Abstract
Adipose tissue, as the largest endocrine organ, secretes many biologically active molecules circulating in the bloodstream, collectively termed adipocytokines, which not only regulate the metabolism but also play a role in pathophysiological processes. C1q tumor necrosis factor (TNF)-related protein 3 (CTRP3) is a member of C1q tumor necrosis factor-related proteins (CTRPs), which is a paralog of adiponectin. CTRP3 has a wide range of effects on glucose/lipid metabolism, inflammation, and contributes to cardiovascular protection. In this review, we comprehensively discussed the latest research on CTRP3 in obesity, diabetes, metabolic syndrome, and cardiovascular diseases.
Highlights
Adipose tissue (AT) is widely known as an endocrine organ and a sensor/regulator of energy homeostasis (Rosen and Spiegelman, 2006; Scherer, 2006)
When we focus on the changes of C1Q/tumor necrosis factor (TNF)-RELATED PROTEIN-3 (CTRP3) levels, we found that it was significantly increased in subjects with pre-diabetic subjects (Choi et al, 2012), and decreased significantly in newly diagnosed type 2 diabetes mellitus (T2DM) (Ban et al, 2014) or T2DM (Deng et al, 2015; Qu et al, 2015; Moradi et al, 2019)
CTRP3 significantly increases the expression of disulfide bond-A oxidoreductase-like protein (DsbAL) and adiponectin in 3T3-L1 adipocytes by activating AMPK signaling (Liu et al, 2012); in addition, DsbAL promotes the multimerization of adiponectin, thereby enhancing the biological activity of adiponectin, and prevents the reduction of adiponectin induced by endoplasmic reticulum stress, thereby improving insulin sensitivity (Pajvani et al, 2003; Liu et al, 2008, 2012; Liu and Liu, 2014). 5. recently, the level of CTRP3 in the circulation is related to β cell function
Summary
Adipose tissue (AT) is widely known as an endocrine organ and a sensor/regulator of energy homeostasis (Rosen and Spiegelman, 2006; Scherer, 2006). CTRP3 significantly increases the expression of disulfide bond-A oxidoreductase-like protein (DsbAL) and adiponectin in 3T3-L1 adipocytes by activating AMPK signaling (Liu et al, 2012); in addition, DsbAL promotes the multimerization of adiponectin, thereby enhancing the biological activity of adiponectin, and prevents the reduction of adiponectin induced by endoplasmic reticulum stress, thereby improving insulin sensitivity (Pajvani et al, 2003; Liu et al, 2008, 2012; Liu and Liu, 2014).
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