Table 1.

Therapeutic agents for managing HDL level and prevention of diabetes.

Drugs	Mechanism	Members	The effect on HDL	The effects on other lipids	Glucose tolerance	Side effects	References
Statins	Facilitating the LDL removal by upregulating LDL receptors	Atorvastatin	15% increase	LDL and TG reduction	Increased IR and insulin secretion	Neuromuscular side effects	[78, 90, 91, 92, 93, 94]
		Pravastatin
Niacin	Inhibiting the production of LDL‐C precursors	Niacor	15%‐35% increase	LDL reduction	Minimally worsened	Limited use due to difficulty in tolerating clinically relevant dose	[10, 88, 92, 95, 96]
		Niaspan
Fibrates	Inducing the expression of LpL, inhibition of the Apo C‐III expression, and Apo B‐100 and VLDL synthesis	Gemfibrozil	10%‐15% increase	LDL, TG, and VLDL reduction	Gemfibrozil is more efficient in T2DM patients	Increased serum creatinine and kidney disease	[92, 95, 97, 98]
		Bezafibrate
CETP inhibitors	Inhibiting the transfer of cholesterol esters from HDL‐C to LDL or IDL in exchange for TG	Torcetrapib	106% increase (dose‐dependent)	LDL reduction	A combination of CETP inhibitors and infusion of rHDL (Apo A‐I and phospholipids) is beneficial for T2DM patients	CETP inhibitors are required for LDL uptake by RCT a pathway	[12, 90, 95, 99, 100, 101]
		Dalcetrapib (JTT‐705)	34% increase (dose‐dependent)

Abbreviations: Apo, apo lipoprotein; CETP, cholesterol ester transfer protein; HDL, high‐density lipoprotein; HDL‐C, high‐density lipoprotein cholesterol; IDL, intermediate‐density lipoprotein; IR, insulin resistance; LDL, low‐density lipoprotein; LDL‐C, low‐density lipoprotein cholesterol; LPL, lipoprotein lipase; RCT, reverse cholesterol transport; rHDL, reconstituted high‐density lipoprotein; T2DM, type 2 diabetes mellitus; TG, triglyceride; VLDL, very low‐density lipoprotein.

^a RCT pathway; is a critical pathway in the human body and inhibiting this pathway could cause irreversible damages.