Why Doesn’t the Brain Lose Weight, When Obese People Diet?

Why Doesn’t the Brain Lose Weight, When Obese People Diet?
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DOI:
10.1159/000327676
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发表时间:
2011-04
期刊:
影响因子:
3.6
通讯作者:
A. Peters;A. Bosy-Westphal;B. Kubera;D. Langemann;Kristin Goele;Wiebke Later;M. Heller;C. Hubold;M. Müller
A. Peters;A. Bosy-Westphal;B. Kubera;D. Langemann;Kristin Goele;Wiebke Later;M. Heller;C. Hubold;M. Müller
中科院分区:
医学3区
文献类型:
--
作者:
A. Peters;A. Bosy-Westphal;B. Kubera;D. Langemann;Kristin Goele;Wiebke Later;M. Heller;C. Hubold;M. Müller

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目的:正如最近所显示的,肥胖与脑容量不足有关。我们在此采用介入性研究设计来调查肥胖症患者在热量限制后大脑是否萎缩。为了阐明神经保护的机制,我们评估了大脑拉动能力,即大脑从身体适当需求能量的能力。方法:对52例正常体重妇女和42例肥胖妇女(体重减轻前后≈10%)的脑、肝、肾脏器质量(磁共振成像)、脂肪(气移体积描记仪)和肌肉质量(双能x线吸收仪)进行评估。用间接量热法测定机体代谢。为了研究能量是如何在大脑和身体之间分配的,我们使用了比较生物学领域获得的参考数据。我们在脑-体图中计算了每位女性与同等大小的参考哺乳动物之间的距离,并将此距离命名为“脑测量”。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“大脑胰岛素抑制”已被证明是一种大脑拉动机制。结果:正常体重和肥胖女性的脑质量相等(1441.8±14.6 g vs 1479.2±12.8 g; n.s),并且不受体重减轻的影响(1483.8±12.7 g; n.s)。相比之下,减重后肌肉、脂肪、肝脏和肾脏的质量下降了3 ~ 18%(均p < 0.05)。肥胖女性的脑功能指标低于正常体重女性(5.8±0.1比7.4±0.1;p < 0.001)。体重减轻使脑测量增加到6.3±0.1 (p < 0.001)。胰岛素浓度与脑电图呈负相关(r = -0.382; p < 0.001)。结论:肥胖妇女的脑质量正常,在热量限制中受到保护。我们的数据表明,热量限制期间的神经保护是由一个有效的脑牵拉施加脑胰岛素抑制介导的。
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.