Literature DB >> 6327767

Adrenergic blockade alters glucose kinetics during exercise in insulin-dependent diabetics.

D C Simonson, V Koivisto, R S Sherwin, E Ferrannini, R Hendler, A Juhlin-Dannfelt, R A DeFronzo.   

Abstract

We investigated the effects of alpha and/or beta adrenergic blockade (with phentolamine and/or propranolol) on glucose homeostasis during exercise in six normal subjects and in seven Type I diabetic subjects. The diabetics received a low dose insulin infusion (0.07 mU/kg X min) designed to maintain plasma glucose at approximately 150 mg/dl. In normals, neither alpha, beta, nor combined alpha and beta adrenergic blockade altered glucose production, glucose uptake, or plasma glucose concentration during exercise. In diabetics, exercise alone produced a decline in glucose concentration from 144 to 116 mg/dl. This was due to a slightly diminished rise in hepatic glucose production in association with a normal increase in glucose uptake. When exercise was performed during beta adrenergic blockade, the decline in plasma glucose was accentuated. An exogenous glucose infusion (2.58 mg/kg X min) was required to prevent glucose levels from falling below 90 mg/dl. The effect of beta blockade was accounted for by a blunted rise in hepatic glucose production and an augmented rise in glucose utilization. These alterations were unrelated to changes in plasma insulin and glucagon levels, which were similar in the presence and absence of propranolol. In contrast, when the diabetics exercised during alpha adrenergic blockade, plasma glucose concentration rose from 150 to 164 mg/dl. This was due to a significant increase in hepatic glucose production and a small decline in exercise-induced glucose utilization. These alterations also could not be explained by differences in insulin and glucagon levels. We conclude that the glucose homeostatic response to exercise in insulin-dependent diabetics, in contrast to healthy controls, is critically dependent on the adrenergic nervous system.

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Year:  1984        PMID: 6327767      PMCID: PMC437075          DOI: 10.1172/JCI111371

Source DB:  PubMed          Journal:  J Clin Invest        ISSN: 0021-9738            Impact factor:   14.808


  36 in total

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Authors:  A S Luyckx; P J Lefebvre
Journal:  Diabetes       Date:  1974-02       Impact factor: 9.461

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Journal:  Diabetes       Date:  1973-01       Impact factor: 9.461

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Journal:  J Clin Invest       Date:  1971-12       Impact factor: 14.808

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Journal:  Am J Med Sci       Date:  1969-06       Impact factor: 2.378

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Journal:  Diabetologia       Date:  1969-10       Impact factor: 10.122

10.  Substrate turnover during prolonged exercise in man. Splanchnic and leg metabolism of glucose, free fatty acids, and amino acids.

Authors:  G Ahlborg; P Felig; L Hagenfeldt; R Hendler; J Wahren
Journal:  J Clin Invest       Date:  1974-04       Impact factor: 14.808

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  8 in total

Review 1.  Plasma glucose metabolism during exercise in humans.

Authors:  A R Coggan
Journal:  Sports Med       Date:  1991-02       Impact factor: 11.136

2.  Effect of adrenaline on glucose kinetics during exercise in adrenalectomised humans.

Authors:  K Howlett; H Galbo; J Lorentsen; R Bergeron; T Zimmerman-Belsing; J Bülow; U Feldt-Rasmussen; M Kjaer
Journal:  J Physiol       Date:  1999-09-15       Impact factor: 5.182

3.  Studies on the insulin-antagonistic effect of catecholamines in normal man. Evidence for the importance of beta 2-receptors.

Authors:  I Lager; S Attvall; B M Eriksson; H von Schenk; U Smith
Journal:  Diabetologia       Date:  1986-07       Impact factor: 10.122

4.  Beta-adrenergic blockade is more effective in suppressing adrenaline-induced glucose production in Type 1 (insulin-dependent) diabetes.

Authors:  H Shamoon; R Sherwin
Journal:  Diabetologia       Date:  1984-03       Impact factor: 10.122

Review 5.  Physiological bases for the treatment of the physically active individual with diabetes.

Authors:  D H Wasserman; N N Abumrad
Journal:  Sports Med       Date:  1989-06       Impact factor: 11.136

Review 6.  New insights into managing the risk of hypoglycaemia associated with intermittent high-intensity exercise in individuals with type 1 diabetes mellitus: implications for existing guidelines.

Authors:  Kym J Guelfi; Timothy W Jones; Paul A Fournier
Journal:  Sports Med       Date:  2007       Impact factor: 11.136

7.  Glucoregulation during exercise: hypoglycemia is prevented by redundant glucoregulatory systems, sympathochromaffin activation, and changes in islet hormone secretion.

Authors:  D R Hoelzer; G P Dalsky; W E Clutter; S D Shah; J O Holloszy; P E Cryer
Journal:  J Clin Invest       Date:  1986-01       Impact factor: 14.808

8.  Hyperinsulinaemia during exercise does not suppress hepatic glycogen concentrations in patients with type 1 diabetes: a magnetic resonance spectroscopy study.

Authors:  K Chokkalingam; K Tsintzas; J E M Snaar; L Norton; B Solanky; E Leverton; P Morris; P Mansell; I A Macdonald
Journal:  Diabetologia       Date:  2007-07-18       Impact factor: 10.122

  8 in total

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