The following study was conducted by Scientists from Mouse Cancer Genetics Program, CCR, NCI, NIH, Frederick, USA; Molecular Signaling Section, Laboratory of Bioorganic Chemistry, NIDDK, NIH, Bethesda, USA; Mouse Metabolism Core Laboratory, NIDDK, NIH, Bethesda, USA. Study is published in Nature Communications Journal as detailed below.
Nature Communications; Volume 11, Article number: 1950; (2020)
Novel Metabolic Role for BDNF in Pancreatic β-Cell Insulin Secretion
Abstract
BDNF signaling in hypothalamic circuitries regulates mammalian food intake. However, whether BDNF exerts metabolic effects on peripheral organs is currently unknown. Here, we show that the BDNF receptor TrkB.T1 is expressed by pancreatic β-cells where it regulates insulin release. Mice lacking TrkB.T1 show impaired glucose tolerance and insulin secretion. β-cell BDNF-TrkB.T1 signaling triggers calcium release from intracellular stores, increasing glucose-induced insulin secretion. Additionally, BDNF is secreted by skeletal muscle and muscle-specific BDNF knockout phenocopies the β-cell TrkB.T1 deletion metabolic impairments. The finding that BDNF is also secreted by differentiated human muscle cells and induces insulin secretion in human islets via TrkB.T1 identifies a new regulatory function of BDNF on metabolism that is independent of CNS activity. Our data suggest that muscle-derived BDNF may be a key factor mediating increased glucose metabolism in response to exercise, with implications for the treatment of diabetes and related metabolic diseases.
Source:
Nature Communications
URL: https://www.nature.com/articles/s41467-020-15833-5
Citation:
Fulgenzi, G., Z. Hong, et al. (2020). “Novel metabolic role for BDNF in pancreatic β-cell insulin secretion.” Nature Communications 11(1): 1950.
