Plasma cholesteryl ester transfer protein and lipoprotein levels during treatment of growth hormone-deficient adult humans

Citation
Ajf. Carrilho et al., Plasma cholesteryl ester transfer protein and lipoprotein levels during treatment of growth hormone-deficient adult humans, LIPIDS, 36(6), 2001, pp. 549-554
Citations number
52
Categorie Soggetti
Agricultural Chemistry","Biochemistry & Biophysics
Journal title
LIPIDS
ISSN journal
00244201 → ACNP
Volume
36
Issue
6
Year of publication
2001
Pages
549 - 554
Database
ISI
SICI code
0024-4201(200106)36:6<549:PCETPA>2.0.ZU;2-8
Abstract
The incidence of atherosclerosis is increased in growth hormone (GH) defici ent-individuals. Nonetheless, the antiatherogenic benefits of GH replacemen t therapy remain uncertain. In this study the effect of human recombinant g rowth hormone (hrGH) replacement therapy administered to GH-deficient adult s on the plasma cholesteryl ester transfer protein (CETP) concentration and activity was analyzed. These findings were related to changes in the conce ntrations of the plasma lipoproteins. The hrGH was administered for 12 mon to human GH-deficient patients (n = 13; 8 men, 5 women). During the study p lasma lipoproteins were separated by ultracentrifugation, and plasma choles terol esterification rate (CER), endogenous CETP activity, and CETP concent ration were measured. GH replacement therapy transiently (at 3 mon) lowered plasma concentration of CETP and low density lipoprotein-cholesterol (LDL- C) and raised total triglycerides. Furthermore, hrGH permanently increased both the plasma lipoprotein(a) [Lp(a)] concentration, which is known as ath erogenic, and the proportion of cholesteryl ester in the high density lipop rotein(2) (HDL2) particles, which is potentially atheroprotective. The simu ltaneous decrease of the plasma CETP and LDL-C concentrations elicited by h rGH indicated a close relationship between LDL metabolism and the regulatio n of the CETP gene expression. Endogenous CETP activity and the CER were no t modified because these parameters are regulated in opposite ways by plasm a levels of triglycerides; that is, CER increased and CETP decreased.