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Cited by 151Diabetes, Cardiovascular Risks, and LipoproteinsAdipose Tissue and MetabolismDiet, Metabolism, and Disease

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

Evidence that insulin resistance is responsible for the decreased thermic effect of glucose in human obesity

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Ravussin, E, Acheson, K J, Vernet, O, Danforth, E, Jéquier, E·1985·Journal of Clinical Investigation
DOI 10.1172/jci112083PMC PMC424038
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Abstract

The thermic effect of glucose was investigated in nine obese and six lean subjects in whom the same rate of glucose uptake was imposed. Continuous indirect calorimetry was performed for 240 min on the supine subject. After 45 min, 20% glucose was infused (609 mg/min) for 195 min and normoglycemia was maintained by adjusting the insulin infusion rate. At 2 h, propranolol was infused (bolus 100 micrograms/kg; 1 microgram/kg X min) for the remaining 75 min. To maintain the same glucose uptake (0.624 g/min), it was necessary to infuse insulin at 3.0 +/- 0.6 (leans) and 6.6 +/- 1.2 mU/kg X min (obese) (P less than 0.02). At this time, glucose oxidation was 0.248 +/- 0.019 (leans) and 0.253 +/- 0.022 g/min (obese) (NS), and nonoxidative glucose disposal was 0.375 +/- 0.011 and 0.372 +/- 0.029 g/min, respectively. Resting metabolic rate (RMR) rose significantly by 0.13 +/- 0.02 kcal/min in both groups, resulting in similar thermic effects, i.e., 5.5 +/- 0.7% (leans) 5.4 +/- 0.9% (obese) (NS) and energy costs of glucose storage 0.35 +/- 0.06 and 0.39 +/- 0.09 kcal/g (NS), respectively. With propranolol, glucose uptake and storage remained the same, while RMR fell significantly in both groups, with corresponding decreases (P less than 0.05) in the thermic effects of glucose to 3.7 +/- 0.6% and 2.9 +/- 0.8% (NS) and the energy costs of glucose storage 0.23 +/- 0.04 and 0.17 +/- 0.05 kcal/g (NS) in the lean and obese subjects, respectively. These results suggest that the defect in the thermic effect of glucose observed in obese subjects is due to their insulin resistance, which is responsible for a lower rate of glucose uptake and hence decreased rate of glucose storage, which is an energy-requiring process.

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Metadata

Authors
Ravussin, E., Acheson, K. J., Vernet, O., Danforth, E., & Jéquier, E.
Affiliations
University of Vermont (US)
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1985-09-01
Volume
76
Issue
3
Pages
1268-1273
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci112083
PMC
PMC424038
OpenAlex
W2018043022
Cited by
151
References
32
Citations by year
2025: 1 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 7 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 5 · 2014: 3 · 2013: 5 · 2012: 2
FWCI
5.62
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • IRIS (submittedVersion)
  • SERVAL (Université de Lausanne) (submittedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
insulin resistance, obesity, glucose oxidation, glucose storage, resting metabolic rate, propranolol, glucose uptake, nonoxidative glucose disposal, energy expenditure, beta-adrenergic blockade, insulin infusion, glucose infusion, indirect calorimetry, energy balance, weight loss, weight gain
MeSH terms
Adult, Blood Glucose, Blood Pressure, Body Temperature, Energy Metabolism, Female, Glucose, Heart Rate, Humans, Insulin, Insulin Resistance, Male, Obesity

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