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Proopiomelanocortin (POMC) neurons are major negative regulators of energy balance. A distinct developmental property of POMC neurons is that they can adopt an orexigenic neuropeptide Y (NPY) phenotype. However, the mechanisms underlying the differentiation of  Pomc  progenitors remain unknown. Here, we show that the loss of the microRNA (miRNA)-processing enzyme  Dicer  in POMC neurons causes metabolic defects, an age-dependent decline in the number of  Pomc mRNA-expressing cells, and an increased proportion of  Pomc  progenitors acquiring a NPY phenotype. miRNome microarray screening further identified miR-103/107 as candidates that may be involved in the maturation of  Pomc  progenitors. In vitro inhibition of miR-103/107 causes a reduction in the number of  Pomc -expressing cells and increases the proportion of  Pomc  progenitors differentiating into NPY neurons. Moreover, in utero silencing of miR-103/107 causes perturbations in glucose homeostasis. Together, these data suggest a role for prenatal miR-103/107 in the maturation of  Pomc  progenitors and glucose homeostasis.

Central Dicer-miR-103/107 controls developmental switch of POMC progenitors into NPY neurons and impacts glucose homeostasis