( A and B) Dual ISH for POMC and ICC for GFP was performed on hypothalamic sections from RIPCreZEG mice. Our findings demonstrate a critical role for IRS2 in β cell and hypothalamic function and provide insights into the role of RIPCre neurons, a distinct hypothalamic neuronal population, in growth and energy homeostasis.Ĭharacterization of RIPCre neurons by ICC, ISH, and electrophysiological analysis. Insulin hyperpolarized and leptin depolarized POMC neurons. Insulin and a melanocortin agonist depolarized RIPCre neurons, whereas leptin was ineffective. RIPCre neurons did not express POMC or neuropeptide Y. NesCreIrs2KO and POMCCreIrs2KO mice did not display reduced β cell mass, but NesCreIrs2KO mice displayed mild abnormalities of glucose homeostasis. RIPCreIrs2KO and NesCreIrs2KO mice retained leptin sensitivity, which suggests that CNS Irs2 pathways are not required for leptin action. POMCCreIrs2KO mice did not display this phenotype. RIPCreIrs2KO and NesCreIrs2KO mice displayed hyperphagia, obesity, and increased body length, which suggests altered melanocortin action. Overt diabetes did not ensue, because β cells escaping Cre-mediated recombination progressively populated islets. RIPCreIrs2KO mice displayed impaired glucose tolerance and reduced β cell mass. We generated mice lacking Irs2 in β cells and a population of hypothalamic neurons (RIPCreIrs2KO), in all neurons (NesCreIrs2KO), and in proopiomelanocortin neurons (POMCCreIrs2KO) to determine the role of Irs2 in the CNS and β cell. Insulin receptor substrate 2 (Irs2) plays complex roles in energy homeostasis.
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