Hyperglucagonemia increases resting metabolic rate in man during insulin deficiency

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Abstract

The physiological significance of the hyperglucagonemia that occurs in patients with many catabolic conditions is unclear. The effect of hyperglucagonemia on resting metabolic rate (RMR) was studied in six normal subjects. Infusion of somatostatin (SRIH; 500 μg/h for 210 min) resulted in a 5-fold decrease in plasma C-peptide and a 2-fold decrease in plasma insulin and glucagon concentrations, but did not change RMR significantly. When glucagon (0.2 μg/kg·h), was infused with SRIH (500 μg/h for 210 min), the decreases in plasma C-peptide and insulin were similar to that during the infusion of SRIH alone, but plasma glucagon increased from 160 ± 24 (±SEM) to 560 ± 80 pg/mL (P < 0.001). There was a significant increase in RMR during the entire period (210 min) of glucagon infusion (P < 0.01). During the last hour of the glucagon plus SRIH infusion, the RMR was 1.38 ± 0.10 Cal/min, which was 15% higher than the preinfusion RMR (1.19 ± 0.10 Cal/min; P < 0.01) and 14% higher than the RMR during the same period when SRIH alone was infused (1.21 ± 0.11 Cal/min; P < 0.01). When SRIH and glucagon were infused, protein oxidation (calculated from urinary nitrogen loss) was 52 ± 5 mg/min; 29% higher than when SRIH alone was infused (40 ± 5 mg/min; P < 0.05). These results indicate that hyperglucagonemia during insulin deficiency results in an increase in energy expenditure, which may contribute to the catabolic state in many conditions.

Original languageEnglish (US)
Pages (from-to)896-901
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume64
Issue number5
StatePublished - 1987
Externally publishedYes

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Basal Metabolism
Glucagon
Insulin
Plasmas
C-Peptide
Somatostatin
Energy Metabolism
Nitrogen
Oxidation
Scanning electron microscopy
Proteins

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Hyperglucagonemia increases resting metabolic rate in man during insulin deficiency",
abstract = "The physiological significance of the hyperglucagonemia that occurs in patients with many catabolic conditions is unclear. The effect of hyperglucagonemia on resting metabolic rate (RMR) was studied in six normal subjects. Infusion of somatostatin (SRIH; 500 μg/h for 210 min) resulted in a 5-fold decrease in plasma C-peptide and a 2-fold decrease in plasma insulin and glucagon concentrations, but did not change RMR significantly. When glucagon (0.2 μg/kg·h), was infused with SRIH (500 μg/h for 210 min), the decreases in plasma C-peptide and insulin were similar to that during the infusion of SRIH alone, but plasma glucagon increased from 160 ± 24 (±SEM) to 560 ± 80 pg/mL (P < 0.001). There was a significant increase in RMR during the entire period (210 min) of glucagon infusion (P < 0.01). During the last hour of the glucagon plus SRIH infusion, the RMR was 1.38 ± 0.10 Cal/min, which was 15{\%} higher than the preinfusion RMR (1.19 ± 0.10 Cal/min; P < 0.01) and 14{\%} higher than the RMR during the same period when SRIH alone was infused (1.21 ± 0.11 Cal/min; P < 0.01). When SRIH and glucagon were infused, protein oxidation (calculated from urinary nitrogen loss) was 52 ± 5 mg/min; 29{\%} higher than when SRIH alone was infused (40 ± 5 mg/min; P < 0.05). These results indicate that hyperglucagonemia during insulin deficiency results in an increase in energy expenditure, which may contribute to the catabolic state in many conditions.",
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T1 - Hyperglucagonemia increases resting metabolic rate in man during insulin deficiency

AU - Nair, K Sreekumaran

PY - 1987

Y1 - 1987

N2 - The physiological significance of the hyperglucagonemia that occurs in patients with many catabolic conditions is unclear. The effect of hyperglucagonemia on resting metabolic rate (RMR) was studied in six normal subjects. Infusion of somatostatin (SRIH; 500 μg/h for 210 min) resulted in a 5-fold decrease in plasma C-peptide and a 2-fold decrease in plasma insulin and glucagon concentrations, but did not change RMR significantly. When glucagon (0.2 μg/kg·h), was infused with SRIH (500 μg/h for 210 min), the decreases in plasma C-peptide and insulin were similar to that during the infusion of SRIH alone, but plasma glucagon increased from 160 ± 24 (±SEM) to 560 ± 80 pg/mL (P < 0.001). There was a significant increase in RMR during the entire period (210 min) of glucagon infusion (P < 0.01). During the last hour of the glucagon plus SRIH infusion, the RMR was 1.38 ± 0.10 Cal/min, which was 15% higher than the preinfusion RMR (1.19 ± 0.10 Cal/min; P < 0.01) and 14% higher than the RMR during the same period when SRIH alone was infused (1.21 ± 0.11 Cal/min; P < 0.01). When SRIH and glucagon were infused, protein oxidation (calculated from urinary nitrogen loss) was 52 ± 5 mg/min; 29% higher than when SRIH alone was infused (40 ± 5 mg/min; P < 0.05). These results indicate that hyperglucagonemia during insulin deficiency results in an increase in energy expenditure, which may contribute to the catabolic state in many conditions.

AB - The physiological significance of the hyperglucagonemia that occurs in patients with many catabolic conditions is unclear. The effect of hyperglucagonemia on resting metabolic rate (RMR) was studied in six normal subjects. Infusion of somatostatin (SRIH; 500 μg/h for 210 min) resulted in a 5-fold decrease in plasma C-peptide and a 2-fold decrease in plasma insulin and glucagon concentrations, but did not change RMR significantly. When glucagon (0.2 μg/kg·h), was infused with SRIH (500 μg/h for 210 min), the decreases in plasma C-peptide and insulin were similar to that during the infusion of SRIH alone, but plasma glucagon increased from 160 ± 24 (±SEM) to 560 ± 80 pg/mL (P < 0.001). There was a significant increase in RMR during the entire period (210 min) of glucagon infusion (P < 0.01). During the last hour of the glucagon plus SRIH infusion, the RMR was 1.38 ± 0.10 Cal/min, which was 15% higher than the preinfusion RMR (1.19 ± 0.10 Cal/min; P < 0.01) and 14% higher than the RMR during the same period when SRIH alone was infused (1.21 ± 0.11 Cal/min; P < 0.01). When SRIH and glucagon were infused, protein oxidation (calculated from urinary nitrogen loss) was 52 ± 5 mg/min; 29% higher than when SRIH alone was infused (40 ± 5 mg/min; P < 0.05). These results indicate that hyperglucagonemia during insulin deficiency results in an increase in energy expenditure, which may contribute to the catabolic state in many conditions.

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