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Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs 125 31 31 6 6 PD Dr. M. J. Müller P. E. Mitchinson U. Paschen H. J. Seitz Klinische Endokrinologie Medizinische Hochschule Hannover Konstanty Gutschow Straße 7 D-3000 Hannover 61 Germany Biochemische Endokrinologie Institut für Physiologische Chemie, Universitäts-Krankenhaus Eppendorf Hamburg FRG Summary The glucoregulatory function of glucagon was investigated in hypo-, eu- and hyperthyroid miniature pigs. Infusion glucagon, (3 ng x kg body weight −1 · min −1 ) transiently increased blood glucose (p<0.01) and hepatic glucose production (p<0.01) in euthyroidism, but was without effect in hyperthyroidism. Infusing glucagon plus somatostatin (2 ng x kg body weight −1 · min −1 and 0.2 μg x kg body weight −1 · min −1 ) transiently increased blood glucose (Δ 3.0 to 4.3 mmol/l) and hepatic glucose production (Δ 3.3 to 7.7 umol x kg body weight −1 · min −1 ) in all thyroid states, the effect was less pronounced in hyperthyroid pigs. By contrast, hypoglucagonaemia (74 to 107 pg/ml) at basal insulin (28 to 35 μU/ml) provoked hypoglycaemia (1.4 to 2.2 mmol/l) and a fall in glucose production (Δ 4.7 to 8.3 umol x kg body weight −1 · min −1 ), which was independent of the thyroid state; the effect was most pronounced in hyperthyroidism (p<0.01). Hepatic glycogen content, arterial gluconeogenic precursor concentrations as well as the glycaemic response (Δ 0.60 mmol/l) to alanine infusion (23 umol x kg body weight −1 · min −1 ) were all unaffected by hyperthyroidism. We conclude that moderate experimental hyperthyroidism reduces glucagon action due to reduced glycogen mobilisation. This may in part result from increased insulin sensitivity. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetologia Springer Journals

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs

Müller, M.; Mitchinson, P.; Paschen, U.; Seitz, H.
Diabetologia , Volume 31 (6) – Jun 1, 1988
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References (32)

Publisher
Springer Journals
Copyright
Copyright © 1988 by Springer-Verlag
Subject
Medicine & Public Health; Human Physiology; Internal Medicine; Metabolic Diseases
ISSN
0012-186X
eISSN
1432-0428
DOI
10.1007/BF02341505
Publisher site
See Article on Publisher Site

Abstract

125 31 31 6 6 PD Dr. M. J. Müller P. E. Mitchinson U. Paschen H. J. Seitz Klinische Endokrinologie Medizinische Hochschule Hannover Konstanty Gutschow Straße 7 D-3000 Hannover 61 Germany Biochemische Endokrinologie Institut für Physiologische Chemie, Universitäts-Krankenhaus Eppendorf Hamburg FRG Summary The glucoregulatory function of glucagon was investigated in hypo-, eu- and hyperthyroid miniature pigs. Infusion glucagon, (3 ng x kg body weight −1 · min −1 ) transiently increased blood glucose (p<0.01) and hepatic glucose production (p<0.01) in euthyroidism, but was without effect in hyperthyroidism. Infusing glucagon plus somatostatin (2 ng x kg body weight −1 · min −1 and 0.2 μg x kg body weight −1 · min −1 ) transiently increased blood glucose (Δ 3.0 to 4.3 mmol/l) and hepatic glucose production (Δ 3.3 to 7.7 umol x kg body weight −1 · min −1 ) in all thyroid states, the effect was less pronounced in hyperthyroid pigs. By contrast, hypoglucagonaemia (74 to 107 pg/ml) at basal insulin (28 to 35 μU/ml) provoked hypoglycaemia (1.4 to 2.2 mmol/l) and a fall in glucose production (Δ 4.7 to 8.3 umol x kg body weight −1 · min −1 ), which was independent of the thyroid state; the effect was most pronounced in hyperthyroidism (p<0.01). Hepatic glycogen content, arterial gluconeogenic precursor concentrations as well as the glycaemic response (Δ 0.60 mmol/l) to alanine infusion (23 umol x kg body weight −1 · min −1 ) were all unaffected by hyperthyroidism. We conclude that moderate experimental hyperthyroidism reduces glucagon action due to reduced glycogen mobilisation. This may in part result from increased insulin sensitivity.

Journal

Diabetologia – Springer Journals

Published: Jun 1, 1988

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