Metabolic flexibility.
Source
AstraZeneca R&D, Pepparedsleden 3, Mölndal 431 83, Sweden. leonard.storlien@astrazeneca.comAbstract
Human physiology needs to be well adapted to cope with major discontinuities in both the supply of and demand for energy. This adaptability requires 'a clear capacity to utilize lipid and carbohydrate fuels and to transition between them' (Kelley et al. 2002b).人類生理上需要對不穩定的能量來源與能量需求有良好的適應能力。
這樣的適應需要明確的能力來代謝脂肪與碳水化合物並且交互利用（文獻 Kelley et al. 2002b）
Such capacities characterize the healthy state and can be termed 'metabolic flexibility'.
這代表健康狀態也可被稱為『代謝的靈活度』。
However, increasing evidence points to metabolic inflexibility as a key dysfunction of the cluster of disease states encompassed by the term 'metabolic syndrome'.
然而，愈多證據指出代謝靈活度也可被當做病態的『代謝症候群』主要的原因之一。
In obese and diabetic individuals this inflexibility is manifest in a range of metabolic pathways and tissues including:
在肥胖與糖尿病的病患裡這樣的靈活性可表現代謝的路徑與組織包含：
(1) failure of cephalic-phase insulin secretion (impaired early-phase prandial insulin secretion concomitant with failure to suppress hepatic glucose production and NEFA efflux from adipose tissue);
無法在進食先行階段分泌胰島素（無法在進食前期分泌胰島素伴隨無法抑制肝醣製造與非主要脂肪酸由脂肪組織流出）
(2) failure of skeletal muscle to appropriately move between use of lipid in the fasting state and use of carbohydrate in the insulin-stimulated prandial state;
骨骼肌無法正常交互的在節食階段利用脂肪酸，在用餐時胰島素分泌下利用碳水化合物。
(3) impaired transition from fatty acid efflux to storage in response to a meal.
無法在用餐時正常轉換脂肪酸的流出與儲存
Finally, it is increasingly clear that reduced capacity for fuel usage in, for example, skeletal muscle, as indicated by reduced mitochondrial size and density, is characteristic of the metabolic syndrome state and a fundamental component of metabolic inflexibility.
最後，能量利用的能力顯著減少，例如：
骨骼肌細胞內粒線體的體積減少密度縮小，粒線體代謝症候群的特徵也是代謝靈活性的基本的要素。
Key questions that remain are how metabolic flexibility is lost in obese and diabetic individuals and by what means it may be regained.
要題在：肥胖與糖尿病的病患是怎麼失去代謝靈活度的？並且，要如何才能夠重獲代謝靈活度。
Gaby
