Affiliation:
1. Department of Anatomy and Physiology, The University, Dundee, Scotland, U.K.
2. Department of Medicine, Ninewells Hospital and Medical School, Dundee, Scotland, U.K.
3. Metabolism Division, Washington University School of Medicine, St Louis, Missouri, U.S.A.
4. Department of Medicine, University College and Middlesex Medical School, London
Abstract
1. Energy expenditure, plasma glucose and palmitate kinetics and leg glycerol release were determined simultaneously both before and during adrenaline infusion in lean and obese human subjects. Seven lean subjects (mean 96.5% of ideal body weight) were studied in the post-absorptive state and also during mixed nutrient liquid feeding, eight obese subjects (mean 165% of ideal body weight) were studied in the post-absorptive state and six obese subjects (mean 174% of ideal body weight) were studied during feeding.
2. Resting energy expenditure was higher in the obese subjects, but the thermic response to adrenaline, both in absolute and percentage terms, was similar in lean and obese subjects. Plasma adrenaline concentrations attained (3 nmol/l) were comparable in all groups and the infusion had no differential effects on the plasma insulin concentration. Before adrenaline infusion the plasma glucose flux was higher in the obese than in the lean subjects in the fed state only (45.8 ± 3.8 versus 36.6 ± 1.0 mmol/h, P <0.05); it increased to the same extent in both groups with the adrenaline infusion.
3. Before the adrenaline infusion plasma palmitate flux was higher in the obese than in the lean subjects (by 51%, P <0.01, in the post-absorptive state and by 78%, P <0.05, in the fed state). However, there was no significant change during adrenaline infusion in the obese subjects (from 13.5 ± 1.00 to 15.0 ± 1.84 mmol/h, not significant, in the post-absorptive state and from 14.4 ± 2.13 to 15.7 ± 1.74 mmol/h, not significant, in the fed state), whereas there were increases in the lean subjects (from 8.93 ± 1.10 to 11.2 ± 1.19 mmol/h, P <0.05, in the post-absorptive state, and from 8.06 ± 1.19 to 9.86 ± 0.93 mmol/h, P <0.05, in the fed state).
4. Before adrenaline infusion the palmitate oxidation rate was also higher in the obese than in the lean subjects (1.86 ± 0.14 versus 1.22 ± .09 mmol/h, P <0.01, in the post-absorptive state and 1,73 ± 0.25 versus 1.12 ± 0.12 mmol/h, P <0.05, in the fed state). However, in response to adrenaline the fractional oxidation rate (% of flux) increased less in the obese than in the lean subjects, especially in the post-absorptive state (from 13.8 ± 1.02 to 14.9 ± 1.39%, not significant, versus from 13.7 ± 0.98 to 19.3 ± 1.92%, P <0.05). These effects were independent of feeding. Leg glycerol release increased more in the lean subjects with adrenaline infusion, although increases in the plasma glycerol concentration did not differ between the groups.
5. These results suggest that in obese subjects plasma inter-organ transport of fatty acids and the subsequent fractional oxidation responses favour storage of triacylglycerol. These factors may be important determinants for the development and maintenance of the obese state.
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