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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 #338360

Research Project: Biology of Obesity Prevention

Location: Healthy Body Weight Research

Title: Modulations of calcium in adipose tissue by TRPC1: a key player in obesity

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

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: Schaar, A., Krout, D.P., Roemmich, J.N., Larson, K.J., Singh, B. 2017. Modulations of calcium in adipose tissue by TRPC1: a key player in obesity [abstract]. Journal of Federation of American Societies for Experimental Biology. 31:lb155.

Interpretive Summary:

Technical Abstract: The disruption of metabolic homeostasis, the regulation of energy the body extracts, stores and uses, leads to excess adipose tissue accumulation and the onset of obesity. White adipose tissue (WAT) is a metabolically dynamic endocrine organ responsible for maintaining metabolic homeostasis through mitochondrion function and the secretion of cytokines. A key modulator of glucose and lipid metabolism is the WAT secreted cytokine adiponectin, however, the regulation of it is not fully known. Transient Receptor Potential Canonical (TRPC) channels are a major class of Ca2+ permeable channels found in key metabolic tissues (hypothalamus, adipocytes, and skeletal muscle). Fluctuations in intracellular Ca2+ are due to the release of Ca2+ stores from the endoplasmic reticulum (ER) that initiates store-operated Ca2+ entry (SOCE) mechanism, or by direct Ca2+ entry from the extracellular space upon membrane depolarization. Within our work, we provide evidence that Ca2+ entry into the cell, especially upon store-depletion, plays an important role in WAT functionality and subsequently metabolic regulation. It was found that mice deficient in the Ca2+ channel TRPC1-/- have significantly increased adipose deposition without an increase in overall weight as compared to control. When investigating WAT, the reduced Ca2+ influx due to a loss of TRPC1 resulting in a decline in mitochondria function. Further, TRPC1-/- mice were found to have reduced serum adiponectin levels along with a reduction in the downstream enzymes adiponectin regulates necessary for lipid metabolism. Combined, these results indicate that TRPC1 may have an important role in the regulation of metabolic homeostasis and the onset of obesity through the regulation of WAT.