HDL biology
Chronic growth hormone replacement lowers CETP activity alongside LCAT, improving the lipoprotein profile (J Lipid Res 2000)
Original title: Effect of growth hormone replacement therapy on plasma lecithin:cholesterol acyltransferase and lipid transfer protein activities in growth hormone-deficient adults
Twenty-four growth-hormone-deficient adults were randomized to placebo, low-dose GH (1 U/day), or high-dose GH (2 U/day) for six months, followed by a six-month open extension on high-dose GH. Placebo produced no significant changes in lipoproteins or LCAT, CETP, or PLTP activities. After six months of GH (combined, n=24), VLDL+LDL cholesterol and apoB decreased while HDL-cholesterol and HDL cholesteryl ester increased (all P<0.05), with comparable effects on prolonged treatment; apoA-I and Lp[a] were unchanged. After 12 months of GH (n=15), plasma LCAT and CETP activities both decreased (P<0.01), alongside decreased cholesterol esterification and cholesteryl ester transfer rates (P<0.01 for both), while PLTP activity did not change; changes in esterification and transfer rates were independently linked to changes in LCAT (P=0.001) and CETP activity (P=0.01). Chronic GH replacement thus improves the lipoprotein profile while lowering CETP and LCAT activities, with implications for HDL metabolism and reverse cholesterol transport.
Original abstract
The effects of growth hormone (GH) replacement on plasma lecithin:cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP), and phospholipid transfer protein (PLTP), factors involved in high density lipoprotein (HDL) metabolism, are unknown. We carried out a 6 months study in 24 GH-deficient adults who were randomized to placebo (n = 8), low dose GH (1 U daily, n = 8), and high dose GH (2 U daily, n = 8), followed by a 6 months open extension study with high dose GH (1 drop-out). No significant changes in plasma lipoproteins, LCAT, CETP, and PLTP activities, cholesterol esterification (EST) and cholesteryl ester transfer (CET) were observed after placebo. After 6 months of GH (combined data, n = 24), very low + low density lipoprotein (VLDL + LDL) cholesterol (P < 0.05) and apolipoprotein B (P < 0.05) decreased, whereas HDL cholesterol and HDL cholesteryl ester increased (P < 0. 05). Prolonged treatment showed comparable effects. Plasma apolipoprotein A-I and Lp[a] remained unchanged. Plasma LCAT (P < 0. 01) and CETP activities (P < 0.01), as well as EST (P < 0.01) and CET decreased (P < 0.01) after 12 months of GH (n = 15), but PLTP activity did not significantly change. Changes in EST and CET after 12 months of treatment were independently related to changes in plasma LCAT (P = 0.001 and CETP activity (P = 0.01). In conclusion, GH replacement therapy improves the lipoprotein profile in GH-deficient adults. Chronic GH replacement lowers plasma LCAT and CETP activities, contributing to a decrease in cholesterol esterification and cholesteryl ester transfer. These effects may have consequences for HDL metabolism and reverse cholesterol transport.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.