Carta Gianfranca, Murru Elisabetta, Banni Sebastiano, Manca Claudia
Dipartimento Scienze Biomediche, Università degli studi di Cagliari, Cagliari, Italy.
Front Physiol. 2017 Nov 8;8:902. doi: 10.3389/fphys.2017.00902. eCollection 2017.
Palmitic acid (PA) has been for long time negatively depicted for its putative detrimental health effects, shadowing its multiple crucial physiological activities. PA is the most common saturated fatty acid accounting for 20-30% of total fatty acids in the human body and can be provided in the diet or synthesized endogenously via lipogenesis (DNL). PA tissue content seems to be controlled around a well-defined concentration, and changes in its intake do not influence significantly its tissue concentration because the exogenous source is counterbalanced by PA endogenous biosynthesis. Particular physiopathological conditions and nutritional factors may strongly induce DNL, resulting in increased tissue content of PA and disrupted homeostatic control of its tissue concentration. The tight homeostatic control of PA tissue concentration is likely related to its fundamental physiological role to guarantee membrane physical properties but also to consent protein palmitoylation, palmitoylethanolamide (PEA) biosynthesis, and in the lung an efficient surfactant activity. In order to maintain membrane phospholipids (PL) balance may be crucial an optimal intake of PA in a certain ratio with unsaturated fatty acids, especially PUFAs of both n-6 and n-3 families. However, in presence of other factors such as positive energy balance, excessive intake of carbohydrates (in particular mono and disaccharides), and a sedentary lifestyle, the mechanisms to maintain a steady state of PA concentration may be disrupted leading to an over accumulation of tissue PA resulting in dyslipidemia, hyperglycemia, increased ectopic fat accumulation and increased inflammatory tone via toll-like receptor 4. It is therefore likely that the controversial data on the association of dietary PA with detrimental health effects, may be related to an excessive imbalance of dietary PA/PUFA ratio which, in certain physiopathological conditions, and in presence of an enhanced DNL, may further accelerate these deleterious effects.
长期以来,棕榈酸(PA)因其假定的有害健康影响而被负面描述,掩盖了其多种关键的生理活动。PA是最常见的饱和脂肪酸,占人体总脂肪酸的20%-30%,可通过饮食摄入或通过脂肪生成(DNL)内源性合成。PA的组织含量似乎在一个明确的浓度附近受到控制,其摄入量的变化不会显著影响其组织浓度,因为外源性来源被PA的内源性生物合成所抵消。特定的生理病理状况和营养因素可能会强烈诱导DNL,导致PA的组织含量增加,及其组织浓度的稳态控制被破坏。PA组织浓度的严格稳态控制可能与其保证膜物理性质的基本生理作用有关,也与蛋白质棕榈酰化、棕榈酰乙醇胺(PEA)生物合成以及在肺中高效的表面活性有关。为了维持膜磷脂(PL)平衡,以特定比例摄入PA与不饱和脂肪酸,尤其是n-6和n-3家族的多不饱和脂肪酸(PUFA)可能至关重要。然而,在存在正能量平衡、碳水化合物(特别是单糖和双糖)摄入过多以及久坐不动的生活方式等其他因素的情况下,维持PA浓度稳态的机制可能会被破坏,导致组织PA过度积累,进而导致血脂异常、高血糖、异位脂肪积累增加以及通过Toll样受体4导致炎症反应增强。因此,关于膳食PA与有害健康影响之间关联的有争议数据,可能与膳食PA/PUFA比例的过度失衡有关,在某些生理病理状况下,以及在DNL增强的情况下,这种失衡可能会进一步加速这些有害影响。