A Model of NEFA Dynamics with Focus on the Postprandial State
A Model of NEFA Dynamics with Focus on the Postprandial State
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DOI：
10.1007/s10439-009-9738-6
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发表时间：
2009-09-01
影响因子：
3.8
通讯作者：
Colding-Jorgensen, Morten
中科院分区：
文献类型：
--
作者：
Jelic, Katarina;Hallgreen, Christine E.;Colding-Jorgensen, Morten
为了更好地理解血浆非酯化脂肪酸(NEFA)在餐后状态下的行为机制，我们建立了一个基于生理学的血浆NEFA动态数学模型。已知的生理机制被量化并用于描述NEFA动力学。胰岛素是餐后状态下NEFA代谢的主要调节剂。因此，血浆NEFA水平高度依赖于胰岛素浓度、脂肪组织的胰岛素敏感性和最大脂解率。在吸收后状态下，例如在低胰岛素时，脂肪组织的脂肪分解导致NEFA从脂肪组织净输出到其他组织。餐后，胰岛素的增加导致：脂解减少；脂蛋白脂酶(LPL)活性增加；脂肪组织刺激再酯化，降低NEFA的摄取和再酯化。结果是在一顿含碳水化合物的餐后，血浆NEFA含量下降。当胰岛素恢复到吸收后水平时，血浆NEFA通常会反弹。这种反弹是由于脂肪分解作用的恢复，脂肪组织对NEFA的再酯化作用的减少，以及LPL的增加--因为胰岛素延迟了几个小时激活LPL。总而言之，NEFA的运动强烈依赖于胰岛素--在健康人中，餐后血浆NEFA与胰岛素浓度几乎呈负相关。该模型提供了NEFA动力学的一个综合视图，并为定量和概念性地理解等离子体NEFA通量提供了一个框架。
To improve the understanding of the mechanisms underlying the behavior of plasma non-esterified fatty acids (NEFA) in the postprandial state, we have developed a physiology-based mathematical model of plasma NEFA dynamics. Known physiological mechanisms are quantified and used to describe NEFA dynamics. Insulin is the major regulator of NEFA metabolism in the postprandial state. Plasma NEFA levels are thus highly dependent on the insulin concentration, the insulin sensitivity of adipose tissue, and the maximal lipolytic rate. In the postabsorptive state, e.g., at low insulin, adipose tissue lipolysis results in a net export of NEFA from adipose tissue to other tissues. Postprandially, the rise in insulin results in: Decreased lipolysis; a higher rate of lipoprotein lipase (LPL) activity; and decreased NEFA uptake and reesterification by adipose tissue stimulation of reesterification. The result is a drop in plasma NEFA after a carbohydrate containing meal. When insulin returns to postabsorptive levels, a rebound in plasma NEFA often occurs. This rebound is due to a restoration of lipolysis, a decrease in NEFA reesterification by adipose tissue and an increased LPL-as insulin activates LPL with a delay of several hours. In conclusion, movements of NEFA depend strongly on insulin-with postprandial plasma NEFA being almost inversely related to the insulin concentration in healthy humans. The model provides an integrative view of NEFA dynamics and a framework for quantitative and conceptual understanding of plasma NEFA fluxes.