Neuromedin U (NMU), a highly conserved peptide in mammals, is implicated in energy homeostasis and glycemic control, and may also be involved in the regulation of adipoinsular axis function. However, the role of NMU in regulating insulin secretion has not been clearly established. In this study, we investigated the role of NMU in the regulation of insulin secretion both in vitro and in vivo. We found that NMU and NMU receptor (NMUR) 1 were expressed in mouse islets and β cell-derived MIN6-K8 cells. In mice, NMU suppressed glucose-stimulated insulin secretion (GSIS) both in vitro and in vivo. Additionally, an NMUR1 agonist inhibited GSIS in both MIN6-K8 cells and mice islets. Moreover, NMU attenuated intracellular Ca2+ influx in MIN6-K8 cells, potentially causing a decrease in insulin secretion. siNmu-transfected MIN6-K8 cells showed elevated GSIS. Treatment with anti-NMU IgG increased GSIS in isolated mouse pancreatic islets. These results suggested that NMU can act directly on β cells through NMUR1 in an autocrine or paracrine fashion to suppress insulin secretion. Collectively, our results highlight the crucial role of NMU in suppressing pancreatic insulin secretion, and may improve our understanding of glucose homeostasis.
Neuromedin U suppresses glucose-stimulated insulin secretion in pancreatic β cells.
Weidong Zhang,H. Sakoda,Ayako Miura,K. Shimizu,K. Mori,M. Miyazato,Kentaro Takayama,Y. Hayashi,M. Nakazato
Published 2017 in Biochemical and Biophysical Research Communications - BBRC
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- Publication year
2017
- Venue
Biochemical and Biophysical Research Communications - BBRC
- Publication date
2017-11-04
- Fields of study
Biology, Medicine
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- Source metadata
Semantic Scholar, PubMed
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