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    The leptin receptor and its role in obesity and type 2 diabetes

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    Obesity is considered as a major public health problem, which is often associated with type 2 diabetes mellitus, cardiovascular diseases and cancer. In most cases, obesity is accompanied by a decreased responsiveness for a hormone called leptin. This cytokine is primarily secreted by the white adipose tissue and targets specific receptors in the arcuate nucleus of the hypothalamus to regulate energy expenditure and food intake. Stimulation of leptin receptors (OB-R) activates several intracellular signaling pathways such as the JAK2/STAT3, MAPK, PI3K and AMPK pathways. Mutations that abolish leptin or OB-R expression result in massive obesity in mice and humans. However, the prevalence of such mutants are not very high in the human population. Most obese individuals have paradoxically high leptin levels and are unable to respond adequately to this hormone. This pathological state is termed "leptin resistance". Several hypothesis attempt to explain this leptin resistance such as impaired transport of leptin across the blood-brain-barrier, impaired OB-R signaling or altered OB-R trafficking.

    Research aims:


    Our research is oriented towards three major topics aiming to understand the mechanism of OB-R function, which regulates the sensitivity to leptin:

    A)    Interaction between leptin – OB-R
    B)    Modulation of OB-R function by the endospanin family
    C)    Leptin transport into the brain
    D)    Gastro-intestinal hormones and the contol of food intake.


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