Search

Evidence from rodent studies indicates that the [beta]-cell-derived neurohormone amylin exerts multiple effects on eating behavior, including reductions in meal size, intake of highly palatable foods, and stress-induced sucrose consumption. To assess the effect of amylin agonism on human eating behavior we conducted a randomized, blinded, placebo-controlled, multicenter study investigating the effects of the amylin analog pramlintide on body weight, 24-h caloric intake, portion sizes, 'fast food' intake, and perceived control of eating in 88 obese subjects. After a 2-day placebo lead-in, subjects self-administered pramlintide (180 [micro]g) or placebo by subcutaneous injection 15 rain before meals for 6 wk without concomitant lifestyle modifications. Compared with placebo, pramlintide treatment elicited significant mean reductions from baseline in body weight on day 44 (-2.1 [+ or-] 0.3 vs. +0.1 [+ or-] 0.4%, P < 0.001), 24-h caloric intake (-990 [+ or-] 94 vs. -243 [+ or-] 126 kcal on day 3, P < 0.0001; -680 [+ or-] 86 vs. -191 [+ or-] 161 kcal on day 43, P < 0.01), portion sizes, and caloric intake at a 'fast food challenge' (-385 [+ or-] 61 vs. -109 [+ or-] 88 kcal on day 44, P < 0.05). Pramlintide treatment also improved perceived control of eating, as demonstrated by a 45% placebo-corrected reduction in binge eating scores (P < 0.01). The results of this translational research study confirm in humans various preclinical effects of amylin agonism, demonstrating that pramlintide-mediated weight loss in obese subjects is accompanied by sustained reductions in 24-h food intake, portion sizes, fast food intake, and binge eating tendencies. obesity; weight loss; satiety; food intake; neuroendocrine hormones