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Effect of diet-induced obesity on uterine function in mice.

ABSTRACT: Effect of diet-induced obesity on uterine function in mice.

PROVIDER: PRJNA1117027 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29195256_1.fastq.gz	Fastqsanger.gz
	SRR29195256_2.fastq.gz	Fastqsanger.gz
	SRR29195257_1.fastq.gz	Fastqsanger.gz
	SRR29195257_2.fastq.gz	Fastqsanger.gz
	SRR29195258_1.fastq.gz	Fastqsanger.gz

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Effect of diet-induced obesity on uterine function in mice.

Project description:To gain insight into the mechanism(s) by which obesogenic diet caused decreased uterine contractility at term, we collected uterine tissue from mice fed either a control (CON) or an obesogenic (DIO) diet at day 18.5 of pregnancy and performed RNA sequencing.

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microRNA expression profiles in myocardium of diet-induced obesity rat

Project description:Diet induced obesity in rat was associated with myocardial dysfunction, hypertension and fibrosis. This study aimed to explore microRNA expression profiles in diet obesity-induced rat myocardium. Wistar rats were feed normal chow or high-fat diet for 20 weeks. After that, cardiac function was evaluated by echocardiography. Left ventricular myocardium was harvest to assess the extent of hypertension and fibrosis, meanwile, the left ventricular microRNA expression was analyzed using Agilent Rat miRNA microarray. Significant cardiac dysfunction, hypertension and fibrosis were found in diet-induced obesity rats as compared with normal diet rats. rno-miR-141-3p and rno-miR-144-3p were also significantly increased in myocardium of diet-induced obesity rat. These findings suggest that specific miRNA differences may contribute to the alteration in cardiac function, hypertension and fibrosis which responses to diet-induced obesity.

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Genome-wide analysis of uterine natural killer cell gene expression from control diet-fed and high fat diet-fed female mice in early pregnancy

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Project description:The experimental goals of this study were to determine the differences in hypothalamus gene expression in genetically identical mice that have variability in their susceptibility towards diet-induced obesity following 6 weeks feeding a high fat diet, 2 weeks low fat diet and 6 weeks high fat diet. Keywords: Comparative gene expression analysis

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MOF haploinsufficiency triggers diet-induced obesity resistance

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EP3 deletion in macrophages aggravates diet-induced obesity in mice by suppressing SPARC

Project description:Macrophages are primary immune cells involved in obesity-triggered chronic low-grade inflammation in adipose tissues. Prostaglandin (PG) E2, mainly generated from macrophages, can regulate adipose tissue remodeling. Here, we observed that PGE2 receptor subtype 3 (EP3) was remarkably downregulated in adipose tissue macrophages from high-fat diet (HFD)-fed mice and patients with obesity. Notably, macrophage-specific deletion of EP3 exacerbated HFD-induced obesity in mice, whereas EP3α isoform overexpression in macrophages alleviated obesity phenotype in HFD-fed mice. EP3 deficiency suppressed anti-adipogenic secreted protein acidic and rich in cysteine (SPARC) secretion in macrophages. SPARC deletion in macrophages abrogated the protection of EP3α-overexpression against HFD-induced obesity in mice. Mechanistically, EP3 activation promoted SPARC expression by suppressing DNA methylation in macrophages through the PKA/Sp1/Dnmt1/3a signaling cascade. EP3 agonist treatment ameliorates HFD-induced obesity in mice. Thus, EP3 inhibits adipogenesis through promoting macrophage releasing SPARC and may serve as a therapeutic target for managing diet-induced obesity.

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Gene expression in diet-induced obesity resistent (DIO non-responder) and diet-induced obesity susceptible (DIO responder) C57BL/6J mouse strain

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