Macho L, Ficková M, Seböková E, Mitková A, Klimes I
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava.
Ann N Y Acad Sci. 1993 Jun 14;683:237-43. doi: 10.1111/j.1749-6632.1993.tb35712.x.
High sucrose diet-induced insulin resistance and mild glucose intolerance are associated with decreased insulin binding to isolated adipocytes and reduced insulin action in adipose tissue. Enhanced dietary intake of omega-3 polyunsaturated fatty acids (n-3-FA) counteracts these disorders. To provide more information on the possible role of membrane-related glucose transport processes, basal and insulin-stimulated 2-deoxy-D-3H glucose uptake was evaluated in isolated adipocytes obtained from rats on various dietary regimens. For 2 weeks animals were fed three different isocaloric (18 cal% proteins, 19 cal% fat, and 63 cal% carbohydrate) diets: (1) a standard rat chow (B), (2) a high sucrose diet (S, 63 cal% sucrose), or (3) an S diet supplemented with marine fish oil (S + FO, Martens, 30 wt% of n-3-FA). High dietary n-3-FA intake resulted in a significant decline in both basal (0.05 +/- 0.01 pmol/10(6) fat cells; mean +/- SEM) and insulin-stimulated (10(-6) M) (0.20 +/- 0.01) glucose uptake when compared with the control (basal: 0.12 +/- 0.02; insulin: 0.35 +/- 0.02) and/or the S group (basal: 0.18 +/- 0.03; insulin: 0.43 +/- 0.03), indicating decreases in insulin responsiveness and sensitivity (ED50: B: 0.03 +/- 0.01; S: 0.03 +/- 0.01; S + FO: 0.73 +/- 0.2 nM; p < 0.01 for S + FO vs B and S + FO vs S). Fish oil supplementation induced an increase in adipocyte size (B: 69 +/- 1.6; S: 70 +/- 2.5 and S + FO: 76 +/- 2.2 microns; B: S + FO p < 0.05) and a decrease in plasma membrane microviscosity (B: 4.08 +/- 0.3; S: 5.39 +/- 0.5; S + FO: 3.10 +/- 0.3; p < 0.05). Rates of basal and insulin-stimulated glucose uptake did not correlate with plasma membrane microviscosity; however, a negative relation to fat cell size was found (r = -0.484; p < 0.05). On the other hand, a positive correlation between both basal (r = 0.504; p < 0.05) and insulin-stimulated (10(-6) M, r = 0.640; p < 0.02) glucose uptake and blood glucose levels was observed. In conclusion, these data (a) suggest a less important role of diet-induced changes in plasma membrane microviscosity for glucose uptake in adipose tissue, and (b) leave unclear the mechanism of why dietary fish oil decreases the sensitivity of glucose uptake to insulin in isolated rat adipocytes.
高蔗糖饮食诱导的胰岛素抵抗和轻度葡萄糖不耐受与分离的脂肪细胞胰岛素结合减少及脂肪组织中胰岛素作用降低有关。增加ω-3多不饱和脂肪酸（n-3-FA）的饮食摄入量可抵消这些紊乱。为了提供更多关于膜相关葡萄糖转运过程可能作用的信息，在从不同饮食方案喂养的大鼠分离得到的脂肪细胞中评估基础和胰岛素刺激的2-脱氧-D-3H葡萄糖摄取。动物连续2周喂食三种不同的等热量（18%热量为蛋白质，19%热量为脂肪，63%热量为碳水化合物）饮食：（1）标准大鼠饲料（B），（2）高蔗糖饮食（S，63%热量为蔗糖），或（3）添加鱼油的S饮食（S + FO，马滕斯，30%重量的n-3-FA）。与对照组（基础：0.12±0.02；胰岛素：0.35±0.02）和/或S组（基础：0.18±0.03；胰岛素：0.43±0.03）相比，高饮食n-3-FA摄入量导致基础（0.05±0.01 pmol/10(6)个脂肪细胞；平均值±标准误）和胰岛素刺激（10(-6) M）（0.20±0.01）葡萄糖摄取均显著下降，表明胰岛素反应性和敏感性降低（半数有效剂量：B组：0.03±0.01；S组：0.03±0.01；S + FO组：0.73±0.2 nM；S + FO组与B组及S + FO组与S组相比，p < 为0.01）。补充鱼油导致脂肪细胞大小增加（B组：69±1.6；S组：70±2.5；S + FO组：76±2.2微米；B组与S + FO组相比，p < 0.05），质膜微粘度降低（B组：4.08±0.3；S组：5.39±0.5；S + FO组：3.10±0.3；p < 0.05）。基础和胰岛素刺激的葡萄糖摄取速率与质膜微粘度无关；然而，发现与脂肪细胞大小呈负相关（r = -0.484；p < 0.05）。另一方面，观察到基础（r = 0.504；p < 0.05）和胰岛素刺激（10(-6) M，r = 0.640；p < 0.02）葡萄糖摄取与血糖水平均呈正相关。总之，这些数据（a）表明饮食诱导的质膜微粘度变化对脂肪组织中葡萄糖摄取的作用较小，（b）尚不清楚饮食鱼油降低分离的大鼠脂肪细胞中葡萄糖摄取对胰岛素敏感性的机制。
