Giacco R, Clemente G, Busiello L, Lasorella G, Rivieccio A M, Rivellese A A, Riccardi G
Institute of Food Science and Technology of National Research Council, Avellino, Italy.
Int J Obes Relat Metab Disord. 2004 Feb;28(2):342-8. doi: 10.1038/sj.ijo.0802589.
To evaluate whether postprandial abnormalities of energy expenditure and/or lipid oxidation are present in healthy, normal-weight subjects with a strong family history of obesity and thus at high risk to become obese.
Case-control study.
A total of 16 young healthy men participated in the study. Eight subjects had both parents overweight (father's and mother's body mass index (BMI) >25 kg/m(2)) and eight had both parents with normal body weight (father's and mother's BMI<25 kg/m(2), respectively). The group of subjects with overweight parents was similar to that with normal-weight parents (control group) in terms of BMI (23.7+/-1.7 vs 22.7+/-1.1 kg/m(2)) (M+/-s.d.) and fat-free body mass (FFM) (60.5+/-4.9 vs 58.4+/-2.0 kg), but was slightly older than the control group (25.4+/-3.3 vs 22.7+/-2.4 y; P<0.05).
Energy expenditure (EE) was measured by indirect calorimetry, and blood samples were taken for the evaluation of metabolic variables in the fasting state and every hour for 8 h after a standard fat-rich meal (protein 15%, carbohydrate 34%, fat 51%, 4090 kJ).
: Fasting plasma glucose, cholesterol, HDL-cholesterol, triglyceride, free fatty acid (FFA) and leptin concentrations were similar in both groups of participants, but subjects with overweight parents has significantly lower plasma insulin concentrations (5.11+/-0.51 vs 7.07+/-1.56 microU/ml; P<0.007) and HOMA index of insulin resistance (1.1+/-0.1 vs 1.6+/-0.4; P<0.01). Postprandial plasma glucose, triglyceride, FFA and leptin concentrations were similar in the two groups, whereas insulin levels were significantly lower in the group with both parents overweight at 3, 5, 6, 7 and 8 h. Fasting and postprandial EE, and fasting lipid and carbohydrate oxidation were similar in both groups. On the contrary, postprandial carbohydrate oxidation (incremental area under curve) was significantly higher (196.25+/-94.75 vs 75.88+/-74.72 mg/kg FFM x 8 h; P<0.007) and that of lipid oxidation lower (90.93+/-80.32 vs 163.68+/-108.22 mg/kg FFM x 8 h; P<0.05) in the group of subjects with overweight parents.
Normal-weight subjects with a strong family history of obesity present a reduced lipid oxidation in the postprandial period and a metabolic profile characterized by low plasma insulin levels and the HOMA index, which is compatible with increased insulin sensitivity. These metabolic characteristics may be considered as early predictors of weight gain and are probably genetically determined.
评估有肥胖家族史的健康、体重正常的受试者是否存在餐后能量消耗和/或脂质氧化异常，这些受试者因而有很高的肥胖风险。
病例对照研究。
共有16名年轻健康男性参与该研究。8名受试者的父母均超重（父亲和母亲的体重指数（BMI）>25 kg/m²），8名受试者的父母体重均正常（父亲和母亲的BMI分别<25 kg/m²）。父母超重的受试者组与体重正常父母的受试者组（对照组）在BMI（23.7±1.7 vs 22.7±1.1 kg/m²）（均值±标准差）和去脂体重（FFM）（60.5±4.9 vs 58.4±2.0 kg）方面相似，但年龄略大于对照组（25.4±3.3 vs 22.7±2.4岁；P<0.05）。
通过间接测热法测量能量消耗（EE），并采集血样以评估空腹状态下的代谢变量，以及在标准高脂餐（蛋白质15%，碳水化合物34%，脂肪51%，4090 kJ）后8小时内每小时的代谢变量。
两组参与者的空腹血糖、胆固醇、高密度脂蛋白胆固醇、甘油三酯、游离脂肪酸（FFA）和瘦素浓度相似，但父母超重的受试者血浆胰岛素浓度显著较低（5.11±0.51 vs 7.07±1.56 μU/ml；P<0.007），胰岛素抵抗的HOMA指数也较低（1.1±0.1 vs 1.6±0.4；P<0.01）。两组餐后血浆葡萄糖、甘油三酯、FFA和瘦素浓度相似，而在3、5、6、7和8小时时，父母均超重的组胰岛素水平显著较低。两组的空腹和餐后EE，以及空腹脂质和碳水化合物氧化相似。相反，父母超重的受试者组餐后碳水化合物氧化（曲线下增量面积）显著更高（196.25±94.75 vs 75.88±74.72 mg/kg FFM×8小时；P<0.007），脂质氧化则较低（90.93±80.32 vs 163.68±108.22 mg/kg FFM×8小时；P<0.05）。
有肥胖家族史的体重正常受试者在餐后脂质氧化减少，代谢特征为血浆胰岛素水平低和HOMA指数低，这与胰岛素敏感性增加相符。这些代谢特征可能被视为体重增加的早期预测指标，且可能由基因决定。
