中年時的胰島素阻抗性會影響腦部功能


  【24drs.com】一篇新研究指出,有阿茲海默氏症風險的中年後期成人,胰島素阻抗性與腦部葡萄糖代謝降低及記憶不佳有關。
  
  威斯康辛阿茲海默氏症研究中心、威斯康辛大學公衛學院的Barbara B. Bendlin博士表示,多年來,我們已知第二型糖尿病患者發生阿茲海默氏症的風險增加,而風險增加的實際機轉則難以捉摸。
  
  我們的研究結果認為,胰島素阻抗性這個糖尿病的主要特徵會增加阿茲海默氏症風險,因為改變了腦部使用葡萄糖的方式,而葡萄糖是腦部的主要燃料。
  
  這篇研究線上登載於7月27日JAMA Neurology期刊。
  
  研究對象包括150名認知正常成年人、平均年齡60.7歲,研究開始時讓他們進行認知測試、空腹抽血、腦部氟-18去氧葡萄糖標示正子攝影;他們有一些人來自威斯康辛阿茲海默預防登記資料庫(WRAP),這是雙親中有阿茲海默氏症的社區樣本。這150名參與者中,108人(72%)是女性、103人(68.7%)的雙親之一有阿茲海默氏症,61人(40.7%)有一個APOE ε4等位基因,7人(4.7%)有第二型糖尿病。
  
  研究者報告指出,大部分正面、側面、頂部、顳側和內側顳葉,週邊胰島素阻抗性的穩定狀態模式評估較高,這與較低的全身葡萄糖代謝(P < .01)和局部葡萄糖代謝(P < .05)顯著有關。
  
  他們指出,這個關聯在左側顳葉內側特別強,這個區域的葡萄糖代謝較低與立即和延遲記憶測試表現較差有關(兩者都是P < .001)。
  
  Bendlin博士表示,除了發現有胰島素阻抗性者有較低的腦部葡萄糖代謝,我們還發現腦部某些區域的葡萄糖吸收降低,而這對記憶功能很重要,與記憶表現不佳有關。她指出,重點在於,研究對象是中年後期、且大部分沒有糖尿病;讓中年人改變胰島素阻抗性,或許有助於預防記憶衰退。
  
  Bendlin博士認為,適當範圍的葡萄糖與胰島素值是健康腦部功能所必須,特別是糖尿病前期者,維持胰島素敏感性(例如:完整的飲食與運動調整)對於整體健康很重要,對腦部健康也是很重要。
  
  未參與此研究的加拿大安大略渥太華大學心理系Claude Messier博士表示,雖然本文重申了已知的觀察現象(腦中代謝降低與APOE4基因型有關,且與代謝症狀有關),這篇研究將此關係延伸為中年後期成人的阿茲海默氏症風險增加。
  
  他表示,雖然這篇研究並未證實第二型糖尿病(或代謝症狀)與阿茲海默氏症之間的因果關係,但是它證明了胰島素敏感性與腦部阿茲海默氏症敏感區域的代謝活性降低有關。
  
  Messier博士指出,它現在相當清楚地提出,糖尿病會加速認知功能衰退且與其他疾病狀態(血管疾病與阿茲海默氏症)有關,會加速它們的病程。目前還無法說是否可以透過改變生活型態而避免糖尿病,但是或許可以降低早期阿茲海默氏症的機會。
  
  西雅圖華盛頓大學醫學院Laura D. Baker博士表示,這些新發現建立了讓我們將焦點轉變到中年健康狀態是發生阿茲海默氏症之有力預測因子的研究基礎。
  
  未參與該研究的Baker博士表示,這篇研究也擴展了她的團隊之前的研究,她們發現初期阿茲海默氏症患者與胰島素阻抗的年長者之間,腦部糖代謝特徵有著驚人的相似處。[新]研究結果指出,這個相似之處延伸到中年成人,因此得到阿茲海默氏症風險增加可能與葡萄糖代謝失能有關的重點,且不論是否發生於成年時。
  
  Baker博士表示,當逐漸在年輕成人診斷出第二型糖尿病時,[新]研究結果對於發生阿茲海默氏症的年齡有重要的影響-除了50多歲的人報告的症狀增加,甚至在他們40多歲時就可能有症狀。這些結果與其他結果強調了中年健康狀態對於阿茲海默氏症風險的重要性,對於何時啟動介入以預防或延緩疾病具有重要意義。
  
  資料來源: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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