Stefan Norbert, Vozarova Barbora, Funahashi Tohru, Matsuzawa Yuji, Ravussin Eric, Weyer Christian, Tataranni P Antonio
Clinical Diabetes and Nutrition Section, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85016, USA.
Obes Res. 2002 Oct;10(10):1016-20. doi: 10.1038/oby.2002.138.
To test the hypothesis that low adiponectin is associated with low fat oxidation in humans.
We measured plasma adiponectin concentrations in 75 healthy, nondiabetic Pima Indians (age, 28 +/- 7 years; 55 men and 20 women; body fat, 29.7 +/- 7.5%) and 18 whites [(age, 33 +/- 8 years; 14 men and 4 women; body fat, 28.2 +/- 10.8% (means +/- SD)] whose body composition was measured by DXA and 24-hour energy expenditure (24-hour EE) by a respiratory chamber. Respiratory quotient (an estimate of whole-body carbohydrate/lipid oxidation rate) was calculated over 24 hours (24-hour RQ).
Before correlational analyses, waist-to-thigh ratio (WTR) and percentage of body fat (PFAT) were adjusted for age, sex, and race; 24-hour EE was adjusted for fat mass and fat-free mass, and 24-hour RQ were adjusted for energy balance. Plasma adiponectin concentrations were negatively correlated with WTR (r = -0.42, p < 0.0001) and PFAT (r = -0.46, p < 0.0001). There was no correlation between plasma adiponectin concentrations and 24-hour RQ, (r = 0.09, p = 0.36) before or after adjustment for PFAT (r = 0.001, p = 0.99, respectively, partial correlation), and no correlation was found between plasma adiponectin concentrations and 24-hour EE (r = -0.12, p = 0.27).
Our cross-sectional data do not suggest physiological concentrations of fasting plasma adiponectin play a role in the regulation of whole-body fat oxidation or energy expenditure in resting conditions. Whether administration of adiponectin to individuals with low levels of this hormone will increase their fat oxidation rates/energy expenditure remains to be established.
检验低脂联素与人类低脂氧化相关的假设。
我们测量了75名健康、非糖尿病的皮马印第安人(年龄28±7岁;55名男性和20名女性;体脂29.7±7.5%)和18名白人(年龄33±8岁;14名男性和4名女性;体脂28.2±10.8%(均值±标准差))的血浆脂联素浓度,其身体成分通过双能X线吸收法测量,24小时能量消耗(24小时EE)通过呼吸室测量。计算24小时的呼吸商(全身碳水化合物/脂质氧化率的估计值)(24小时RQ)。
在进行相关性分析之前,腰臀比(WTR)和体脂百分比(PFAT)根据年龄、性别和种族进行了调整;24小时EE根据脂肪量和去脂体重进行了调整,24小时RQ根据能量平衡进行了调整。血浆脂联素浓度与WTR呈负相关(r = -0.42,p < 0.0001)和PFAT呈负相关(r = -0.46,p < 0.0001)。在调整PFAT之前或之后,血浆脂联素浓度与24小时RQ之间均无相关性(r = 0.09,p = 0.36;r = 0.001,p = 0.99,偏相关),血浆脂联素浓度与24小时EE之间也无相关性(r = -0.12,p = 0.27)。
我们的横断面数据并不表明空腹血浆脂联素的生理浓度在静息状态下对全身脂肪氧化或能量消耗的调节中起作用。对于这种激素水平较低的个体,给予脂联素是否会提高其脂肪氧化率/能量消耗仍有待确定。