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Integrated Analysis of lncRNA and mRNA Expression Profiles in brown adipose tissue of obesity-prone and obesity-resistant mice

ABSTRACT: Integrated Analysis of lncRNA and mRNA Expression Profiles in brown adipose tissue of obesity-prone and obesity-resistant mice

PROVIDER: PRJNA853392 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19879201.fastq.gz	Fastqsanger.gz
	SRR19879202.fastq.gz	Fastqsanger.gz
	SRR19879203.fastq.gz	Fastqsanger.gz
	SRR19879204.fastq.gz	Fastqsanger.gz
	SRR19879205.fastq.gz	Fastqsanger.gz

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Transcript Profiling of High Fat Diet induced Obesity-prone and Obesity-resistant Rats

Project description:Rodents respond to chronic high fat diet in at least two ways: some of them may readily gain body weight and become obese (termed obesity-prone), and others may not (termed obesity-resistant). An integrated approach of transcript and metabolic profiling of obesity-prone and obesity-resistant rats has been conducted, showing significantly different transcript and metabolic profiles in the two phenotypes. The major transcriptional differences involved hepatic fatty acid metabolism and ketogenesis in response to 16 weeks of high fat diet. At the same time, the different metabolic profiles (in liver tissue extracts, serum, and urine) between the two phenotypes could be ascribed to the corresponding pathways identified with multivariate statistical analysis, including fatty acid metabolism, Krebs cycle, and amino acid metabolism. The integration of results from both transcript and metabolic profiling revealed the different responses to dietary intervention of the two phenotypes and the physiological basis of susceptibility to metabolic disease in obesity-prone rats from a systematic view.

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LncRNA and mRNA expression profiles in brown adipose tissue of obesity-prone and obesity-resistant mice.

Project description:Obesity-prone or obesity-resistant phenotypes can exist in individuals who consume the same diet type. Brown adipose tissue functions to dissipate energy in response to cold exposure or overfeeding. Long noncoding RNAs play important roles in a wide range of biological processes. However, systematic examination of lncRNAs in phenotypically divergent mice has not yet been reported. Here, the lncRNA expression profiles in BAT of HFD-induced C57BL/6J mice were investigated by high-throughput RNA sequencing. Genes that play roles in thermogenesis and related pathways were identified. We found lncRNA (Gm44502) may play a thermogenic role in obesity resistance by interacting with six mRNAs. Our results also indicated that seven differentially expressed lncRNAs (4930528G23Rik, Gm39490, Gm5627, Gm15551, Gm16083, Gm36860, Gm42002) may play roles in reducing heat production in obesity susceptibility by interacting with seven differentially expressed mRNAs. The screened lncRNAs may participate in the pathogenesis of weight regulation and provide insight into obesity therapy.

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Integrated Analysis of lncRNA and mRNA Expression Profiles in brown adipose tissue of obesity-prone and obesity-resistant mice

Project description:The expression profiles of lncRNAs in BAT were investigated by high-throughput RNA sequencing using HFD-induced C57BL/6J mice. Genes that play roles in thermogenesis and related pathways were identified.

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Project description:Brown adipose tissue (BAT) is a thermogenic organ that dissipates stored energy as heat to maintain body temperature in infants and small mammals. This process may also provide protection from development of diet-induced obesity. We found that the bioactive lipid mediator lysophosphatidic acid (LPA) markedly decreases differentiation of cultured primary brown adipocyte precursors, while potent selective inhibitors of the LPA-generating enzyme autotaxin (ATX) promote differentiation. Transgenic mice overexpressing ATX exhibited reduced expression of BAT-related genes in peripheral white adipose tissue and accumulated significantly more fat than wild-type controls when fed a high fat diet. Our results indicate that ATX and its product LPA are physiologically relevant negative regulators of brown fat adipogenesis and suggest that a decrease in peripheral brown adipose tissue results in increased susceptibility to diet-induced obesity in mice.

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