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Type 2 diabetes, insulin resistance and inflammation

Type 2 diabetes, insulin resistance and inflammation - molecular mechanisms and genes   

The focus of this project is to characterize molecular mechanisms and genes involved in insulin resistance, Type 2 diabetes and its complications including systemic inflammation and cardiovascular disease.

- We perform Genom Wide Association (GWA) studies using SNP chips and the unique EUGENE2 cohort. This includes >1000 healthy first-degree relatives (FDR) of Type 2 diabetic individuals who have undergone extensive phenotyping for insulin sensitivity, insulin secretion, intima/media thickness of the carotid artery etc. 

- We characterize the effects and mechanisms of a new secreted adipokine that we have identified. This adipokine is induced by Wnt signalling and TNFalpha. Wnt signalling is increased in the adipose tissue in obesity. This has been shown to have unique properties such as proliferation of preadipocytes and monocytes/macrophages. It is also proinflammatory and inhibits the normal differentiation of preadipocytes. 

- We characterize the molecular mechanisms for STAT-induced inflammation and the anti-inflammatory effects of insulin that we have identified. The focus will be on PKCdelta and SHP-2 and the possibility to develop new anti-inflammatory molecules.

Type 2 diabetes, insulin resistance and inflammation - role of Wnt signalling

In previous work, we have identified several differences in the gene and protein expression in adipose cells from Type 2 diabetic and insulin-resistant individuals. These abnormalities are consistent with an impaired adipocyte differentiation leading to an abnormal secretion pattern of different hormones and cytokines that are produced by the fat cells (adipokines). We have now shown that there is a direct correlation between these adipocyte abnormalities and insulin sensitivity measured in patients in vivo.

Additional recent experiments have shown that certain cytokines impair the normal early differentiation of preadipocytes and, instead , promote an inflammatory phenotype by activating the Wnt signalling cascade. This complex signalling pathway antagonizes cell differentiation and maintains, for instance, stem cells in an undifferentiated state.

This project is focused on the role and mechanisms for the increased Wnt signalling, which we have seen in the adipose cells from insulin-resistant states including obesity and Type 2 diabetes.

Differentiated human preadipocytes in oil red staining (top)

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Page Manager: Gunilla Lindell|Last update: 8/30/2011
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