• Clinical endocrinology · May 1994

    Comparative Study

    The effect of pharmacological dosages of glucocorticoids on free living total energy expenditure in man.

    • P K Chong, R T Jung, C M Scrimgeour, and M J Rennie.
    • Department of Medicine, Ninewells Hospital and Medical School, Dundee, Scotland.
    • Clin. Endocrinol. (Oxf). 1994 May 1; 40 (5): 577-81.

    ObjectivesWeight gain had previously been thought to be due to increased calorie intake alone though no information on its effect on total energy expenditure is available in humans. We therefore assessed whether weight gain associated with glucocorticoids is due to a reduction in energy expenditure.DesignWe performed an open study with 1 mg of betamethasone given orally twice a day for 21 days.SubjectsSeven healthy female volunteers, age range 26-55 years, body mass index 19 to 40, mean 27 kg/m2.MeasurementsTotal free living energy expenditure was measured by the doubly labelled water method (D2 18O), resting metabolic rate by ventilated hood indirect calorimetry and fat free mass from the dilution volume of oxygen-18 labelled water. Body composition and components of energy expenditure were assessed before and during the final 14 days of betamethasone administration.ResultsWeight increased by a mean of 1.2 kg (P < 0.05) because of a significant rise in fat mass (1.5 kg) with no change in fat free mass. Resting metabolic rate remained unaltered on betamethasone but total energy expenditure increased in all subjects with a significant mean rise of 26% from 11.7 to 14.7 MJ/24 h (P < 0.05). The energy component of physical activity with thermogenesis increased on average 52% (from 5.8 to 8.9 MJ/24 h; P < 0.05). The rise in energy expenditure was still apparent after correction for the increase in body weight. Fasting respiratory quotient (RQ) increased from 0.81 to 0.86 with no change in fasting blood glucose. Betamethasone did not result in an energy sparing effect on the two components of energy expenditure studied.ConclusionsBody weight increased on betamethasone entirely due to an increase in fat mass. This occurred despite a rise in total energy expenditure which involved specifically that component accounted for by physical activity plus thermogenesis. The most likely explanation is that betamethasone increased dietary energy intake significantly in excess of expenditure. We estimate that an average extra energy intake of 2.8 MJ/day would have had to be consumed for this rise in fat mass to occur even before taking into account the energy intake cost of the rise in expenditure.

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