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Growth hormone overexpression in the central nervous system results in hyperphagia-induced obesity associated with insulin resistance and dyslipidemia.

Journal article
Authors Mohammad Bohlooly-Yeganeh
Bob Olsson
Carl E G Bruder
Daniel Lindén
Klara Sjögren
Mikael Bjursell
Emil Egecioglu
Lennart Svensson
Peter Brodin
John C Waterton
Olle Isaksson
Frank Sundler
Bo Ahrén
Claes Ohlsson
Jan Oscarsson
Jan Törnell
Published in Diabetes
Volume 54
Issue 1
Pages 51-62
ISSN 0012-1797
Publication year 2005
Published at Wallenberg Laboratory
Institute of Internal Medicine, Dept of Medicine
Institute of Internal Medicine, Dept of Body Composition and Metabolism
Institute of Physiology and Pharmacology, Dept of Physiology
Pages 51-62
Language en
Keywords Adipose Tissue, anatomy & histology, Animals, Base Sequence, Blood Glucose, metabolism, Body Weight, Calorimetry, Indirect, Cattle, DNA Probes, Energy Intake, drug effects, Female, Gene Expression Regulation, genetics, physiology, Genome, Growth Hormone, administration & dosage, genetics, pharmacology, physiology, Hyperinsulinism, chemically induced, Hyperlipidemias, genetics, Hyperphagia, blood, genetics, physiopathology, Hypothalamus, physiology, Injections, Intraventricular, Insulin Resistance, genetics, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Obesity, blood, etiology
Subject categories Medical and Health Sciences


It is well known that peripherally administered growth hormone (GH) results in decreased body fat mass. However, GH-deficient patients increase their food intake when substituted with GH, suggesting that GH also has an appetite stimulating effect. Transgenic mice with an overexpression of bovine GH in the central nervous system (CNS) were created to investigate the role of GH in CNS. This study shows that overexpression of GH in the CNS differentiates the effect of GH on body fat mass from that on appetite. The transgenic mice were not GH-deficient but were obese and showed increased food intake as well as increased hypothalamic expression of agouti-related protein and neuropeptide Y. GH also had an acute effect on food intake following intracerebroventricular injection of C57BL/6 mice. The transgenic mice were severely hyperinsulinemic and showed a marked hyperplasia of the islets of Langerhans. In addition, the transgenic mice displayed alterations in serum lipid and lipoprotein levels and hepatic gene expression. In conclusion, GH overexpression in the CNS results in hyperphagia-induced obesity indicating a dual effect of GH with a central stimulation of appetite and a peripheral lipolytic effect.

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