Pancreatic β Cell Mass Preserved in Heterozygous PDK1 Knockout Mice

概要

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We have demonstrated that 3-phosphoinositide-dependent protein kinase 1 (PDK1)contributes to signaling by insulin or insulin-like growth fctor-1 (IGF-1) that isresponsible for the regulation of both the number and size of pancreatic β cells in mice.Complete ablation of PDK1 in pancreatic β cells leads to progressive hyperglycemia asa result of loss of β cell mass. In this study, we generated heterozygous pancreatic βcell-specific PDK1 knockout (βPDK1+/–) mice and fed them a high-fat diet as a model ofhuman type 2 diabetes. The βPDK1+/– mice exhibited normal glucose tolerance even ona high-fat diet. Further, islet morphology and β cell mass were normal in βPDK1+/–mice, and haploinsufficiency of PDK1 did not impair the compensatory hyperplasia ofβ cells on a high-fat diet. The phosphorylation and expression of the molecules that areexpressed downstream of PDK1 were similar in the islets of the βPDK1+/– and controlmice. Eventually, we concluded that glucose homeostasis and islet mass weremaintained in βPDK1+/– mice.
神戸大学の論文