Influence of growth hormone on glucose-glucose 6-phosphate cycle and insulin action in normal humans
Autor: | Patrick M. Bell, D. P. Rooney, R. D. G. Neely, Elisabeth R. Trimble, A. B. Atkinson, Brian Sheridan, N. P. Bell |
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Rok vydání: | 1992 |
Předmět: |
Adult
Blood Glucose Male medicine.medical_specialty Physiology Endocrinology Diabetes and Metabolism medicine.medical_treatment Glucose-6-Phosphate Biology chemistry.chemical_compound Insulin resistance Reference Values Physiology (medical) Internal medicine Acromegaly medicine Humans Insulin Infusions Intravenous Pancreatic hormone Fatty acid metabolism Osmolar Concentration Glucosephosphates Metabolism Glucose clamp technique medicine.disease Hormones Kinetics Endocrinology Glucose 6-phosphate chemistry Growth Hormone Glucose Clamp Technique |
Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 263:E980-E987 |
ISSN: | 1522-1555 0193-1849 |
DOI: | 10.1152/ajpendo.1992.263.5.e980 |
Popis: | Increased activity of the hepatic glucose-glucose 6-phosphate (G/G-6-P) cycle is associated with hepatic and peripheral insulin resistance in acromegaly. To determine whether a similar association occurs after short-term growth hormone (GH) elevation within the physiological range, two-step euglycemic hyperinsulinemic clamps were performed in normal human males after 12-h GH (2.2 ng.kg-1 x h-1) and control infusions. G/G-6-P cycle activity and endogenous glucose production (EGP) were determined by [2-3H]- and [6-3H]-glucose using labeled exogenous glucose infusions and selective enzymatic detritiation. GH increased levels of circulating lipid intermediates despite a twofold increase in basal insulin (P < 0.005), but plasma glucose, EGP, and G/G-6-P cycle activity were unchanged. GH impaired insulin suppression of EGP and lipid intermediates and impaired insulin stimulation of glucose disposal, but G/G-6-P cycle activity was unchanged. We conclude that increased activity of the G/G-6-P cycle does not contribute to the hepatic insulin resistance induced by GH under these conditions but that changes in fatty acid metabolism may be partly responsible for the impairment in hepatic and peripheral insulin action. |
Databáze: | OpenAIRE |
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