucose, insulin, triglycerides, and free fatty acids in U9-KO mice in comparison with WT. U90926 deficiency did not have a major effect on perigonadal white adipose tissue morphology and gene expression profile. Furthermore, in mice fed a high fat diet, we found increased expression of U90926, yet no effect of U90926 deficiency on weight gain, fat mass, adipogenesis marker expression, and immune cell infiltration into the adipose tissue. Taken together, these data suggest that the lncRNA U90926 lacks an essential role in obesity-related phenotypes as well as adipocyte biology in vivo.

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