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摘要


近年來由於人類飲食習慣的改變,糖的攝取大量增加。糖除了提供甜味,本身缺乏營養價值,大量攝取糖分更增加熱量來源。大型的流行病學研究顯示,糖分的攝取跟肥胖、代謝症候群以及心血管疾病有關,甚至在調整了體重與常見之心血管風險因子後,糖分的攝取仍會增加心血管疾病相關死亡率。除了提供熱量以外,糖分更因為含有大量的果糖分子(fructose),而成為科學研究的焦點。相較於葡萄糖,果糖分子的代謝不受到能量狀態的調控。大量的果糖分子在肝臟中代謝,容易造成肝臟內生性脂質合成(de novo lipogenesis)以及消耗大量三磷酸腺苷(ATP)。三磷酸腺苷的快速消耗會進一步造成細胞內尿酸堆積以及透過丙二醯基輔酶A(malonyl CoA)影響食慾中樞。細胞內尿酸升高則造成氧化壓力上升、脂肪堆積以及胰島素阻抗性增加。除了透過丙二醯基輔酶A影響食慾外,果糖還會影響局部腦血流造成食慾的上升。基於糖分對於人體的各種不良影響,更積極限制糖分的攝取將是健康的選擇。

並列摘要


There has been a marked increase in the consumption of dietary sugar during the past decades. Many randomized clinical trials and epidemiologic studies have shown that individuals who consume higher amounts of added sugar tend to gain more weight and have a higher risk of obesity, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease (CVD). Thus, the World Health Organization recommends those added sugar make up less than 10% of total calories. As for the mechanisms of sugar-related health hazard, increasing evidences suggested that fructose from sugar may play a pivotal role. Without negative feedback by energy status as seen in the metabolism of glucose, fructose is associated with increased de novo lipogenesis and the consumption of intracellular ATP. The fast depletion in ATP level further leads to accumulation of uric acid. Increased intracellular uric acid is associated with increased oxidative stress, insulin resistance, and hypertriglyceridemia. Malonyl CoA acts as a signal molecule in the satiety center in hypothalamus. Opposite to the effect of glucose consumption, fructose metabolism leads to lowered malonyl CoA level and increased food intake. Based on the above reasons and the lack of nutritional values, a further reduction of sugar consumption to below 5% of total energy intake per day may have additional benefits.

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