Adiponectin belongs to the family of fatty tissue hormones (adipokines). Adiponectin is a larger peptide consisting of 244 amino acids. It is mainly produced in adipocytes (fat tissue cells), but also in skeletal muscle cells (Liu Y et al. 2014). Adiponectin is encoded by ADIPOQ gene located on chromosome 3q27. Various gene polymorphisms are associated with an increased risk of diabetes and obesity.
Adiponectin exerts its effect via the receptors, AdipoR1 (in skeletal muscle) and AdipoR2 (in the liver). It has strong insulin-sensitive, anti-inflammatory and anti-diabetic effects via various signaling pathways (Liu M et al. 2014).
Its main function is to control glucose homeostasis. Hepatic gluconeogenesis is inhibited and fatty acid oxidation is increased. Adiponectin thus induces processes that reduce the risk of type 2 diabetes, obesity and atherosclerosis (Lim S et al. 2014). Several genetic variants are associated with increased risk of diabetes.
Low fat stores lead to increased expression of adiponectin. Full fat stores reduce the formation of the peptide.
Adiponectin levels are decreased in obesity, insulin resistance, type 2 diabetes, hypertension; high fasting glucose, elevated LDL and total cholesterol. The value is decreased in the blood already at the stage of prediabetes. Thus, it can serve as a prognostic marker for increased risk of type 2 diabetes. The adiponectin level correlates positively with the level of HDL cholesterol.
Adiponectin promotes fat storage in adipocytes and counteracts the development of insulin resistance . It reduces the risk of developing type 2 diabetes. Furthermore, adiponectin has a vasoprotective effect, reduces the risk of developing atherosclerosis. It modulates adiponectin the function of cardiomyocytes, endothelial cells and smooth muscle cells of blood vessels, counteracting pathological processes (cardiomyopathy, angiopathy).
Overweight and obese individuals with metabolic syndrome were found to have significantly lower levels of adiponectin and IL-6 in their blood than those without metabolic syndrome.
Adiponectin is able to suppress cellular inflammatory signals. Thus, UV-irradiated keratinocytes express significantly greater amounts of hBD2. Adiponectin is able to suppress this hBD2 overexpression (Kim M et al. 2016).