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RNA-seq of livers from glucagon receptor knock-out (GcgrKO) mice compared to wildtype littermates

ABSTRACT: RNA-seq of livers from glucagon receptor knock-out (GcgrKO) mice compared to wildtype littermates

PROVIDER: PRJEB55291 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR10041005_1.fastq.gz	Fastqsanger.gz
	ERR10041005_2.fastq.gz	Fastqsanger.gz
	ERR10041006_1.fastq.gz	Fastqsanger.gz
	ERR10041006_2.fastq.gz	Fastqsanger.gz

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RNA-seq of livers from glucagon receptor knock-out (GcgrKO) mice compared to wildtype littermates

Project description:Glucagon is a key regulator of glucose homeostasis, amino acid catabolism, and lipid metabolism. Glucagon receptor knock-out (GcgrKO) mice have slightly reduced blood glucose levels whereas plasma levels of amino acids are vastly increased reflecting disruption of hepatic amino acid catabolism. To dissect the molecular mechanisms underlying this effect, RNA sequencing of livers from male GcgrKO mice and wild-type littermates were performed. The mice were 10 weeks of age and were subjected to a short-term fast of 4 h before anesthesia with 2.5% isoflurane.

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AMPK gamma3 knock-out and mutant (R225Q) transgenic mice compared to corresponding wild type littermates

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Project description:Chronic glucagon receptor inhibition with a glucagon receptor antibody decreases amino acid catabolism and ureagenesis, while increasing plasma triglyceride concentrations, plasma very-low density lipoprotein cholesterol concentrations, and liver triglyceride concentrations. To dissect the molecular mechanism underlying these effects, RNA sequencing of liver biopsies from female mice treated for eight weeks with the glucagon receptor antibody, REGN1193, or a control antibody, REGN1945, were performed.

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RNA-seq of livers from female mice treated for eight weeks with the glucagon analogue, NNC9204-0043, compared to female mice treated with PBS (control group)

Project description:Chronic glucagon receptor activation with a long-acting glucagon analogue increases amino acid catabolism, and to dissect the molecular mechanism underlying this effect, RNA sequencing of liver biopsies from female mice treated for eight weeks with GCGA or PBS were performed.

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Gene expression in skeletal muscle in AMPK gamma3 knock-out mice and wild type littermates

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Project description:Glucagon and insulin are counter-regulatory pancreatic hormones that precisely control blood glucose homeostasis1. Type 2 diabetes mellitus (T2DM) is characterized by inappropriately elevated blood glucagon2-5 levels as well as insufficient glucose stimulated insulin secretion (GSIS) by pancreatic ß-cells6. Early in the pathogenesis of T2DM, hyperglucagonemia is observable antecedent to ß-cell dysfunction7-9; and in mice, liver-specific activation of glucagon receptor-dependent signaling results in impaired GSIS10. However, the mechanistic relationship between hyperglucagonemia, hepatic glucagon action, and ß-cell dysfunction remains poorly understood. Here we show that glucagon action stimulates hepatic production of the neuropeptide kisspeptin1, which acts in an endocrine manner on ß-cells to suppress GSIS. In vivo glucagon administration acutely stimulates hepatic kisspeptin1 production, and kisspeptin1 is increased in livers from humans with T2DM and from mouse models of diabetes mellitus. Synthetic kisspeptin1 potently suppresses GSIS in vivo and in vitro from normal isolated islets, which express the kisspeptin1 receptor Kiss1R. Administration of a Kiss1R antagonist in diabetic Leprdb/db mice potently augments GSIS and reduces glycemia. Our observations indicate in the pathogenesis of T2DM an endocrine mechanism sequentially linking hyperglucagonemia via hepatic kisspeptin1 production to impaired insulin secretion. In addition, our findings suggest Kiss1R antagonism as a therapeutic avenue to improve ß-cell function in T2DM. Total RNA from L-Δprkar1a KO mice compared to control D-glucose mice

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