Document Type

Article

Publication Date

2019

Publication Title

Journal of Cell Science

Volume

132

Abstract

Adipocyte functionality, including adipocyte differentiation and adipokine secretion, is essential in obesity-associated metabolic syndrome. Here, we provide evidence that Ca2+ influx in primary adipocytes, especially upon store-depletion, plays an important role in adipocyte differentiation, functionality, and subsequently metabolic regulation. The endogenous Ca2+ entry channel in both subcutaneous and visceral adipocytes was dependent on TRPC1-STIM1 and blocking Ca2+ entry with SKF-96365 or TRPC1-/- derived adipocytes inhibited adipocyte differentiation. Additionally, TRPC1-/- mice have decreased organ weight, but increased adipose deposition and reduced serum adiponectin and leptin concentrations, without affecting total adipokine expression. Mechanistically, TRPC1- mediated Ca2+ entry regulated SNARE complex formation and agonist –mediated secretion of adipokine loaded vesicles was inhibited in TRPC1-/- adipose. These results suggest an unequivocal role of TRPC1 in adipocytes differentiation and adiponectin secretion, and loss of TRPC1 disturbs metabolic homeostasis.

Issue

13

DOI

10.1242/jcs.231878

ISSN

00219533

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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