Meal‐induced thermogenesis in obese patients before and after weight reduction
- 1 October 1989
- journal article
- research article
- Published by Wiley in Clinical Physiology and Functional Imaging
- Vol. 9 (5) , 481-498
- https://doi.org/10.1111/j.1475-097x.1989.tb01002.x
Abstract
The purpose of this study was to find out whether human obesity is associated with a diminished meal-induced thermogenesis and, if so, to what extent this response is influenced by weight reduction. Ten obese subjects (body mass index 42 .+-. 2) and 10 age- and sex-matched non-obese volunteers were studied with continuous indirect calorimetry in the basal stage and after the ingestion of a standardized test meal. Six obese subjects (body mass index 44 .+-. 2) were examined on two occasions, once before and once after gastric banding and an average weight reduction of 18 .+-. 3 kg. Basal oxygen uptake and energy expenditure were 30% (P < 0.001) greater in the obese subjects compared to non-obese controls. After the meal, pulmonary oxygen uptake and energy expenditure increase rapidly and reached a relatively constant level after 60 min; for pulmonary oxygen uptake the average rise above basal was less in the obese (17.7 .+-. 1.6%) than the non-obese (27.8 .+-. 1.9%, P < 0.001); the increase in energy expenditure was 18.5 .+-. 1.7% in obese and 30.8 .+-. 2.1% in non-obese subjects (P < 0.001). After weight reduction, oxygen uptake and energy expenditure in the basal state were 20% lower (P < 0.05) than before weight reduction. The average postprandial increase in oxygen uptake was greater after weight reduction (24.8 .+-. 2.0%) than before (16.7 .+-. 1.6%, P < 0.001). Corresponding values for energy expenditure were 27.2 .+-. 2.2 and 18.2 .+-. 2.2% (P < 0.001). It is concluded that: (1) the thermogenic response to a mixed meal is lower in obese compared to non-obese individuals; and, (2) this impaired response is partly normalized after weight reduction. These findings suggest that a diminished meal-induced thermogenesis is a secondary phenomenon rather than a primary pathogenic factor in human obesity.Keywords
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