探討含不同脂肪種類之高果糖高油飲食介入下對大鼠腦部瘦體素阻抗、神經退化相關蛋白及大鼠認知功能的影響

肥胖及代謝症候群是神經退化性疾病及認知功能衰退的危險因子之一，其中阿茲海默症是常見的神經退化性疾病，佔所有失智症中的 60-80%。造成阿茲海默症的確切原因仍尚未完全清楚，主要病理特徵為腦中細胞外有類澱粉樣蛋白 (β-amyloid, Aβ) 堆積及細胞內有神經纖維糾結的現象。飲食中過多的果糖及飽和脂肪酸會增加血中三酸甘油酯的含量，促進肝臟合成醣類及脂肪，造成肥胖及高胰島素血症，提高罹患心血管疾病及阿茲海默症的風險。胰島素阻抗及肥胖常伴隨有瘦體素抗性的情形產生。先前研究指出，瘦體素與大腦中細胞外Aβ 的產生減少有關，且具有神經保護作用。本實驗主要探討在高果糖高脂飲食中，飽和脂肪酸對於瘦體素及神經退化疾病的影響，結果顯示在椰子油介入的組別中瘦體素濃度較控制組高，且血液生化檢驗中血糖、胰島素及三酸甘油酯較控制組高。在水迷宮第四天實驗中，控制組較介入組有較好的空間學習記憶能力。因此含高飽和脂肪酸及高果糖飲食會增加血中三酸甘油酯、胰島素及瘦體素濃度，降低大腦中瘦體素含量及瘦體素接受器的表現量，造成瘦體素阻抗，且增加大腦中類澱粉樣蛋白堆積，造成大鼠認知功能表現下降。

關鍵字

瘦體素；飽合脂肪酸；高果糖高油飲食；阿茲海默症

並列摘要

Metabolic syndromes and obesity are the risks of neurodegeneration. Alzheimer’s disease (AD) is the most common neurodegeneration, but the specific mechanism is unclear. AD shows intraneuronal aggregates called neurofibrillary tangles and extracellular amyloid plaques. Excessive fructose and saturated fatty acid in the diet not only increase triglyceride level in serum but also promote hepatic’s lipogenesis and gluconeogenesis. High-fructose-high-fat diet may result in obesity, insulin resistance and leptin resistance. Leptin can decrease amyloid plaques in brain and protect neuron by reducing oxidative damage. We show here that, compares to control group, high-fructose-high-coconut oil group has higher leptin level and higher level of triglyceride, insulin and blood sugar. In Morris water maze test, Control group shows better spatial learning and memory. High-fructose-high-saturated fat diet induces leptin resistance by increasing leptin level in blood, decreaseing leptin level in brain and down regulating leptin receptor expression, which will induce amyloid plaques accumulation and effect rats cognitive performence.

並列關鍵字

Leptin ； Saturated fatty acid ； High-fructose-high-fat diet ； Alzheimer’s disease

參考文獻

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Med Biol 2004, 541:135-152.

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探討含不同脂肪種類之高果糖高油飲食介入下對大鼠腦部瘦體素阻抗、神經退化相關蛋白及大鼠認知功能的影響

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