Segal K R, Albu J, Chun A, Edano A, Legaspi B, Pi-Sunyer F X
Department of Pediatrics, Mount Sinai School of Medicine, New York 10029.
J Clin Invest. 1992 Mar;89(3):824-33. doi: 10.1172/JCI115661.
The putative blunted thermogenesis in obesity may be related to insulin resistance, but insulin sensitivity and obesity are potentially confounding factors. To determine the independent effects of obesity and insulin resistance on the thermic effect of food, at rest and after exercise, lean and obese men were matched at two levels of insulin sensitivity determined by insulin-stimulated glucose disposal (milligrams per kilogram fat-free mass [FFM] per minute) during the euglycemic, hyperinsulinemic (40 mU/m2.min) clamp: 5.4 mg/kg FFM for the lean and obese groups with low insulin sensitivity, and 8.1 mg/kg FFM for the groups with high insulin sensitivity. The two lean groups were matched for percent fat (approximately 15 +/- 1% fat), as were the two obese groups (approximately 33 +/- 2% fat). Energy expenditure was measured for 3 h in the fasting state and for 3 h after a 720-kcal mixed meal, each at rest and immediately after 1 h of cycling at 100 W. The thermic effect of food (TEF) was calculated as the postprandial minus fasting energy expenditure (kcal/3 h) during rest and after exercise. During rest, TEF was blunted by both obesity (24 +/- 5 and 34 +/- 6 kcal/3 h for obese groups with low and high insulin sensitivity vs. 56 +/- 6 and 74 +/- 6 kcal/3 h for the lean groups with low and high insulin sensitivity; P less than 0.01 lean vs. obese) and insulin resistance (insulin-resistant less than insulin-sensitive, at both levels of obesity; P less than 0.01). After exercise, TEF was also impaired in the obese (47 +/- 6 and 44 +/- 5 kcal/3 h for the insulin-resistant and -sensitive groups) and in the lean insulin-resistant (55 +/- 5 kcal/3 h), compared with the lean insulin-sensitive men (71 +/- 3 kcal/3 h), P less than 0.01. Compared with rest, TEF after exercise was improved, but not normalized, in both obese groups (P less than 0.05), but unchanged in the lean groups. These results suggest that both insulin resistance and obesity are independently associated with impaired TEF at rest, but the responsiveness of thermogenesis to exercise before a meal is related to the obese state and not independently to insulin resistance per se.
肥胖中假定的产热减弱可能与胰岛素抵抗有关，但胰岛素敏感性和肥胖是潜在的混杂因素。为了确定肥胖和胰岛素抵抗对食物热效应在静息和运动后的独立影响，将瘦人和肥胖男性按照胰岛素刺激的葡萄糖处置（每千克去脂体重每分钟毫克数）所确定的两种胰岛素敏感性水平进行匹配，在正常血糖、高胰岛素血症（40 mU/m²·min）钳夹试验中：低胰岛素敏感性的瘦人和肥胖组为5.4 mg/kg去脂体重，高胰岛素敏感性的组为8.1 mg/kg去脂体重。两个瘦人组的体脂百分比相匹配（约15±1%脂肪），两个肥胖组也是如此（约33±2%脂肪）。在空腹状态下测量3小时的能量消耗，并在摄入720千卡混合餐后测量3小时的能量消耗，均在静息时以及以100瓦功率骑行1小时后立即测量。食物热效应（TEF）计算为静息和运动后餐后减去空腹的能量消耗（千卡/3小时）。在静息时，肥胖（低和高胰岛素敏感性肥胖组分别为24±5和34±6千卡/3小时，而低和高胰岛素敏感性瘦人组分别为56±6和74±6千卡/3小时；瘦人与肥胖相比P<0.01）和胰岛素抵抗（在两种肥胖水平下，胰岛素抵抗组均低于胰岛素敏感组；P<0.01）都会使TEF减弱。运动后，与胰岛素敏感的瘦人男性（71±3千卡/3小时）相比，肥胖者（胰岛素抵抗和敏感组分别为47±6和44±5千卡/3小时）以及胰岛素抵抗的瘦人（55±5千卡/3小时）的TEF也受损，P<0.01。与静息相比，运动后两个肥胖组的TEF均有所改善，但未恢复正常（P<0.05），而瘦人组则无变化。这些结果表明，胰岛素抵抗和肥胖均独立地与静息时受损的TEF相关，但餐前运动时产热的反应性与肥胖状态有关，而非独立于胰岛素抵抗本身。
