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Acute and Short-Term Effects of Growth Hormone on Insulin-Like Growth Factors and Their Binding Proteins: Serum Levels and Hepatic Messenger Ribonucleic Acid Responses in Humans¹

Gastroenterology Center (H.O., H.B., B.N.), Department of Surgery, Molecular Nutrition Unit (H.O., B.A.), Center for Nutrition and Toxicology, Center for Metabolism and Endocrinology (B.A.), Department of Medicine, Karolinska Institute at Huddinge University Hospital, S-141 86 Huddinge, Sweden; Endocrinology and Diabetes Unit (A.H., C.M., M.T.), Department of Molecular Medicine, Department of Clinical Neuroscience (C.E., T.J.E.), Center for Molecular Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden; and Kolling Institute of Medical Research (P.J.D., R.C.B.), University of Sydney, Royal North Shore Hospital, St. Leonards, NSW 2065, Australia

Address all correspondence and requests for reprints to: Tomas J. Ekström, Ph.D., Center for Molecular Medicine, Karolinska Institute at Karolinska Hospital, S-171 76 Stockholm, Sweden. E-mail: tomas.ekstrom{at}cmm.ki.se

We investigated the acute (4–5 h) and short-term (5 days) effects of GH treatment on hepatic messenger RNA (mRNA) levels of the genes for the insulin-like growth factors (IGFs), insulin-like growth factor binding protein-1, -2, and -3 (IGFBPs), and the acid labile subunit (ALS), as well as serum levels of these proteins in humans. At the mRNA level, we observed an increase in IGF-1 transcription (+173%) following GH treatment in the acute group, which remained elevated in the short-term treatment group. IGFBP-2 mRNA decreased after short-term GH treatment, without changes in IGFBP-1 or -3 expression. The ALS transcript level increased after 5 days. In serum, we found increased levels of IGF-I and insulin, and decreased levels of IGF-II, in the short-term treatment group. IGFBP-1 decreased in both treatment groups, whereas IGFBP-2 was reduced after 5 days treatment. ALS increased in the short-term group. We observed increased IGFBP-3 serum levels after 5 days of GH treatment, likely due to increased formation of the ternary complex. Our results show that the metabolic effects by GH on the IGF axis are complex. In addition to a direct stimulation of IGF-I and ALS expression, GH inhibits IGFBP-1 serum levels and IGFBP-2 expression in an indirect manner, possibly facilitating enhanced IGF bioavailability to target tissues.

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