Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, Louisiana 70808, USA.
J Clin Endocrinol Metab. 2010 Feb;95(2):851-5. doi: 10.1210/jc.2009-1739. Epub 2010 Jan 8.
Leptin regulates energy homeostasis by suppressing food intake; however, its role in energy expenditure and fat oxidation remains uncertain in humans.
The aim of the study was to assess 24-h energy metabolism before and after weight loss induced by leptin treatment in congenital leptin-deficient subjects or low-calorie diet in controls.
We measured 24-h energy expenditure, 24-h fat oxidation, and body fat in three null homozygous leptin-deficient obese adults before and after weight loss induced by a 19-wk leptin replacement period (0.02-0.04 mg/kg/d). The same measures were performed in three obese controls pair-matched for sex, age, and weight loss induced by a 10- to 21-wk low-calorie diet. Measurements were preceded for 1 wk of weight stabilization. Energy expenditure was adjusted for fat-free mass, fat mass, sex, and age based on a reference population (n = 842; R(2) = 0.85; P < 0.0001). Similarly, fat oxidation was adjusted for fat-free mass, percentage body fat, energy balance, and diet composition during the 24-h respiratory chamber stay (R(2) = 0.38; P < 0.0001).
Before weight loss, congenital leptin-deficient and control subjects had similar energy expenditure. However, after weight loss ( approximately 15 kg), controls had energy expenditures lower than expected for their new weight and body composition (-265 +/- 76 kcal/d; P = 0.04), whereas leptin-treated subjects had values not different from the reference population (-128 +/- 119 kcal/d; P = 0.67). Before weight loss, fat oxidation was similar between groups. However, after weight loss, leptin-treated subjects had higher fat oxidation than controls (P = 0.005) and higher than the reference population (P = 0.0001).
In congenital leptin-deficient subjects, leptin replacement prevented the decrease in energy expenditure and fat oxidation often observed after weight loss.
瘦素通过抑制食物摄入来调节能量平衡；然而，其在人类能量消耗和脂肪氧化中的作用仍不确定。
本研究旨在评估先天性瘦素缺乏症患者接受瘦素治疗或对照组接受低热量饮食导致体重减轻前后 24 小时的能量代谢。
我们测量了 3 名纯合子先天性瘦素缺乏症肥胖成年人在接受 19 周瘦素替代治疗（0.02-0.04mg/kg/d）导致体重减轻前后的 24 小时能量消耗、24 小时脂肪氧化和体脂肪。在接受 10-21 周低热量饮食导致体重减轻的情况下，对 3 名肥胖对照组进行了相同的测量，这些对照组在性别、年龄和体重减轻方面与患者相匹配。测量前进行了 1 周的体重稳定期。根据参考人群（n=842；R²=0.85；P<0.0001），基于脂肪量、脂肪量、性别和年龄对能量消耗进行了调整。同样，根据 24 小时呼吸室停留期间的无脂肪量、体脂百分比、能量平衡和饮食组成，对脂肪氧化进行了调整（R²=0.38；P<0.0001）。
在体重减轻之前，先天性瘦素缺乏症患者和对照组的能量消耗相似。然而，在体重减轻（约 15 公斤）后，对照组的能量消耗低于其新体重和身体成分的预期值（-265±76kcal/d；P=0.04），而接受瘦素治疗的患者的能量消耗与参考人群无差异（-128±119kcal/d；P=0.67）。在体重减轻之前，两组之间的脂肪氧化相似。然而，在体重减轻后，接受瘦素治疗的患者的脂肪氧化高于对照组（P=0.005），也高于参考人群（P=0.0001）。
在先天性瘦素缺乏症患者中，瘦素替代治疗可预防体重减轻后经常观察到的能量消耗和脂肪氧化的下降。
