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为什么肥胖的人节食时大脑不会减重?

Why doesn't the brain lose weight, when obese people diet?

机构信息

Medical Clinic I, University of Lübeck, Lübeck, Germany.

出版信息

Obes Facts. 2011;4(2):151-7. doi: 10.1159/000327676. Epub 2011 Apr 7.

DOI:10.1159/000327676
PMID:21577022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6444703/
Abstract

OBJECTIVE

As has been shown recently, obesity is associated with brain volume deficits. We here used an interventional study design to investigate whether the brain shrinks after caloric restriction in obesity. To elucidate mechanisms of neuroprotection we assessed brain-pull competence, i.e. the brain's ability to properly demand energy from the body.

METHODS

In 52 normal-weight and 42 obese women (before and after ≈10% weight loss) organ masses of brain, liver and kidneys (magnetic resonance imaging), fat (air displacement plethysmography) and muscle mass (dual-energy X-ray absorptiometry) were assessed. Body metabolism was measured by indirect calorimetry. To investigate how energy is allocated between brain and body, we used reference data obtained in the field of comparative biology. We calculated the distance between each woman and a reference mammal of comparable size in a brain-body plot and named the distance 'encephalic measure'. To elucidate how the brain protects its mass, we measured fasting insulin, since 'cerebral insulin suppression' has been shown to function as a brain-pull mechanism.

RESULTS

Brain mass was equal in normal-weight and obese women (1,441.8 ± 14.6 vs. 1,479.2 ± 12.8 g; n.s.) and was unaffected by weight loss (1,483.8 ± 12.7 g; n.s.). In contrast, masses of muscle, fat, liver and kidneys decreased by 3-18% after weight loss (all p < 0.05). The encephalic measure was lower in obese than normal-weight women (5.8 ± 0.1 vs. 7.4 ± 0.1; p < 0.001). Weight loss increased the encephalic measure to 6.3 ± 0.1 (p < 0.001). Insulin concentrations were inversely related to the encephalic measure (r = -0.382; p < 0.001).

CONCLUSION

Brain mass is normal in obese women and is protected during caloric restriction. Our data suggest that neuroprotection during caloric restriction is mediated by a competent brain-pull exerting cerebral insulin suppression.

摘要

目的

最近的研究表明,肥胖与脑容量不足有关。我们采用干预性研究设计,来研究肥胖患者在热量限制后大脑是否会缩小。为了阐明神经保护的机制,我们评估了大脑吸引力,即大脑从身体获取能量的能力。

方法

对 52 名正常体重女性和 42 名肥胖女性(减肥前后)的脑、肝、肾器官质量(磁共振成像)、脂肪(空气置换体描记法)和肌肉质量(双能 X 射线吸收法)进行评估。通过间接测热法测量身体代谢。为了研究能量在大脑和身体之间是如何分配的,我们使用了比较生物学领域获得的参考数据。我们在脑体图上计算每个女性与体型相当的参考哺乳动物之间的距离,并将该距离命名为“脑体比”。为了阐明大脑如何保护其质量,我们测量了空腹胰岛素,因为已经证明“大脑胰岛素抑制”作为一种大脑吸引力机制发挥作用。

结果

正常体重女性和肥胖女性的脑质量相等(1441.8 ± 14.6 与 1479.2 ± 12.8 g;n.s.),且不受体重减轻的影响(1483.8 ± 12.7 g;n.s.)。相反,减肥后肌肉、脂肪、肝和肾的质量分别减少了 3-18%(均 p < 0.05)。肥胖女性的脑体比低于正常体重女性(5.8 ± 0.1 与 7.4 ± 0.1;p < 0.001)。减肥后脑体比增加至 6.3 ± 0.1(p < 0.001)。胰岛素浓度与脑体比呈负相关(r = -0.382;p < 0.001)。

结论

肥胖女性的脑质量正常,并且在热量限制期间得到保护。我们的数据表明,热量限制期间的神经保护是通过有效的大脑吸引力来介导的,这种吸引力发挥了大脑胰岛素抑制作用。

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