Key result
Growth hormone replacement in GH-deficient adults decreased VLDL+LDL cholesterol (P<0.05) and increased HDL cholesterol (P<0.05), while lowering LCAT and CETP activities (P<0.01).
Why the study?
Does growth hormone replacement therapy alter lipid transfer protein activities and lipoprotein profiles in growth hormone-deficient adults?
RCT (n=24)
randomized
Does growth hormone replacement therapy alter lipid transfer protein activities and lipoprotein profiles in growth hormone-deficient adults?
Growth hormone replacement therapy in GH-deficient adults improves the lipoprotein profile and lowers plasma LCAT and CETP activities, which may influence HDL metabolism and reverse cholesterol transport.
Supports GH replacement to improve atherogenic lipids in deficient adults; extends evidence on LCAT/CETP modulation of HDL metabolism.
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.
No takes yet. Share an insight, caveat, or question.
Beentjes et al. (2000) conducted an RCT in Growth hormone deficiency (n=24). Growth hormone replacement vs. Placebo was evaluated on Plasma lipoproteins, LCAT, CETP, and PLTP activities. Growth hormone replacement in GH-deficient adults decreased VLDL+LDL cholesterol (P<0.05) and increased HDL cholesterol (P<0.05), while lowering LCAT and CETP activities (P<0.01).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: