Kim Jin Nam, Han Sung Nim, Kim Hye-Kyeong
Department of Food Science and Nutrition, The Catholic University of Korea, Bucheon, Republic of Korea.
Department of Food & Nutrition, Seoul National University, Seoul, Republic of Korea.
Nutr Res. 2014 Aug;34(8):723-31. doi: 10.1016/j.nutres.2014.07.015. Epub 2014 Jul 30.
Phytic acid, also known as myo-inositol hexaphosphate, has been shown to lower blood glucose levels and to improve insulin sensitivity in rodents. We investigated the effects of phytic acid and myo-inositol on differentiation, insulin-stimulated glucose uptake, and lipolysis of adipocytes to test the hypothesis that the antidiabetic properties of phytic acid and myo-inositol are mediated directly through adipocytes. 3T3-L1 cells were treated with 10, 50, or 200 μmol/L of phytic acid or myo-inositol. Oil Red O staining and an intracellular triacylglycerol assay were used to determine lipid accumulation during adipocyte differentiation. Immunoblotting and real-time polymerase chain reaction (PCR) were performed to evaluate expression of transcription factors, a target protein, and insulin signaling molecules. Phytic acid and myo-inositol exposures increased lipid accumulation in a dose-dependent manner (P < .01). The expression of key transcription factors associated with adipocyte differentiation, such as peroxisome proliferator-activated receptor γ (PPARγ) and sterol regulatory element-binding protein 1c, and the expression of fatty acid synthase increased upon treatments with phytic acid and myo-inositol (P < .05). Insulin-stimulated glucose uptake in mature adipocytes increased with phytic acid and myo-inositol treatments (P < .01). In addition, mRNA levels of insulin receptor substrate 1 (IRS1), mRNA levels of glucose transporter 4, and phosphorylation of tyrosine in IRS1 increased upon phytic acid and myo-inositol treatments. In fully differentiated adipocytes, phytic acid and myo-inositol reduced basal lipolysis dose dependently (P < .01). These results suggest that phytic acid and myo-inositol increase insulin sensitivity in adipocytes by increasing lipid storage capacity, improving glucose uptake, and inhibiting lipolysis.
植酸，又称肌醇六磷酸，已被证明可降低啮齿动物的血糖水平并改善其胰岛素敏感性。我们研究了植酸和肌醇对脂肪细胞分化、胰岛素刺激的葡萄糖摄取及脂肪分解的影响，以验证植酸和肌醇的抗糖尿病特性直接通过脂肪细胞介导这一假说。用10、50或200μmol/L的植酸或肌醇处理3T3-L1细胞。采用油红O染色和细胞内三酰甘油测定法来确定脂肪细胞分化过程中的脂质积累。进行免疫印迹和实时聚合酶链反应（PCR）以评估转录因子、靶蛋白和胰岛素信号分子的表达。植酸和肌醇处理以剂量依赖方式增加脂质积累（P <.01）。用植酸和肌醇处理后，与脂肪细胞分化相关的关键转录因子，如过氧化物酶体增殖物激活受体γ（PPARγ）和固醇调节元件结合蛋白1c的表达以及脂肪酸合酶的表达增加（P <.05）。植酸和肌醇处理可增加成熟脂肪细胞中胰岛素刺激的葡萄糖摄取（P <.01）。此外，植酸和肌醇处理后，胰岛素受体底物1（IRS1）的mRNA水平、葡萄糖转运蛋白4的mRNA水平以及IRS1中酪氨酸的磷酸化增加。在完全分化的脂肪细胞中，植酸和肌醇剂量依赖性地降低基础脂肪分解（P <.01）。这些结果表明，植酸和肌醇通过增加脂质储存能力、改善葡萄糖摄取和抑制脂肪分解来提高脂肪细胞中的胰岛素敏感性。
