中年时的胰岛素阻抗性会影响脑部功能


  【24drs.com】一篇新研究指出,有阿兹海默氏症风险的中年后期成人,胰岛素阻抗性与脑部葡萄糖代谢降低及记忆不佳有关。
  
  威斯康辛阿兹海默氏症研究中心、威斯康辛大学公卫学院的Barbara B. Bendlin博士表示,多年来,我们已知第二型糖尿病患者发生阿兹海默氏症的风险增加,而风险增加的实际机转则难以捉摸。
  
  我们的研究结果认为,胰岛素阻抗性这个糖尿病的主要特征会增加阿兹海默氏症风险,因为改变了脑部使用葡萄糖的方式,而葡萄糖是脑部的主要燃料。
  
  这篇研究在线登载于7月27日JAMA Neurology期刊。
  
  研究对象包括150名认知正常成年人、平均年龄60.7岁,研究开始时让他们进行认知测试、空腹抽血、脑部氟-18去氧葡萄糖标示正子摄影;他们有一些人来自威斯康辛阿兹海默预防登记资料库(WRAP),这是双亲中有阿兹海默氏症的社区样本。这150名参与者中,108人(72%)是女性、103人(68.7%)的双亲之一有阿兹海默氏症,61人(40.7%)有一个APOE ε4等位基因,7人(4.7%)有第二型糖尿病。
  
  研究者报告指出,大部分正面、侧面、顶部、颞侧和内侧颞叶,外围胰岛素阻抗性的稳定状态模式评估较高,这与较低的全身葡萄糖代谢(P < .01)和局部葡萄糖代谢(P < .05)显著有关。
  
  他们指出,这个关联在左侧颞叶内侧特别强,这个区域的葡萄糖代谢较低与立即和延迟记忆测试表现较差有关(两者都是P < .001)。
  
  Bendlin博士表示,除了发现有胰岛素阻抗性者有较低的脑部葡萄糖代谢,我们还发现脑部某些区域的葡萄糖吸收降低,而这对记忆功能很重要,与记忆表现不佳有关。她指出,重点在于,研究对象是中年后期、且大部分没有糖尿病;让中年人改变胰岛素阻抗性,或许有助于预防记忆衰退。
  
  Bendlin博士认为,适当范围的葡萄糖与胰岛素值是健康脑部功能所必须,特别是糖尿病前期者,维持胰岛素敏感性(例如:完整的饮食与运动调整)对于整体健康很重要,对脑部健康也是很重要。
  
  未参与此研究的加拿大安大略渥太华大学心理系Claude Messier博士表示,虽然本文重申了已知的观察现象(脑中代谢降低与APOE4基因型有关,且与代谢症状有关),这篇研究将此关系延伸为中年后期成人的阿兹海默氏症风险增加。
  
  他表示,虽然这篇研究并未证实第二型糖尿病(或代谢症状)与阿兹海默氏症之间的因果关系,但是它证明了胰岛素敏感性与脑部阿兹海默氏症敏感区域的代谢活性降低有关。
  
  Messier博士指出,它现在相当清楚地提出,糖尿病会加速认知功能衰退且与其它疾病状态(血管疾病与阿兹海默氏症)有关,会加速它们的病程。目前还无法说是否可以透过改变生活型态而避免糖尿病,但是或许可以降低早期阿兹海默氏症的机会。
  
  西雅图华盛顿大学医学院Laura D. Baker博士表示,这些新发现建立了让我们将焦点转变到中年健康状态是发生阿兹海默氏症之有力预测因子的研究基础。
  
  未参与该研究的Baker博士表示,这篇研究也扩展了她的团队之前的研究,她们发现初期阿兹海默氏症患者与胰岛素阻抗的年长者之间,脑部糖代谢特征有著惊人的相似处。[新]研究结果指出,这个相似之处延伸到中年成人,因此得到阿兹海默氏症风险增加可能与葡萄糖代谢失能有关的重点,且不论是否发生于成年时。
  
  Baker博士表示,当逐渐在年轻成人诊断出第二型糖尿病时,[新]研究结果对于发生阿兹海默氏症的年龄有重要的影响-除了50多岁的人报告的症状增加,甚至在他们40多岁时就可能有症状。这些结果与其它结果强调了中年健康状态对于阿兹海默氏症风险的重要性,对于何时启动介入以预防或延缓疾病具有重要意义。
  
  资料来源:http://www.24drs.com/
  
  Native link:Midlife Insulin Resistance Affects Brain Function

Midlife Insulin Resistance Affects Brain Function

By Megan Brooks
Medscape Medical News

Insulin resistance is associated lower brain glucose metabolism and poorer memory in late-middle-aged adults at risk for Alzheimer's disease (AD), a new study indicates.

"While we have known for several years that people with type 2 diabetes are at increased risk for developing AD, the exact mechanisms underlying increased risk are still elusive," Barbara B. Bendlin, PhD, from University of Wisconsin School of Medicine and Public Health and Wisconsin Alzheimer's Disease Research Center in Madison, told Medscape Medical News.

"Our findings suggest that insulin resistance, a central feature of diabetes, could increase risk for AD by altering the way the brain uses glucose, the primary fuel for the brain."

The study was published online July 27 in JAMA Neurology.

Window of Opportunity

Participants included 150 cognitively normal adults with a mean age of 60.7 years who underwent cognitive testing, fasting blood draw, and fludeoxyglucose F 18–labeled positron emission tomography of the brain at baseline. They are part of the Wisconsin Registry for Alzheimer's Prevention (WRAP), a community sample enriched for AD parental history. Of the 150 participants, 108 (72%) were women, 103 (68.7%) had a parental history of AD, 61 (40.7%) had an APOE ε4 allele, and 7 (4.7%) had type 2 diabetes.

Higher homeostatic model assessment of peripheral insulin resistance was significantly associated with lower global glucose metabolism (P < .01) and regional glucose metabolism (P < .05) "across large portions of the frontal, lateral, parietal, lateral temporal, and medial temporal lobes," the researchers report.

The association was particularly "robust" in the left medial temporal lobe, and lower glucose metabolism in this area correlated significantly with poorer performance on tests of immediate and delayed memory (P < .001 for both), they note.

"In addition to finding that people with insulin resistance have lower brain glucose metabolism, we also found that lower glucose uptake in brain regions, important for memory function, was associated with lower memory performance," Dr Bendlin told Medscape Medical News. It's important to note, she added, that the participants studied are late middle-aged, and the majority do not have diabetes. "Midlife may provide a window of opportunity for altering insulin resistance which may be protective against memory decline," she said.

"We suspect that there are optimal ranges of glucose and insulin levels that are needed for healthy brain function. Especially for individuals who are 'prediabetic', it is likely important to maintain insulin sensitivity (for example, through diet and exercise modification), for overall health, and more specifically for brain health as well," Dr Bendlin said.

Convincing Evidence

"Although this paper reiterates a known observation (decrease in brain metabolism associated with APOE4 genotype and the link with the metabolic syndrome), it extends this relationship to middle-aged people with increased risks for AD," Claude Messier, MD, PhD, from the University of Ottawa School of Psychology in Ontario, Canada, who wasn't involved in the study, told Medscape Medical News.

"Although it does not prove that there is a causal relationship between type 2 diabetes (or the metabolic syndrome) and AD, it demonstrates convincingly that insulin sensitivity is associated with decreases in metabolic activity in brain regions most sensitive to AD," he said.

It is now "pretty clear," Dr Messier added, that being diabetic will "hasten cognitive decline and interact with other disease states (vascular disease and AD) to hasten their progression." At this point, it's fair to say that if "you can avoid diabetes through lifestyle changes, you are probably reducing your odds of early AD."

Laura D. Baker, PhD, from the University of Washington School of Medicine in Seattle, told Medscape Medical News that these new findings "build on the work of others who have helped shift our scientific focus to midlife health status as a potent predictor of those who are likely to develop AD down the road."

Dr Baker, who wasn't involved in the study, said it also expands on previous work conducted by her group that uncovered "striking similarity in brain glucometabolic signatures of older insulin-resistant adults and patients with early AD. The [new] findings indicate that this similarity extends to middle-aged adults and thus makes the important point that increased AD risk may be linked to glucometabolic dysfunction, regardless of when it occurs in adulthood," she said.

"At a time in history when type 2 diabetes is diagnosed in progressively younger adults, the [new] findings have important implications for age of AD onset — with symptoms that will be increasingly reported by adults in their 50s and even possibly even in their 40s. These and other findings that highlight the importance of middle-age health status for AD risk have important implications for when interventions to prevent or slow the disease must be initiated," Dr Baker said.

The study had no commercial funding. The authors have disclosed no relevant financial relationships.

JAMA Neurol. Published online July 27, 2015.

    
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