Effects of curcumin on HDL functionality

Curcumin, a bioactive polyphenol, is a yellow pigment of the Curcuma longa (turmeric) plant. Curcumin has many pharmacologic effects including antioxidant, anti-carcinogenic, anti-obesity, anti-angiogenic and anti-inflammatory properties. Recently, it has been found that curcumin affects lipid metabolism, and subsequently, may alleviate hyperlipidemia and atherosclerosis. Plasma HDL cholesterol (HDL-C) is an independent negative risk predictor of cardiovascular disease (CVD). However, numerous clinical and genetic studies have yielded disappointing results about the therapeutic benefit of raising plasma HDL-C levels. Therefore, research efforts are now focused on improving HDL functionality, independent of HDL-C levels. The quality of HDL particles can vary considerably due to heterogeneity in composition. Consistent with its complexity in composition and metabolism, a wide range of biological activities is reported for HDL, including antioxidant, anti-glycation, anti-inflammatory, anti-thrombotic, anti-apoptotic and immune modulatory activities. Protective properties of curcumin may influence HDL functionality; therefore, we reviewed the literature to determine whether curcumin can augment HDL function. In this review, we concluded that curcumin may modulate markers of HDL function, such as apo-AI, CETP, LCAT, PON1, MPO activities and levels. Curcumin may subsequently improve conditions in which HDL is dysfunctional and may have potential as a therapeutic drug in future. Further clinical trials with bioavailability-improved formulations of curcumin are warranted to examine its effects on lipid metabolism and HDL function.

Heterogeneity, metabolism and biological activities of normal functional HDL (A) and of HDL with defective antiatherogenic function in the dyslipidemia of metabolic diseases (B). Interconversion between lipid-free apolipoprotein AI, discoid lipid-poor pre-β-HDL, spherical small, dense HDL3, and large, light HDL2 mediated by lecithin:cholesterol acyltransferase, cholesteryl ester transfer protein, phospholipid transfer protein, hepatic lipase, endothelial lipase, ABCA1 and scavenger receptor type BI is schematically shown in either solid (A) or dotted (B) lines. In panel (B), key pathways leading to the formation of functionally deficient HDL (elevated hepatic production of serum amyloid A, shedding of apolipoprotein AI and other HDL proteins from HDL particles, enrichment of small HDL3 in triglycerides and depletion in cholesteryl esters mediated by cholesteryl ester transfer protein, and oxidation and glycation of HDL proteins) are shown in solid lines. Biological activities of HDL particles are indicated. Deficient biological activities of small, dense HDL3 are marked in red. HDL components are underlined.108