The α2-adrenergic system is involved in the regulation of food intake in animals but its effects on feeding in humans are unknown. We hypothesized that clonidine administration would stimulate food intake in healthy human subjects. Ten men and 4 women, all physically and psychiatrically healthy, received clonidine 3 μg/kg or placebo, orally, in blinded, balanced, randomized order. Consumption of a liquid test meal was measured; also, serum growth hormone levels were used as a secondary measure of clonidine effects. Visual analog scale ratings of hunger, satiety, and sedation were obtained before, during, and after the test meal. A subset of five subjects also received 1.5 μg/kg clonidine, in addition to the two trials described above. Test meal consumption was greater following placebo than following clonidine. Sedation ratings were substantially higher at all time points after clonidine and correlated with meal consumption (correlation coefficient r = -0.584; p = 0.028). Hunger and satiety ratings did not differ. The 1.5 μg/kg dose did not provide different effects on feeding from that seen with placebo. Contrary to our hypothesis, clonidine did not stimulate food intake in humans. Sedation associated with clonidine administration may have suppressed any effects on feeding. Copyright (C) 1998 Elsevier Science Inc.
Bibliographical noteFunding Information:
This study was supported in part by grants from the University of Minnesota Graduate School, the General Clinical Research Center Grant MO1RR00400 from National Center for Research Resources, and Minnesota Obesity Center Grant #P30 DK50456 from the National Institute of Health, Rockville, MD. The authors wish to thank Janet Holland for her expert assistance in the preparation of this manuscript, and Paul Thuras, Ph.D., for assistance with statistical analyses.
- Feeding behavior
- α-Adrenergic system