Insulin, a pleotrophic hormone, has diverse effects in the body.
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Recent work has highlighted the important role of insulin's action in the nervous system on glucose and energy homeostasis, memory, and mood. Scope of review: Here we review experimental and clinical work that has broadened the understanding of insulin's diverse functions in Michelle Lillerod sex central and peripheral nervous systems, including glucose and body weight homeostasis, memory and mood, with particular emphasis on intranasal insulin. Major conclusions: Implications for the treatment of obesity, type 2 diabetes, dementia, and mood disorders are discussed in the context of brain insulin action.
Intranasal insulin may have potential in the treatment of central nervous system-related metabolic disorders. Transport of pyruvate into the mitochondrial matrix by the Mitochondrial Pyruvate Carrier MPC is an important and rate-limiting step in its metabolism. To evaluate the role that the MPC plays in Lilllerod systemic glucose homeostasis, we used genetically-engineered Drosophila and mice with loss of MPC activity in insulin-producing cells.
In both species, MPC deficiency results in elevated blood sugar concentrations and glucose intolerance accompanied by impaired glucose-stimulated insulin secretion. Moreover, treatment of pancreas-specific MPC knockout mice with glibenclamide, a sulfonylurea KATP channel inhibitor, improved defects in islet insulin secretion and abnormalities in glucose homeostasis in vivo.
Finally, using a recently-developed biosensor for MPC activity, we show that the MPC is rapidly stimulated by glucose treatment in INS-1 insulinoma cells suggesting that glucose sensing is coupled to mitochondrial pyruvate carrier activity. Altogether, these studies suggest that the MPC plays an important and ancestral role in insulin-secreting Michelle Lillerod sex in mediating glucose sensing, regulating Mihelle secretion, and controlling systemic glycemia. The purpose of this work was to characterize the role of microRNAs in the control of brite adipocyte formation.
Using human multipotent adipose derived stem cells, we identified miRb-5p as downregulated upon brite adipocyte formation. In vitrooverexpression and knockdown of miRb-5p decreased and increased mitochondrial biogenesis, respectively.
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