Altered hypothalamic function in response to glucose ingestion in obese humans

Altered hypothalamic function in response to glucose ingestion in obese humans
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DOI:
10.2337/diabetes.48.9.1801
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发表时间:
1999-09-01
期刊:
影响因子:
7.7
通讯作者:
Gao, JH
Gao, JH
中科院分区:
医学1区
文献类型:
--
作者:
Matsuda, M;Liu, YJ;Gao, JH

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下丘脑在能量摄入和摄食行为的调节中起着核心作用。然而,人类下丘脑存在功能异常,可能与能量摄入过多和肥胖有关,这一点尚未在体内得到证实。因此,我们使用功能磁共振成像(FMRI)来监测口服葡萄糖后的下丘脑功能,10名肥胖(34+/-2岁,BMI 34.2+/-1.3 kg/m(2))和10名瘦(32+/-4岁,BMI 22.0+/-0.9 kg/m(2))受试者摄入75g葡萄糖,同时使用传统的T-2加权梯度回波脉冲序列连续成像50分钟。在摄入葡萄糖后,瘦的受试者脑室旁和腹内侧核对应的区域的fMRI信号受到抑制。与消瘦受试者相比,肥胖者的这种抑制反应明显减弱(4.8+/-1.3比7.0+/-0.6%,P<0.05),并延迟(9.4+/-0.5比6.4+/-0.5分钟,P<0.05)。在瘦体和肥胖者中,达到最大抑制反应所需的时间与空腹血糖(r=0.001,75,P<0.05)和胰岛素(r=0.47,P<0.05)浓度相关。这些结果首次在体内证明,瘦体和肥胖者存在可能继发于肥胖的不同下丘脑功能。
The hypothalamus plays a central role in the regulation of energy intake and feeding behavior. However, the presence of a functional abnormality in the hypothalamus in humans that may be related to excess energy intake and obesity has yet to be demonstrated in vivo. We, therefore, used functional magnetic resonance imaging (fMRI) to monitor hypothalamic function after oral glucose intake, The 10 obese (34 +/- 2 years of age, BMI 34.2 +/- 1.3 kg/m(2)) and 10 lean (32 +/- 4 years of age, BMI 22.0 +/- 0.9 kg/m(2)) subjects with normal glucose tolerance ingested 75 g of glucose while a midsagittal slice through the hypothalamus was continuously imaged for 50 min using a conventional T-2*-weighted gradient-echo pulse sequence. After glucose ingestion, lean subjects demonstrated an inhibition of the fMRI signal in the areas corresponding to the paraventricular and ventromedial nuclei. In obese subjects, this inhibitory response was markedly attenuated (4.8 +/- 1.3 vs. 7.0 +/- 0.6% inhibition, P < 0.05) and delayed (9.4 +/- 0.5 vs. 6.4 +/- 0.5 min, P < 0.05) compared with that observed in lean subjects. The time taken to reach the maximum inhibitory response correlated with the fasting plasma glucose (r = 0,75, P < 0.001) and insulin (r = 0,47, P < 0.05) concentrations in both lean and obese subjects, These results demonstrate in vivo, for the first time, the existence of differential hypothalamic function in lean and obese humans that may be secondary to obesity.