The aim of this present investigation was to study the relationship between the reduction in insulin sensitivity accompanying 5 days of treatment with growth hormone (GH; 0.05mgċ24h-1ċkg-1) and intracellular substrate oxidation rates in six healthy subjects, while maintaining glucose flux by a constant glucose infusion and adjusting insulin infusion rates to achieve normoglycaemia (feedback clamp). Protein synthesis rates in skeletal muscle (flooding dose of L-[2H5]phenylalanine) were determined under these conditions. We also compared changes in insulin sensitivity after GH treatment with simultaneous changes in energy requirements, protein synthesis rates, nitrogen balance, 3-methylhistidine excretion in urine, body composition and the hormonal milieu. After GH treatment, 70% more insulin was required to maintain normoglycaemia (P < 0.01). The ratio between glucose infusion rate and serum insulin levels decreased by 34% at the two levels of glucose infusion tested (P < 0.05). Basal levels of C-peptide, insulin-like growth factor (IGF)-I and IGF-binding protein-3 increased almost 2-fold, while levels of glucose, insulin, glucagon, GH and IGF-binding protein-1 remained unchanged. Non-esterified fatty acid levels decreased (P < 0.05). In addition, 24h urinary nitrogen excretion decreased by 26% (P < 0.01) after GH treatment, while skeletal muscle protein synthesis and 3-methylhistidine excretion in urine remained unchanged. Energy expenditure increased by 5% (P < 0.05) after treatment, whereas fat and carbohydrate oxidation were unaltered. In conclusion, when glucose flux was normalized by compensatory hyperinsulinaemia under conditions of GH-induced insulin resistance, intracellular rates of oxidation of glucose and fat remained unchanged. The nitrogen retention accompanying GH treatment seems to be due largely to improved nitrogen balance in non-muscle tissue.
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Research Article|
March 18 2002
Glucose flux is normalized by compensatory hyperinsulinaemia in growth hormone-induced insulin resistance in healthy subjects, while skeletal muscle protein synthesis remains unchanged
Jonas NYGREN;
*Centre for Gastrointestinal Disease, Ersta Hospital, Karolinska Institute, 116 91 Stockholm, Sweden
Correspondence: Dr Jonas Nygren, Centre for Gastrointestinal Disease, Ersta Hospital, Box 4622, 116 91 Stockholm, Sweden (e-mail jonas.nygren@ersta.se).
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Anders THORELL;
Anders THORELL
*Centre for Gastrointestinal Disease, Ersta Hospital, Karolinska Institute, 116 91 Stockholm, Sweden
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Kerstin BRISMAR;
Kerstin BRISMAR
†Department of Endocrinology, Karolinska Hospital, Karolinska Institute, 171 76 Stockholm, Sweden
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Pia ESSÉN;
Pia ESSÉN
‡Department of Anaesthesia, Huddinge University Hospital, Karolinska Institute, 141 86 Stockholm, Sweden
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Jan WERNERMAN;
Jan WERNERMAN
‡Department of Anaesthesia, Huddinge University Hospital, Karolinska Institute, 141 86 Stockholm, Sweden
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Margaret A. MCNURLAN;
Margaret A. MCNURLAN
§Department of Surgery, State University of New York, Stony Brook, NY 11794, U.S.A.
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Peter J. GARLICK;
Peter J. GARLICK
§Department of Surgery, State University of New York, Stony Brook, NY 11794, U.S.A.
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Olle LJUNGQVIST
Olle LJUNGQVIST
*Centre for Gastrointestinal Disease, Ersta Hospital, Karolinska Institute, 116 91 Stockholm, Sweden
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Publisher: Portland Press Ltd
Received:
October 08 2001
Accepted:
December 04 2001
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2002
2002
Clin Sci (Lond) (2002) 102 (4): 457–464.
Article history
Received:
October 08 2001
Accepted:
December 04 2001
Citation
Jonas NYGREN, Anders THORELL, Kerstin BRISMAR, Pia ESSÉN, Jan WERNERMAN, Margaret A. MCNURLAN, Peter J. GARLICK, Olle LJUNGQVIST; Glucose flux is normalized by compensatory hyperinsulinaemia in growth hormone-induced insulin resistance in healthy subjects, while skeletal muscle protein synthesis remains unchanged. Clin Sci (Lond) 1 April 2002; 102 (4): 457–464. doi: https://doi.org/10.1042/cs1020457
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