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Fig. 1 | Lipids in Health and Disease

Fig. 1

From: Emerging evidences for the opposite role of apolipoprotein C3 and apolipoprotein A5 in lipid metabolism and coronary artery disease

Fig. 1

The opposite role of apoC3 and apoA5 in TRL metabolism. ApoC3 and apoA5 regulated TRL metabolism through multiple pathways: (a). hepatic VLDL lipidation and secretion; (b). LPL mediated TRL hydrolysis; (c). TRL remnant clearance via hepatic uptake. ApoC3 inhibited LPL mediated TRL hydrolysis, circulating TRL remnant clearance and promoted hepatic VLDL-TG secretion. Conversely, apoA5 accelerated TRL hydrolysis, TRL remnant uptake by liver while inhibited hepatic VLDL-TG secretion. ApoC3, apolipoprotein C3; apoA5, apolipoprotein A5; TRL, triglyceride rich lipoprotein; VLDL, very low density lipoprotein; LPL, lipoprotein lipase; IDL, intermediate density lipoprotein; LDL, low density lipoprotein; CM, chylomicron

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