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餐后脂联素水平不太可能导致普拉德-威利综合征的肥胖发病机制。

Postprandial adiponectin levels are unlikely to contribute to the pathogenesis of obesity in Prader-Willi syndrome.

作者信息

Caixàs Assumpta, Giménez-Palop Olga, Giménez-Pérez Gabriel, Potau Neus, Berlanga Eugenio, González-Glemente José-Miguel, Arroyo Jaume, Laferrère Blandine, Mauricio Dídac

机构信息

Diabetes Endocrinology and Nutrition Unit, Hospital de Sabadell, and UDIAT, Institut Universitari Parc Taulí, Sabadell, Spain.

出版信息

Horm Res. 2006;65(1):39-45. doi: 10.1159/000090513. Epub 2005 Dec 22.

DOI:10.1159/000090513
PMID:16374018
Abstract

AIM

To investigate fasting and postprandial adiponectin levels in PWS patients as compared to obese and lean subjects and whether they could contribute to the pathogenesis of obesity in this syndrome.

METHODS

We studied 7 patients with PWS, 16 obese patients and 42 lean subjects for the fasting study. From this group, we evaluated 7 patients with PWS, 7 age-sex-BMI-matched obese non-PWS patients and 7 age-sex-matched lean subjects before and after the administration of 3,139.5 kJ (750 kcal) of a standard liquid meal (53.2% carbohydrate, 30% fat, 16.7% protein) after an overnight fast. Blood samples were obtained every 15 min for the first hour and every 30 min thereafter until 6 h. Adiponectin, IGF-I, glucose, triglycerides, cholesterol, and insulin were measured.

RESULTS

Fasting plasma adiponectin levels were lower in PWS than in lean subjects (5.24+/-2.56 vs. 8.28+/-4.63 microg/ml, p=0.041) but higher than in obese patients (4.01+/-1.27 microg/ml, p=0.047). After the meal, adiponectin concentrations mildly decreased in PWS at time point 240 min, while in obese and lean subjects no changes were observed. However, 6-hour postprandial AUC for adiponectin was similar in all three groups.

CONCLUSION

Fasting adiponectin levels are low in PWS, but they are so mildly modulated postprandially that these changes do not seem significant for the pathogenesis of obesity in this syndrome.

摘要

目的

研究普拉德-威利综合征(PWS)患者空腹及餐后脂联素水平,并与肥胖和消瘦受试者进行比较,探讨其是否与该综合征肥胖的发病机制有关。

方法

我们对7例PWS患者、16例肥胖患者和42例消瘦受试者进行空腹研究。在这组患者中,我们评估了7例PWS患者、7例年龄、性别、体重指数匹配的非PWS肥胖患者和7例年龄、性别匹配的消瘦受试者,在禁食过夜后给予3139.5千焦(750千卡)标准流食(碳水化合物53.2%、脂肪30%、蛋白质16.7%)前后的情况。在进食后的第一小时内每15分钟采集一次血样,之后每30分钟采集一次,直至6小时。检测脂联素、胰岛素样生长因子-I、葡萄糖、甘油三酯、胆固醇和胰岛素水平。

结果

PWS患者空腹血浆脂联素水平低于消瘦受试者(5.24±2.56对8.28±4.63微克/毫升,p=0.041),但高于肥胖患者(4.01±1.27微克/毫升,p=0.047)。进食后,PWS患者在240分钟时间点脂联素浓度轻度下降,而肥胖和消瘦受试者未观察到变化。然而,三组餐后6小时脂联素的曲线下面积相似。

结论

PWS患者空腹脂联素水平较低,但餐后变化轻微,这些变化对该综合征肥胖的发病机制似乎无显著意义。

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