Abstract
Cidea and Cidec play an important role in regulating triglyceride storage in liver and adipose tissue. It is not known if the Cidea and Cidec genes respond to a high fat diet (HFD) or exercise training, two interventions that alter lipid storage. The purpose of the present study was to determine the effect of a HFD and voluntary wheel running (WR) on Cidea and Cidec mRNA and protein expression in adipose tissue and liver of mice. A HFD promoted a significant increase in Cidea and Cidec mRNA levels in adipose tissue and liver. The increase in Cidea and Cidec mRNAs in adipose tissue and liver in response to a HFD was prevented by WR. Similar to the changes in Cidea mRNA, Cidea protein levels in adipose tissue significantly increased in response to a HFD, a process that was, again, prevented by WR. However, in adipose tissue the changes in Cidec mRNA did not correspond to the changes in Cidec protein levels, as a HFD decreased Cidec protein abundance. Interestingly, in adipose tissue Cidea protein expression was significantly related to body weight (R=.725), epididymal adipose tissue (EWAT) mass (R=.475) and insulin resistance (R=.706), whereas Cidec protein expression was inversely related to body weight (R=-.787), EWAT mass (R=-.706), and insulin resistance (R=-.679). Similar to adipose tissue, Cidea protein expression in liver was significantly related to body weight (R=.660), EWAT mass (R=.468), and insulin resistance (R=.599); however, unlike adipose tissue, Cidec protein levels in liver were not related to body weight or EWAT mass and only moderately associated with insulin resistance (R=-.422, P=0.051). Overall, our findings indicate that Cidea is highly associated with adiposity and insulin resistance, whereas Cidec is related to insulin sensitivity. The present study suggests that Cide proteins might play an important functional role in the development of obesity, hepatic steatosis, as well as the pathogenesis of type 2 diabetes.
Highlights
The most recent data from the CDC reveals that diabetes affects almost 26 million people in the United States [1], resulting in an estimated $245 billion in total health care costs [2]
Since previous studies have shown the role of Cidea and Cidec in triglyceride accumulation in adipocytes [16, 17], the effect of a high fat diet (HFD) and wheel running (WR) was assessed on the expression of these genes in liver and adipose tissues
Cidec protein levels increased in response to WR in HFD-fed mice, WR produced a significant decrease in Cidec levels in low fat diet (LFD)-fed mice
Summary
The most recent data from the CDC reveals that diabetes affects almost 26 million people in the United States [1], resulting in an estimated $245 billion in total health care costs [2]. Because of the prevalence and devastating health consequences of obesity, it is important to gain a better understanding of factors that regulate fat storage in insulin sensitive tissues, since lipids have been shown to disrupt insulin signaling and promote insulin resistance [4]. Plin has been shown to promote lipid droplet growth through an interaction with fat specific protein 27 (Fsp27), a member of the cell deathinducing DFF45 effector (Cide) family of proteins [7]. The lipid binding domain of Cidea and Cidec has been identified [8], and several reports indicate that Cide proteins play an important role in regulating lipid droplet size and triglyceride accumulation [9,10,11]. Similar to Plin knockout mice [12], genetic ablation of Cidea or Cidec results in a lean phenotype, enhanced insulin sensitivity, and resistance to dietary induced obesity [13, 14]
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