Growth hormone (GH) therapy in GH-deficient adults influences the response to a dietary load of cholesterol and saturated fat in terms of cholesterol synthesis, but not serum low density lipoprotein cholesterol levels.
An increased dietary load of cholesterol (ch) and saturated fat increases serum low density lipoprotein ch (LDL-ch) levels. GH therapy in GH-deficient adults decreases serum LDL-ch levels. In the rat, GH is important for resistance to dietary cholesterol in terms of serum cholesterol levels. The aim of this study was to investigate the influence of GH on the effects of an increase in the intake of cholesterol and saturated fat on serum lipoproteins and markers for cholesterol synthesis in man. Six GH-deficient adults were given an isocaloric diet enriched in cholesterol and saturated fat for 17 days with and without GH therapy (1-1.5 U/day). Serum cholesterol, LDL-ch, apolipoprotein B (apoB), and apoA1 levels increased during the diet period with GH therapy and tended to increase during the diet period without GH. However, GH therapy did not influence the dietary effect on serum cholesterol, LDL-ch, apoA1, or apoB levels. Serum levels of triglycerides, very low density lipoprotein ch, high density lipoprotein ch, and apoE were not affected by diet or GH therapy. GH therapy increased serum lipoprotein(a) levels, but did not affect the response to diet. The serum total delta7-lathosterol/cholesterol ratio increased less during the diet period with GH therapy than during the diet period without GH. Serum 7alpha-hydroxy-4-cholesten-3-one levels tended to increase during both diet periods, but were not influenced by GH treatment. Serum plant sterol levels did not change. These results indicate that GH counteracts an increase in cholesterol synthesis induced by a high fat diet without affecting bile acid synthesis or sterol absorption. GH therapy did not have any major influence on the dietary effects on serum lipoprotein levels.
Leonsson
M
M
Research Center for Endocrinology and Metabolism, Sahlgrenska University Hospital, Goteborg, Sweden. maria.leonsson@ss.gu.se
Oscarsson
J
J
Bosaeus
I
I
Lundgren
B K
BK
Johannsson
G
G
Wiklund
O
O
Bengtsson
B A
BA
D000328:Adult; D000368:Aged; D001823:Body Composition; D001835:Body Weight; D002784:Cholesterol / Q000096:biosynthesis*; D002791:Cholesterol, Dietary / Q000008:administration & dosage*; D008078:Cholesterol, LDL / Q000097:blood*; D018592:Cross-Over Studies; D004041:Dietary Fats / Q000008:administration & dosage*; D002149:Energy Intake; D005260:Female; D005947:Glucose / Q000378:metabolism; D019382:Human Growth Hormone / Q000172:deficiency* / Q000627:therapeutic use*; D006801:Humans; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged
D002791:Cholesterol, Dietary; D008078:Cholesterol, LDL; D004041:Dietary Fats; D018972:Insulin-Like Growth Factor Binding Protein 3; D017270:Lipoprotein(a); D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D002784:Cholesterol; D005947:Glucose