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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). 2002 Apr; 102(4):457-64.CS

Abstract

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; 0.05 mg.24 h(-1).kg(-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-[(2)H(5)]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, 24 h 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.

Authors+Show Affiliations

Centre for Gastrointestinal Disease, Ersta Hospital, Box 4622, Karolinska Institute, 116 91 Stockholm, Sweden. jonas.nygren@ersta.seNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11914108

Citation

Nygren, Jonas, et al. "Glucose Flux Is Normalized By Compensatory Hyperinsulinaemia in Growth Hormone-induced Insulin Resistance in Healthy Subjects, While Skeletal Muscle Protein Synthesis Remains Unchanged." Clinical Science (London, England : 1979), vol. 102, no. 4, 2002, pp. 457-64.
Nygren J, Thorell A, Brismar K, et al. 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. 2002;102(4):457-64.
Nygren, J., Thorell, A., Brismar, K., Essén, P., Wernerman, J., McNurlan, M. A., Garlick, P. J., & Ljungqvist, O. (2002). Glucose flux is normalized by compensatory hyperinsulinaemia in growth hormone-induced insulin resistance in healthy subjects, while skeletal muscle protein synthesis remains unchanged. Clinical Science (London, England : 1979), 102(4), 457-64.
Nygren J, et al. 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. 2002;102(4):457-64. PubMed PMID: 11914108.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucose flux is normalized by compensatory hyperinsulinaemia in growth hormone-induced insulin resistance in healthy subjects, while skeletal muscle protein synthesis remains unchanged. AU - Nygren,Jonas, AU - Thorell,Anders, AU - Brismar,Kerstin, AU - Essén,Pia, AU - Wernerman,Jan, AU - McNurlan,Margaret A, AU - Garlick,Peter J, AU - Ljungqvist,Olle, PY - 2002/3/27/pubmed PY - 2002/6/22/medline PY - 2002/3/27/entrez SP - 457 EP - 64 JF - Clinical science (London, England : 1979) JO - Clin. Sci. VL - 102 IS - 4 N2 - 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; 0.05 mg.24 h(-1).kg(-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-[(2)H(5)]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, 24 h 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. SN - 0143-5221 UR - https://www.unboundmedicine.com/medline/citation/11914108/Glucose_flux_is_normalized_by_compensatory_hyperinsulinaemia_in_growth_hormone_induced_insulin_resistance_in_healthy_subjects_while_skeletal_muscle_protein_synthesis_remains_unchanged_ L2 - https://medlineplus.gov/diabetesmedicines.html DB - PRIME DP - Unbound Medicine ER -