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JCI:不是每个胖子都会患机体过重相关的代谢综合征

来源:生物谷 2015-01-05 10:16

2015年1月5日 讯 /生物谷BIOON/ --近日,一项发表于国际杂志The Journal of Clinical Investigation上的研究论文中,来自华盛顿医科大学的研究人员通过研究表示,肥胖并不总是同机体的代谢改变直接相关,而机体的代谢改变常常会引发糖尿病、心脏病及中风,文章中,研究人员发现,一系列的肥胖个体并不会患常见代谢异常相关的肥胖,比如胰岛素耐受、脂质异常、高血压和肝脏脂肪过多。

这项研究中,研究人员对20个肥胖个体进行研究,让这些个体在过去一些月里增重15磅从而来研究体重的额外增加是否会影响个体机体的代谢功能;研究者Elisa Fabbrini说道,我们的目的是让参与者每日消耗额外1000卡路里直至其体重增加6%,但这并不容易,随后研究人员在个体体重增加前后对参与者机体的组成、胰岛素敏感性、血糖调节能力、肝脏脂肪以及其它代谢健康指标进行测定。

结果显示,在个体体重增加后如果个体的体重仍处于正常范围内,那么肥胖个体的代谢特性就会保持正常,但是当个体体重增加到异常状态下后机体的代谢特性就会明显恶化。研究者指出,一些肥胖个体会受到适度增加的脂肪的负面代谢效应的保护,而其它个体则更易于引发机体疾病,该项研究对于临床非常重要,因为大约25%的肥胖个体并不会患代谢综合征,而研究数据显示这些个体甚至是在获得额外体重的情况下也会保持代谢正常。

最后Klein说道,我们还需要更多的研究来理解为何肥胖会引发某些个体发病,这到底是取决于遗传?还是特殊的饮食摄入?抑或着是生活方式、肠道微生物群等,还有待于进一步去探索。(生物谷Bioon.com)

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Metabolically normal obese people are protected from adverse effects following weight gain

Elisa Fabbrini, Jun Yoshino, Mihoko Yoshino, Faidon Magkos, Courtney Tiemann Luecking, Dmitri Samovski, Gemma Fraterrigo, Adewole L. Okunade, Bruce W. Patterson and Samuel Klein

BACKGROUND. Obesity is associated with insulin resistance and increased intrahepatic triglyceride (IHTG) content, both of which are key risk factors for diabetes and cardiovascular disease. However, a subset of obese people does not develop these metabolic complications. Here, we tested the hypothesis that people defined by IHTG content and insulin sensitivity as “metabolically normal obese” (MNO), but not those defined as “metabolically abnormal obese” (MAO), are protected from the adverse metabolic effects of weight gain. METHODS. Body composition, multiorgan insulin sensitivity, VLDL apolipoprotein B100 (apoB100) kinetics, and global transcriptional profile in adipose tissue were evaluated before and after moderate (~6%) weight gain in MNO (n = 12) and MAO (n = 8) subjects with a mean BMI of 36 ± 4 kg/m2 who were matched for BMI and fat mass. RESULTS. Although the increase in body weight and fat mass was the same in both groups, hepatic, skeletal muscle, and adipose tissue insulin sensitivity deteriorated, and VLDL apoB100 concentrations and secretion rates increased in MAO, but not MNO, subjects. Moreover, biological pathways and genes associated with adipose tissue lipogenesis increased in MNO, but not MAO, subjects. CONCLUSIONS. These data demonstrate that MNO people are resistant, whereas MAO people are predisposed, to the adverse metabolic effects of moderate weight gain and that increased adipose tissue capacity for lipogenesis might help protect MNO people from weight gain–induced metabolic dysfunction. TRIAL REGISTRATION. ClinicalTrials.gov NCT01184170. FUNDING. This work was supported by NIH grants UL1 RR024992 (Clinical Translational Science Award), DK 56341 (Nutrition and Obesity Research Center), DK 37948 and DK 20579 (Diabetes Center Grant), and UL1 TR000450 (KL2 Award); a Central Society for Clinical and Translational Research Early Career Development Award; and by grants from the Longer Life Foundation and the Kilo Foundation.

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