Novel metabolic role for BDNF in pancreatic β-cell insulin secretion

Gianluca Fulgenzi, Zhenyi Hong, Francesco Tomassoni-Ardori, Luiz F. Barella, Jodi Becker, Colleen Barrick, Deborah Swing, Sudhirkumar Yanpallewar, Brad St Croix, Jürgen Wess, Oksana Gavrilova and Lino Tessarollo ()
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Gianluca Fulgenzi: CCR, NCI, NIH
Zhenyi Hong: CCR, NCI, NIH
Francesco Tomassoni-Ardori: CCR, NCI, NIH
Luiz F. Barella: Laboratory of Bioorganic Chemistry, NIDDK, NIH
Jodi Becker: CCR, NCI, NIH
Colleen Barrick: CCR, NCI, NIH
Deborah Swing: CCR, NCI, NIH
Sudhirkumar Yanpallewar: CCR, NCI, NIH
Brad St Croix: CCR, NCI, NIH
Jürgen Wess: Laboratory of Bioorganic Chemistry, NIDDK, NIH
Oksana Gavrilova: Mouse Metabolism Core Laboratory, NIDDK, NIH
Lino Tessarollo: CCR, NCI, NIH

Nature Communications, 2020, vol. 11, issue 1, 1-18

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-15833-5

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