Mathakala Vani, Muppuru Muni Kesavulu, Palempalli Uma Maheswari Devi
Department of Applied Microbiology and Biochemistry, Sri Padmavati Mahila Visva vidyalayam, Tirupati, AP, India.
Department of Biosciences, Mohanbabu University, Sree Vidyanikethan Engineering college, Sree Sainath Nagar, Tirupati, AP, India.
Heliyon. 2022 Aug 15;8(8):e10252. doi: 10.1016/j.heliyon.2022.e10252. eCollection 2022 Aug.
The regulation of carbohydrate metabolizing enzymes is an effective way of reducing blood glucose levels and improving glycogen synthesis during the management of type 2 diabetes. The present investigation was conducted to explain the detailed mechanism with which a Seagrass, extract (HBE) enhances the glucose uptake in the 3T3-L1 adipocyte cell culture system in invitro. HBE stimulates the glucose uptake by the translocation of glucose transporter 4 (GLUT4) on to plasma cell membrane through induction of insulin receptor substrate 1 (IRS-1)/protein kinase B (Akt) signaling pathways. To assess the effect of HBE on T2DM, we used invivo experimental diabetes rat models induced with streptozotocin (STZ) to perform oral GTT and ITT. Furthermore, we assessed the enzymatic profile of Glycolysis, Pentose phosphate pathway, and gluconeogenesis from liver tissue homogenate. After long-term exposure with HBE, our results confirmed, that HBE improves the glucose uptake in 3T3-L1 cell lines by up-regulation of glucose transporter type 4 (GLUT4) through uptake of glucose by the adipocytes. The resulting data indicated that HBE had a great potentiality in preventing diabetes and maintaining glucose homeostasis through improving glucose uptake. The present data also showed that HBE with its insulin mimetic activity activates glycogen synthesis and enhances glucose utilization by regulating the carbohydrate metabolic enzymes. The similarity between HBE and insulin indicates that the HBE follows the mechanisms same as the insulin signaling pathway to show the antidiabetic activity.
在2型糖尿病的管理过程中，调节碳水化合物代谢酶是降低血糖水平和改善糖原合成的有效方法。本研究旨在解释海草提取物（HBE）在体外3T3-L1脂肪细胞培养系统中增强葡萄糖摄取的详细机制。HBE通过诱导胰岛素受体底物1（IRS-1）/蛋白激酶B（Akt）信号通路，促使葡萄糖转运蛋白4（GLUT4）转位到浆细胞膜上，从而刺激葡萄糖摄取。为了评估HBE对2型糖尿病的影响，我们使用链脲佐菌素（STZ）诱导的体内实验性糖尿病大鼠模型进行口服葡萄糖耐量试验（GTT）和胰岛素耐量试验（ITT）。此外，我们还评估了肝组织匀浆中糖酵解、磷酸戊糖途径和糖异生的酶谱。长期暴露于HBE后，我们的结果证实，HBE通过上调4型葡萄糖转运蛋白（GLUT4），促进脂肪细胞摄取葡萄糖，从而改善3T3-L1细胞系中的葡萄糖摄取。所得数据表明，HBE在通过改善葡萄糖摄取预防糖尿病和维持葡萄糖稳态方面具有巨大潜力。目前的数据还表明，具有胰岛素模拟活性的HBE通过调节碳水化合物代谢酶来激活糖原合成并增强葡萄糖利用。HBE与胰岛素之间的相似性表明，HBE遵循与胰岛素信号通路相同的机制来显示抗糖尿病活性。
