Whole transcriptome analysis of obese adipose tissue suggests u001kfc.1 as a potential regulator to glucose metabolism
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PROVIDER: PRJNA552542 | ENA |
REPOSITORIES: ENA
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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.
2019-11-04 | GSE133786 | GEO
Project description:Long non-coding RNA (LncRNAs) are newly highlighted key factors controlling brown adipogenesis and development, but their regulatory effect to white adipocyte is still merely understood. Deciphering their underlying mechanism could be a novel way to discovering potential targets of obesity. Therefore, we conducted a whole transcriptome analysis in white adipose tissue from obese patients for the first time. Six obese patients and five control subjects were selected for microarray assay. Differentially expressed coding genes (DEGs), targets of lncRNAs, and alternatively spliced genes in obesity group were systematically compared in a functional framework based on a global gene regulatory network. It was demonstrated that all the three kinds of transcripts were enriched in pathways related to glucose metabolism while only DEGs showed closer proximity to neuro-endocrine-immune system. Thus, a lncRNA-regulated core network was constructed by a stepwise strategy using DEGs as seed nodes. From the core network, we identified a decreased lncRNA, uc001kfc.1, as potential cis-regulator for phosphatase and tensin homolog (PTEN) to enhance insulin sensitivity of white adipocytes in obese patients. We further validated the down-regulation of uc001kfc.1 and PTEN in an independent testing sample set enrolling 22 subjects via qRT-PCR. Although whether the decreased uc001kfc.1 correlated with low risk of diabetes deserved to be examined in an expanded cohort with long-term follow-up visit, the present study highlighted the potential of lncRNA regulating glucose homeostasis in human adipose tissue from a global perspective. With further improvement, such network-based analyzing protocol proposed in this study could be applied to interpreting function of more lncRNAs from other whole transcriptome data.
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Project description:Resveratrol has been reported to improve metabolic function in metabolically-abnormal rodents and humans, but has not been studied in non-obese people with normal glucose tolerance. We conducted a randomized, double-blind, placebo-controlled trial to evaluate the metabolic effects of 12 weeks of resveratrol supplementation (75 mg/day) in non-obese, postmenopausal women with normal glucose tolerance. Although resveratrol supplementation was well-tolerated and increased plasma resveratrol concentration without adverse effects, it did not change body composition, resting metabolic rate, plasma lipids, or inflammatory markers. A two-stage hyperinsulinemic-euglycemic clamp procedure, in conjunction with stable isotopically-labeled tracer infusions, demonstrated that resveratrol did not increase liver, skeletal muscle, or adipose tissue insulin sensitivity. Consistent with the absence of in vivo metabolic effects, resveratrol did not affect its putative molecular targets, including AMPK, Sirt1, Nampt, and Pgc-1α, in either skeletal muscle or adipose tissue. These findings demonstrate that resveratrol supplementation does not have metabolic effects in non-obese women.
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