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Obesity and type 2 diabetes are prevalent diseases of industrialized societies, with an enormous strain on health care systems. The global increase in the development of obesity and the associated metabolic syndrome over the last few decades is an important example of how the interaction between lifestyle and genotype can dramatically impact on health. The familial nature, the marked difference in the prevalence among various racial groups and the difference in concordance rates between monozygotic twins shows that besides environmental factors a genetic component to disease susceptibility exists.
Deranged adipose tissue proliferation, differentiation and maturation contribute significantly to the development of these metabolic diseases, however, the influence and contribution of genetic and environmental factors are so far incompletely understood. It is generally believed that variation in fat distribution and function is not solely a result of influences extrinsic to adipose cells (including hormonal and paracrine microenvironment, local nutrient availability, innervations, and anatomic constraints), but also due to inherent properties of adipose cells. The risk of metabolic complication is increased not only by the amount and location of adipose tissue, but also by the size of the fat cells.
In our group we focus on elucidating the molecular mechanisms underlying the altered preadipocyte and adipocyte biology in different models of obesity, type 2 diabetes and associated metabolic disorders, with special emphasis on gene expression, postranslational modifications and lipid composition of the cell. Using a system biology approach we attempt to achieve a comprehensive understanding of the metabolic pathways that play a role in the development of metabolic diseases using microarray techniques and high throughput siRNA screens. In addition to analysing gene and protein expression patterns we are evaluating lipid composition of differentiated preadipocytes and mature adipocytes in relation to different metabolic disorders. In contrast to previous studies we examine preadipocyte and adipocyte biology in the context of a whole organism by employing a variety of animal models for different metabolic disorders that are available today. By gaining a more thorough understanding of the transcriptional and posttranscriptional networks underlying preadipocyte and adipocyte biology we hope to facilitate the development of more efficient therapeutic approaches for the treatment of metabolic disorders associated with obesity and type 2 diabetes.
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