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Title [sv]
Betacellfunktion, hyperinsulinemi, autofagi, och diabetes
Title [en]
Beta-cell function, hyperinsulinemia, autophagy, and diabetes
Abstract [sv]
Genome wide association studies have emphasized the key role of beta-cell function in type 2 diabetes since most of the type 2 diabetes risk loci are associated with beta-cell function rather than insulin resistance. Aim 1: The HHEX/IDE region has been identified as a type 2 diabetes susceptibility locus and we have discovered an unexpected role for Ide in ensuring insulin secretion and beta-cell autophagy. Using in vitro and in vivo approaches we will now in detail characterize the molecular mechanisms by which Ide ensures beta-cell function and insulin secretion. Aim 2: Increased demand for insulin in response to insulin resistance leads to ER and oxidative stress within beta cells. Autophagy occurs at a basal level to turnover mis-folded proteins and damaged organelles but autophagy is efficiently inhibited by insulin signaling. We hypothesize that hyperinsulinemia, by blocking autophagy, contributes to beta-cell failure during the development of diabetes. Using mouse genetics we will address the role of autophagy for beta-cell function. Aim 3: Hyperinsulinemia stimulates accumulation triglycerides in the liver and we have shown that Gpr40 null mutant mice do not become hyperinsulinemic, develop diabetes, a fatty liver, or upregulate hepatic expression of the fatty acid transporter CD36 in response to high fat diet induced obesity. We now want to explore in further detail the link between hyperinsulinemia, CD36 expression, hepatic steatosis, and hepatic insulin resistance.
Principal InvestigatorEdlund, Helena
Coordinating organisation
Umeå University
Funder
Period
2011-01-01 － 2013-12-31
Identifiers
DiVA, id: project:1032Project, id: 2010-03618_VR

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