Skip to main content
Figure 1 | Cardiovascular Diabetology

Figure 1

From: A dual role of lipasin (betatrophin) in lipid metabolism and glucose homeostasis: consensus and controversy

Figure 1

Roles of lipasin (Angptl8) in regulating triglyceride metabolism and pancreatic beta-cell proliferation. Lipasin is secreted from the liver into the circulation, and is involved in triglyceride metabolism and in promoting pancreatic β -cell proliferation. Active as a dimmer, LPL binds to both HSPG and GPIHPB1 on the surface of capillary microvascular endothelial cells. LPL hydrolyzes TAG in chylomicrons and VLDL, yielding FFAs, which are then taken up by peripheral tissues, including fat, muscle and heart. Both Angptl3 and Angptl4 need to be cleaved to release functional N-termini to inhibit LPL, disrupting dimer formation either reversibly or irreversibly, respectively. Lipasin likely inhibits LPL directly or indirectly by promoting Angptl3 cleavage. Food intake dramatically induces the expression of lipasin, whereas fasting induces Angptl4. Dotted lines denote homologous regions. Angptl3, angiopoietin-like 3; Angptl4, angiopoietin-like 4; EC, endothelial cell; GPIHBP1, glycosylphosphatidylinositol anchored high density lipoprotein binding protein 1; FFA, free fatty acid; HSPG, heparan sulfate proteoglycans; LPL, lipoprotein lipase; TAG, triglyceride; VLDL, very low-density lipoprotein.

Back to article page

Cardiovascular Diabetology

ISSN: 1475-2840