POMC Neurons Dysfunction in Diet-induced Metabolic Disease: Hallmark or Mechanism of Disease?
Neuroscience. 2019-11-01; :
DOI: 10.1016/j.neuroscience.2019.09.031
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Quarta C(1), Fioramonti X(2), Cota D(3).
Author information:
(1)INSERM, Neurocentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33000 Bordeaux, France; University of Bordeaux, Neurocentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33000 Bordeaux, France. Electronic address: .
(2)Université de Bordeaux, Institut National de la Recherche Agronomique, Bordeaux INP, NutriNeuro, UMR 1286, F-33000 Bordeaux, France.
(3)INSERM, Neurocentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33000 Bordeaux, France; University of Bordeaux, Neurocentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33000 Bordeaux, France. Electronic address: .
One important lesson from the last decade of studies in the field of systemic energy metabolism is that obesity is first and foremost a brain disease. Hypothalamic neurons dysfunction observed in response to chronic metabolic stress is a key pathogenic node linking consumption of hypercaloric diets with body weight gain and associated metabolic sequelae. A key hypothalamic neuronal population expressing the neuropeptide Pro-opio-melanocortin (POMC) displays altered electrical activity and dysregulated neuropeptides production capacity after long-term feeding with hypercaloric diets. However, whether such neuronal dysfunction represents a consequence or a mechanism of disease, remains a subject of debate. Here, we will review and highlight emerging pathogenic mechanisms that explain why POMC neurons undergo dysfunctional activity in response to caloric overload, and critically address whether these mechanisms may be causally implicated in the physiopathology of obesity and of its associated co-morbidities.
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