首页> 外文期刊>Journal of clinical biochemistry and nutrition. >Pre-germinated brown rice prevents high-fat diet induced hyperglycemia through elevated insulin secretion and glucose metabolism pathway in C57BL/6J strain mice
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Pre-germinated brown rice prevents high-fat diet induced hyperglycemia through elevated insulin secretion and glucose metabolism pathway in C57BL/6J strain mice

机译:预发芽糙米可通过提高C57BL / 6J品系小鼠的胰岛素分泌和葡萄糖代谢途径来防止高脂饮食诱发的高血糖

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This study investigated the effect and mechanism of pre-germinated brown rice (PGBR) prevented hyperglycemia in C57BL/6J mice fed high-fat-diet (HFD). Normal six-week-old mice were randomly divided into three groups. Group 1 was fed standard-regular-diet (SRD) and group 2 was fed HFD for 16 weeks. In group 3, the mice were fed a HFD with its carbohydrate replaced with PGBR for 16 weeks. Comparing the SRD and HFD groups, we found the HFD group had higher blood pressure, higher concentrations of blood glucose and HbA1c. The HFD group had less protein expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), phosphatidylinositol-3-kinase (PI3K), glucose transporter-4 (GLUT-4) and glucokinase (GCK) and greater expression of glucogen synthase kinase (GSK) in skeletal muscle. The HFD group also had less expression of IR, serine/threonine kinase PI3K-linked protein kinase B (Akt/PKB), AMP-activated protein kinase (AMPK), GCK and peroxisome proliferator-activated receptor γ (PPARγ) in liver. In the HFD?+?PGBR group, the PGBR could reverse the disorders of blood pressure, blood glucose, HbA1c and increase insulin concentration. PGBR increased the IR, IRS-1, PI3K, Akt, GLUT-1 and GLUT-4 proteins, and ameliorated AMPK, GCK, GSK and PPARγ proteins. Together, PGBR prevented HFD-induced hyperglycemia through improving insulin levels, insulin receptor, glucose transporters and enhancing glucose metabolism.
机译:这项研究调查了预发芽糙米(PGBR)预防高脂饮食(HFD)喂养的C57BL / 6J小鼠高血糖的作用和机制。正常的六周龄小鼠随机分为三组。第1组喂食标准饮食(SRD),第2组喂食HFD,持续16周。在第3组中,给小鼠喂食HFD,其碳水化合物被PGBR代替,持续16周。比较SRD组和HFD组,我们发现HFD组的血压更高,血糖浓度和HbA1c更高。 HFD组的胰岛素受体(IR),胰岛素受体底物1(IRS-1),磷脂酰肌醇3激酶(PI3K),葡萄糖转运蛋白4(GLUT-4)和葡萄糖激酶(GCK)的蛋白质表达较少,且较高糖合酶激酶(GSK)在骨骼肌中的表达HFD组在肝脏中的IR,丝氨酸/苏氨酸激酶PI3K连锁蛋白激酶B(Akt / PKB),AMP激活蛋白激酶(AMPK),GCK和过氧化物酶体增殖物激活受体γ(PPARγ)的表达也较少。在HFD + + PGBR组中,PGBR可逆转血压,血糖,HbA1c紊乱并增加胰岛素浓度。 PGBR增加了IR,IRS-1,PI3K,Akt,GLUT-1和GLUT-4蛋白,并改善了AMPK,GCK,GSK和PPARγ蛋白。 PGBR共同通过改善胰岛素水平,胰岛素受体,葡萄糖转运蛋白和增强葡萄糖代谢来预防HFD诱导的高血糖症。

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