The TRPC1 Ca2+-permeable channel inhibits exerciseinduced protection against high-fat diet-induced obesity and type II diabetes

Danielle Krout, Anne Schaar, Yuyang Sun, Pramod Sukumaran, James N. Roemmich, Brij B. Singh, Kate J. Claycombe-Larson

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

The transient receptor potential canonical channel-1 (TRPC1) is a Ca2+-permeable channel found in key metabolic organs and tissues, including the hypothalamus, adipose tissue, and skeletal muscle. Loss of TRPC1 may alter the regulation of cellular energy metabolism resulting in insulin resistance thereby leading to diabetes. Exercise reduces insulin resistance, but it is not known whether TRPC1 is involved in exercise-induced insulin sensitivity. The role of TRPC1 in adiposity and obesity-associated metabolic diseases has not yet been determined. Our results show that TRPC1 functions as a major Ca2+ entry channel in adipocytes. We have also shown that fat mass and fasting glucose concentrations were lower in TRPC1 KO mice that were fed a high-fat (HF) (45% fat) diet and exercised as compared with WT mice fed a HF diet and exercised. Adipocyte numbers were decreased in both subcutaneous and visceral adipose tissue of TRPC1 KO mice fed a HF diet and exercised. Finally, autophagy markers were decreased and apoptosis markers increased in TRPC1 KO mice fed a HF diet and exercised. Overall, these findings suggest that TRPC1 plays an important role in the regulation of adiposity via autophagy and apoptosis and that TRPC1 inhibits the positive effect of exercise on type II diabetes risk under a HF diet-induced obesity environment.

Original languageEnglish (US)
Pages (from-to)20799-20807
Number of pages9
JournalJournal of Biological Chemistry
Volume292
Issue number50
DOIs
StatePublished - Dec 15 2017

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'The TRPC1 Ca<sup>2+</sup>-permeable channel inhibits exerciseinduced protection against high-fat diet-induced obesity and type II diabetes'. Together they form a unique fingerprint.

Cite this