Alteration in lipid metabolism is a benchmark in the development of insulin resistance, type 2 diabetes and related cardiometabolic diseases. Angiopoietin like proteins (ANGPTL) are a family of secreted glycoproteins present in tissues (liver, heart, muscle, adipose tissue), macrophages and blood with pleiotropic effects on vascular cells, stem cell biology, and lipid metabolism. Studies in animals and cell lines have shown that ANGPTL4 is involved in the regulation of lipoprotein lipase (LPL). In plasma, ANGPTL4 inhibits VLDL- and chylomicron triglyceride (TG) hydrolysis while in adipose tissue stimulates lipolysis. However, the relationship between this secreted glycoprotein and lipid metabolism in vivo in humans has not been studied. Since ANGPTL4 is secreted in plasma, we wanted to explore if circulating ANGPTL4 might be related with lipid dysfunction, ectopic fat accumulation and insulin resistance (IR).
Angiopoietin like protein 4 (ANGPTL4): a marker of alteration in lipid metabolism, insulin resistance and ectopic fat accumulation
Gastaldelli A;Gaggini M;Carli F;Buzzigoli E;Ciociaro D;
2016
Abstract
Alteration in lipid metabolism is a benchmark in the development of insulin resistance, type 2 diabetes and related cardiometabolic diseases. Angiopoietin like proteins (ANGPTL) are a family of secreted glycoproteins present in tissues (liver, heart, muscle, adipose tissue), macrophages and blood with pleiotropic effects on vascular cells, stem cell biology, and lipid metabolism. Studies in animals and cell lines have shown that ANGPTL4 is involved in the regulation of lipoprotein lipase (LPL). In plasma, ANGPTL4 inhibits VLDL- and chylomicron triglyceride (TG) hydrolysis while in adipose tissue stimulates lipolysis. However, the relationship between this secreted glycoprotein and lipid metabolism in vivo in humans has not been studied. Since ANGPTL4 is secreted in plasma, we wanted to explore if circulating ANGPTL4 might be related with lipid dysfunction, ectopic fat accumulation and insulin resistance (IR).I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
