Institut des Maladies Métaboliques et Cardiovasculaires, Institut National de la Santé et de la Recherche Médicale (INSERM U1048) and Université Paul Sabatier, I2MC-UPS, 31432, Toulouse Cedex 4, France.
J Physiol Biochem. 2014 Jun;70(2):615-27. doi: 10.1007/s13105-014-0315-6. Epub 2014 Feb 1.
Differential effects of n-3 and n-6 polyunsaturated fatty acids (PUFAs) have been demonstrated on adipose tissue physiology. Facing to the widely recognized beneficial effects of n-3 PUFAs, the n-6 PUFA effects remain controversial. Thus, we further analyzed the linoleic acid (LA) influence on adipocyte functions. To this aim, we treated by LA supplementation at three distinct doses (1, 2.5, or 5% of energy intake) rats with essential fatty acids deficiency (EFAD). PUFA composition was determined in blood and white adipose tissue (WAT), while lipolytic and lipogenic activities were measured in isolated adipocytes. EFAD rats exhibited reduced WAT mass and increased EFAD biomarkers. WAT mass was completely recovered after supplementation, irrespective of LA dose. However, neither body mass nor EFAD biomarkers returned to control with 1% LA, while LA abundance doubled in adipocytes from rats supplemented with 5% LA. Regarding lipolysis, 2.5% LA normalized the EFAD-induced alterations. A trend to decrease the maximal stimulation of lipolysis was observed with 1 and 5% LA. Regarding lipogenesis, the lower and higher LA doses increased basal activity and hampered insulin to further stimulate glucose incorporation into lipids whereas 2.5% LA normalized the basal or insulin-stimulated levels. Our results show that dietary linoleate at 2.5% restored anatomical, biochemical, and functional disturbances induced by EFAD. At higher dose, LA tended to reduce triacylglycerol breakdown, to increase triacylglycerol assembly, and to provoke insulin resistance. Therefore, LA influence on adipocyte functions does not appear to follow a typical dose-response relationship, adding further complexity to the definition of its dietary requirement.
不同类型的多不饱和脂肪酸(PUFA)对脂肪组织生理学有不同的影响。由于 n-3 PUFAs 的广泛有益作用已得到认可,n-6 PUFAs 的作用仍然存在争议。因此,我们进一步分析了亚油酸(LA)对脂肪细胞功能的影响。为此,我们用 LA 以三种不同剂量(能量摄入的 1%、2.5%或 5%)补充必需脂肪酸缺乏(EFAD)大鼠,并检测了血液和白色脂肪组织(WAT)中的 PUFA 组成,同时还测量了分离的脂肪细胞中的脂肪分解和脂肪生成活性。EFAD 大鼠的 WAT 质量减少,EFAD 生物标志物增加。补充后 WAT 质量完全恢复,而与 LA 剂量无关。然而,用 1% LA 补充时,体重和 EFAD 生物标志物都没有恢复到对照水平,而用 5% LA 补充时,脂肪细胞中的 LA 含量增加了一倍。关于脂肪分解,2.5% LA 使 EFAD 引起的改变正常化。用 1% 和 5% LA 观察到最大脂肪分解刺激作用降低的趋势。关于脂肪生成,较低和较高的 LA 剂量增加了基础活性,并阻碍了胰岛素进一步刺激葡萄糖掺入脂质,而 2.5% LA 使基础或胰岛素刺激水平正常化。我们的研究结果表明,饮食中的亚油酸 2.5% 可恢复 EFAD 引起的解剖、生化和功能紊乱。在更高剂量时,LA 倾向于减少甘油三酯分解,增加甘油三酯组装,并引起胰岛素抵抗。因此,LA 对脂肪细胞功能的影响似乎不符合典型的剂量反应关系,这为其膳食需求的定义增加了更多的复杂性。