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UCP2-dependent redox sensing in POMC neurons regulates feeding

Nal Ae Yoon, Sungho Jin, Jung Dae Kim, Zhong Wu Liu, Qiushi Sun, Rebecca Cardone, Richard G. Kibbey, Sabrina Diano

2022Cell Reports21 citationsDOIOpen Access PDF

Abstract

mice have impaired glucose metabolism and are prone to obesity on a high-fat diet. Altogether, our data show that lactate through redox signaling and blocking mitochondrial glucose utilization activates POMC neurons to regulate feeding and glucose metabolism.

Topics & Concepts

EndocrinologyMitochondrionInternal medicineBiologyMetabolismCarbohydrate metabolismCytosolExtracellularPopulationProopiomelanocortinGlycolysisCellular respirationBiochemistryChemistryHypothalamusEnzymeDemographyMedicineSociologyAdipose Tissue and MetabolismRegulation of Appetite and ObesityPancreatic function and diabetes
UCP2-dependent redox sensing in POMC neurons regulates feeding | Litcius