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Molecular and physiological analysis of energy homeostasis in health and disease
Glucose homeostasis and development of type 2 diabetes are critically dependent on the capacity of the insulin secreting beta-cells of the pancreas to secrete insulin according to the metabolic need of the organism. This secretory capacity depends on both the number and secretion capacity of the differentiated beta-cells.
One of our research projects aimed at identying novel genes that regulate beta-cell proliferation, secretion capacity and apoptosis. To this end we are evaluating the mode of action on beta-cells of the gluco-incretin hormones GLP-1 and GIP, which are known to stimulate beta-cell precursor differentiation and proliferation of mature beta-cells, as well as to protect these cells against apoptosis. Our ongoing work was initiated by performing transcript profiling of islets from mice with genetic inactivation of the GLP-1 and GIP receptors, and which showed decreased secretion capacity and increased susceptibility to apoptosis. The function of these genes is investigated by overexpression or down-expression (siRNA) studies in beta-cell lines, primary beta cells and in transgenic mice, followed by functional analysis of proliferation, apoptosis, insulin secretion, as well as whole body glucose homeostasis.
Molecular and physiological analysis of energy homeostasis in health and disease
Glucose homeostasis and development of type 2 diabetes are critically dependent on the capacity of the insulin secreting beta-cells of the pancreas to secrete insulin according to the metabolic need of the organism. This secretory capacity depends on both the number and secretion capacity of the differentiated beta-cells.
One of our research projects aimed at identying novel genes that regulate beta-cell proliferation, secretion capacity and apoptosis. To this end we are evaluating the mode of action on beta-cells of the gluco-incretin hormones GLP-1 and GIP, which are known to stimulate beta-cell precursor differentiation and proliferation of mature beta-cells, as well as to protect these cells against apoptosis. Our ongoing work was initiated by performing transcript profiling of islets from mice with genetic inactivation of the GLP-1 and GIP receptors, and which showed decreased secretion capacity and increased susceptibility to apoptosis. The function of these genes is investigated by overexpression or down-expression (siRNA) studies in beta-cell lines, primary beta cells and in transgenic mice, followed by functional analysis of proliferation, apoptosis, insulin secretion, as well as whole body glucose homeostasis.
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