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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #338359

Research Project: Biology of Obesity Prevention

Location: Healthy Body Weight Research

Title: Transient receptor potential canonical channel-1 (TRPC1) KO mice that exercise are protected from high-fat diet-induced obesity and type 2 diabetes risk

Author
item Krout, Danielle
item Schaar, Anne - University Of North Dakota
item Singh, Brij - University Of North Dakota
item Roemmich, James
item Larson, Kate

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/15/2017
Publication Date: 4/1/2017
Citation: Krout, D.P., Schaar, A., Singh, B., Roemmich, J.N., Larson, K.J. 2017. Transient receptor potential canonical channel-1 (TRPC1) KO mice that exercise are protected from high-fat diet-induced obesity and type 2 diabetes risk [abstract]. Journal of Federation of American Societies for Experimental Biology. 31:31:lb280.

Interpretive Summary:

Technical Abstract: Objective: Transient receptor potential canonical channel-1 (TRPC1) is a major class of calcium permeable channels found in key metabolic tissues, including the hypothalamus, adipose tissue, and skeletal muscle, making them likely candidates for the regulation of cellular energy metabolism. The exact role of TRPC1 in development of obesity, adipose tissue mass changes, and obesity-associated metabolic disease risk has not yet been determined. Method: Four week old male B6129SF2/J (WT) or TRPC1 knockout (TRPC1 KO) mice were fed a control normal-fat (NF) (16% fat) or a high-fat (HF) (45% fat) diet for 3 months and subjected to voluntary wheel running exercise or sedentary activity. Body composition, type 2 diabetes risk, and adipose tissue cellularity were determined. Results: Under sedentary conditions, body fat mass was not different between WT and TRPC1 KO mice. Fat mass was decreased (P<0.05) in TRPC1 KO mice fed a HF diet and exercised compared to WT mice fed a HF diet and exercised. Fasting glucose concentrations were also lower in TRPC1 KO mice fed a HF diet in both exercise and sedentary groups. Adipocyte numbers were decreased in both the subcutaneous and visceral adipose tissue of TRPC1 KO mice fed a HF diet and exercised. Conclusion: These findings suggest that in TRPC1 deficient mice, exercise is very protective against HF diet induced obesity and insulin resistance. Additional studies will be conducted to determine the mechanism underlying exercise-mediated reduction in adiposity and insulin resistance in the absence of TRPC1.