Neuronatin regulates pancreatic β cell insulin content and secretion

摘要: Neuronatin (Nnat) is an imprinted gene implicated in human obesity and widely expressed neuroendocrine metabolic tissues a hormone- nutrient-sensitive manner. However, its molecular cellular functions precise role organismal physiology remain only partly defined. Here we demonstrate that mice lacking Nnat globally or specifically β cells display impaired glucose-stimulated insulin secretion leading to defective glucose handling under conditions of nutrient excess. In contrast, report no evidence for any feeding body weight phenotypes global Nnat-null mice. At the level neuronatin augments signal peptide cleavage by binding peptidase complex facilitates translocation nascent preprohormone. Loss expression therefore reduces content blunts secretion. expression, turn, glucose-regulated. This mechanism represents novel site control cell function whole-animal homeostasis. These data also suggest potential wider regulation metabolism through modulation processing events.