Lambert Jennifer E, Parks Elizabeth J
Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Biochim Biophys Acta. 2012 May;1821(5):721-6. doi: 10.1016/j.bbalip.2012.01.006. Epub 2012 Jan 17.
The intake of dietary fat above energy needs has contributed to the growing rates of obesity worldwide. The concept of disease development occurring in the fed state now has much support and dysregulation of substrate flux may occur due to poor handling of dietary fat in the immediate postprandial period. The present paper will review recent observations implicating cephalic phase events in the control of enterocyte lipid transport, the impact of varying the composition of meals on subsequent fat metabolism, and the means by which dietary lipid carried in chylomicrons can lead to elevated postprandial non-esterified fatty acid concentrations. This discussion is followed by an evaluation of the data on quantitative meal fat oxidation at the whole body level and an examination of dietary fat clearance to peripheral tissues - with particular attention paid to skeletal muscle and liver given the role of ectopic lipid deposition in insulin resistance. Estimates derived from data of dietary-TG clearance show good agreement with clearance to the liver equaling 8-12% of meal fat in lean subjects and this number appears higher (10-16%) in subjects with diabetes and fatty liver disease. Finally, we discuss new methods with which to study dietary fatty acid partitioning in vivo. Future research is needed to include a more comprehensive understanding of 1) the potential for differential oxidation of saturated versus unsaturated fatty acids which might lead to meaningful energy deficit and whether this parameter varies based on insulin sensitivity, 2) whether compartmentalization exists for diet-derived fatty acids within tissues vs. intracellular pools, and 3) the role of reduced peripheral fatty acid clearance in the development of fatty liver disease. Further advancements in the quantitation of dietary fat absorption and disposal will be central to the development of therapies designed to treat diet-induced obesity. This article is part of a Special Issue entitled Triglyceride Metabolism and Disease.
摄入超过能量需求的膳食脂肪导致了全球肥胖率的不断上升。进食状态下疾病发展的概念现在得到了很多支持,并且由于餐后早期对膳食脂肪处理不当,可能会发生底物通量的失调。本文将综述近期的观察结果,这些观察结果涉及头期事件在肠上皮细胞脂质转运控制中的作用、餐食组成变化对后续脂肪代谢的影响,以及乳糜微粒中携带的膳食脂质导致餐后非酯化脂肪酸浓度升高的方式。随后,本文将评估全身水平定量餐食脂肪氧化的数据,并研究膳食脂肪向周围组织的清除情况——鉴于异位脂质沉积在胰岛素抵抗中的作用,特别关注骨骼肌和肝脏。从膳食甘油三酯清除数据得出的估计值与向肝脏的清除情况显示出良好的一致性,在瘦受试者中,向肝脏的清除量相当于餐食脂肪的8-12%,而在糖尿病和脂肪肝病患者中,这个数字似乎更高(10-16%)。最后,我们讨论研究体内膳食脂肪酸分配的新方法。未来的研究需要更全面地了解:1)饱和脂肪酸与不饱和脂肪酸的差异氧化潜力,这可能导致有意义的能量不足,以及该参数是否因胰岛素敏感性而异;2)组织内与细胞内池中的膳食来源脂肪酸是否存在区室化;3)外周脂肪酸清除减少在脂肪肝病发展中的作用。膳食脂肪吸收和处置定量方面的进一步进展对于开发治疗饮食诱导肥胖的疗法至关重要。本文是名为“甘油三酯代谢与疾病”的特刊的一部分。