马苏大马哈鱼籽营养成分分析及其卵磷脂对胰岛素抵抗的改善作用

从氨基酸组成、矿物质含量、维生素和卵磷脂含量等角度分析大马哈鱼（Oncorhynchus keta）和马苏大马哈鱼（Oncorhynchus masou）鱼籽的基本营养组成，并通过构建胰岛素抵抗HepG2肝细胞模型，以葡萄糖吸收水平为指标，研究马苏大马哈鱼籽来源的卵磷脂对HepG2细胞胰岛素抵抗的改善效果。结果表明：马苏大马哈鱼籽中的氨基酸、B族维生素和卵磷脂含量显著高于大马哈鱼籽，其中卵磷脂含量为234 mg/g，约占总质量的23%，是细胞膜的主要构成成分，具有多种生物学活性；二肽基态酶-Ⅳ活性抑制实验结果表明卵磷脂具有潜在的降血糖能力。模型组葡萄糖消耗量为3.87 mmol/L，显著低于正常对照组（5.86 mmol/L）（P＜0.05），说明模型建立成功；与模型组相比，马苏大马哈鱼籽卵磷脂处理组均能够促进胰岛素抵抗HepG2细胞的葡萄糖消耗，其质量浓度为800 μg/mL时，葡萄糖消耗量与空白对照组（5.86 mmol/L）接近，为5.60 mmol/L。采用实时荧光定量聚合酶链式反应测定胰岛素蛋白激酶B信号通路中关键酶基因的表达水平，卵磷脂降低胰岛素抵抗HepG2细胞中磷酸烯醇式丙酮酸羧化酶、葡萄糖-6-磷酸酶和糖原合成酶激酶3β（glycogen synthase kinase 3β，GSK(3)β）基因的相对表达量，其中GSK(3)β相对表达量由模型组的2.60 倍下调至1.59 倍，增加了HepG2细胞中糖原合成酶基因表达水平，促进细胞内糖原合成，糖原相对含量从30.67%增加到73.00%，抑制糖异生过程的发生，改善了胰岛素抵抗HepG2细胞对葡糖糖的利用水平。

Analysis of Nutritional Components and Hypoglycemic Effect of Lecithin in Oncorhynchus masou Roes

The basic nutritional components of Oncorhynchus keta and Oncorhynchus masou roes including amino acids, minerals, vitamins and lecithin were analyzed by high performance liquid chromatography (HPLC). The effect of lecithin from Oncorhynchus masou roes on improving insulin resistance in HepG2 cells was evaluated by determining glucose absorption levels. The results showed that the contents of amino acids, vitamin B and lecithin in Oncorhynchus masou roes were significantly higher than those in Oncorhynchus keta roes; the lecithin content in Oncorhynchus masou roes was 234 mg/g, accounting for 23% of the total mass. Lecithin was the main component of the cell membrane, having many biological activities. The results of dipeptidylpeptidase-Ⅳ (DPP-Ⅳ) inhibition tests showed that lecithin had a potential hypoglycemic activity. Furthermore, glucose consumption was 3.87 mmol/L in the insulin resistance model group, significantly lower than in the normal control group (5.86 mmol/L) (P < 0.05), indicating successful modeling. Compared with the model group, lecithin from Oncorhynchus masou roes could improve the glucose consumption of insulin-resistant cells. The glucose consumption at a lecithin concentration of 800 μg/mL was 5.60 mmol/L, similar to that in the normal control group (5.86 mmol/L). Meanwhile, quantitative real-time polymerase chain reaction was used to detect the expression levels of the key enzymes in the insulin protein kinase B (Akt) signaling pathway, which indicated that lecithin reduced the relative expression levels of phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase (G6Pase), and glycogen synthase kinase 3β (GSK(3)β) genes in insulin-resistant HepG2 cells. Compared with the normal control group, the relative expression level of GSK(3)β was up-regulated by 2.60 folds in the model group, and the up-regulation fold was decreased to 1.59 in the lecithin-treated group. Lecithin increased the expression level of the glycogen synthase (GS) gene in hepatocytes and consequently promoted intracellular glycogen synthesis, increasing glycogen relative content from 30.67% to 73.00%, inhibited gluconeogenesis and improved the utilization of glucose in insulin-resistant HepG2 cells.