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JCI:研究发现饮食引起的肥胖会导致脑损伤

2011/12/30 来源:health canal
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研究人员发现因饮食引起的肥胖会导致啮齿类动物和人类下丘脑某一特殊区域的变化,或导致脑损伤。这有助于解释最令人头疼的体重控制的问题。

研究人员发现因饮食引起的肥胖会导致啮齿类动物和人类下丘脑某一特殊区域的变化,或导致脑损伤。这有助于解释最令人头疼的体重控制的问题。

华盛顿大学医学教授Michael W. Schwartz博士是这项研究的主要著作者。助理教授Josh Thaler博士是这篇论文的第一作者,这篇题为“Obesity Is Associated with Hypothalamic Injury in Rodents and Humans”的论文发表在1月3日的 Journal of Clinical Investigation 杂志上。

今年早些时候已有研究证实通过饮食和健身可以恢复减去的体重,而这种趋势也是肥胖症成功治疗最大的障碍。体重是由大脑下丘脑区域的荷尔蒙和神经细胞复杂的相互作用控制的。这些相互作用影响着食欲、食量,并且对大多数肥胖者来说,还会阻碍永久性减肥。

Schwartz说,“肥胖者生理上对自己体重的上升有防御机制。”这种现象的原理是神经内分泌专家急需研究的课题。

Schwartz说,“为了解释生理上体重增长的设定点,该领域的研究人员已经推断出控制能量平衡的大脑神经回路存在着根本变化。我们的研究首次为大脑存在这样的结构变化提供直接的证据,而且包括人类和鼠类。

他的团队研究了高脂饮食的大小鼠大脑,这些大小鼠是因饮食而肥胖。他们发现这些动物下丘脑的特殊区域有早期并持久的损伤。通过脑成像,他们发现人类大脑的相同部位也有类似的损伤。

Schwartz说我们不能证明下丘脑神经损伤和体重上升防御机制之间的因果关系和影响,这是我们下一步要做的。但是这项研究相当于为影响着下丘脑控制体重的重要区域的变化可能有助于解释这个问题提供了证据。


Obesity is associated with hypothalamic injury in rodents and humans

Joshua P. Thaler, Chun-Xia Yi, Ellen A. Schur, Stephan J. Guyenet, Bang H. Hwang, Marcelo O. Dietrich, Xiaolin Zhao, David A. Sarruf, Vitaly Izgur, Kenneth R. Maravilla, Hong T. Nguyen, Jonathan D. Fischer, Miles E. Matsen, Brent E. Wisse, Gregory J. Morton, Tamas L. Horvath, Denis G. Baskin, Matthias H. Tschöp and Michael W. Schwartz

Obesity has emerged as a major health problem in industrialized nations. Despite substantial progress in understanding the neurobiology of energy homeostasis (the biological process through which energy intake and expenditure are matched to one another so as to promote stability in the amount of fuel stored as fat), little is known regarding how brain systems designed to promote weight stability are altered in common forms of obesity .

Growing evidence implicates immune cell–mediated tissue inflammation as an important mechanism linking obesity to insulin resistance in metabolically active organs, such as liver, skeletal muscle, and adipose tissue. In rodent models of diet-induced obesity (DIO), increased inflammatory signaling in the mediobasal hypothalamus (MBH) similarly contributes to leptin resistance and weight gain , but the cellular interactions underlying this inflammatory response remain uncharacterized. The goal of the current study was to identify the neuroanatomical correlates of obesity-associated hypothalamic inflammation and to determine whether similar responses occur in humans.

We report that unlike inflammation in peripheral tissues, a process that develops over weeks to months of high-fat diet (HFD) feeding in rodent models , markers of hypothalamic inflammation are elevated within 24 hours of HFD exposure. Within the first week of HFD, markers of neuron injury also become evident in the hypothalamic arcuate nucleus (ARC) and adjacent median eminence (ARC-ME) in association with reactive gliosis involving recruitment of both microglia and astrocytes. Although initially transient, suggesting an effective neuroprotective response, inflammation and gliosis return and become established with continued HFD exposure. Using an established MRI method , we also report evidence of increased gliosis in the MBH of obese humans. These findings collectively suggest that, in both humans and rodent models, obesity is associated with injury to a key brain area for energy homeostasis.

文献链接http://www.jci.org/articles/view/59660

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