Effects of exogenous leptin on satiety and satiation in patients with lipodystrophy and leptin insufficiency - PubMed (original) (raw)
Effects of exogenous leptin on satiety and satiation in patients with lipodystrophy and leptin insufficiency
Jennifer R McDuffie et al. J Clin Endocrinol Metab. 2004 Sep.
Abstract
To examine leptin's role in human appetite regulation, we studied recombinant methionyl human leptin's effects on satiation and satiety in a model of leptin insufficiency, lipodystrophy. Eight females with hypoleptinemia and lipodystrophy were given sc injections of A-100 (maximal dose, 200% of that predicted to normalize serum leptin) for 4 months. Satiation and satiety were determined before and again during leptin treatment. Satiation was measured as the time to voluntary cessation of eating from a standardized food array after a 12-h fast. Satiety was determined as the time to hunger sufficient to consume a full meal after consumption of a standardized preload. During leptin treatment, satiation time decreased (41.2 +/- 18.2 to 19.5 +/- 10.6 min; P = 0.01), satiety time increased (62.9 +/- 64.8 to 137.8 +/- 91.6 min; P = 0.04), energy consumed to produce satiation decreased (2034 +/- 405 to 1135 +/- 432 kcal or 8.5 +/- 1.7 to 4.7 +/- 1.8 MJ; P < 0.01), and the amount of food desired in the postabsorptive state decreased (P < 0.02). Ghrelin concentrations also decreased during leptin administration (284.3 +/- 127.9 to 140.6 +/- 104.5 pmol/liter; P < 0.002). We conclude that increased leptin in patients with lipodystrophy results in less caloric, shorter, more satiating meals and longer-lived satiety. These data support the hypothesis that leptin plays an important, permissive role in human appetite regulation.
Figures
FIG. 1
Changes in indicators of appetite before and after leptin therapy. A, Satiation time; B, intake; C, satiety. *, P ≤ 0.05; **, P ≤ 0.01.
Comment in
- Leptin and appetite control in lipodystrophy.
Ahima R, Osei SY. Ahima R, et al. J Clin Endocrinol Metab. 2004 Sep;89(9):4254-7. doi: 10.1210/jc.2004-1232. J Clin Endocrinol Metab. 2004. PMID: 15356017 No abstract available.
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