Abstract
Present study is an attempt to investigate plausible mechanism involved behind antidiabetic activity of standardized Houttuynia cordata Thunb. extract in streptozotocin-induced diabetic rats. The plant is used as a medicinal salad for lowering blood sugar level in North-Eastern parts of India. Oral administration of extract at 200 and 400 mg/kg dose level daily for 21 days showed a significant (P < 0.05) decrease in fasting plasma glucose and also elevated insulin level in streptozotocin-induced diabetic rats. It also significantly reversed all the alterations in biochemical parameters, that is, total lipid profile, blood urea, creatinine, protein, and antioxidant enzymes in liver, pancreas, and adipose tissue of diabetic rats. Furthermore, we have demonstrated that the extract significantly reversed the expression patterns of various glucose homeostatic enzyme genes like GLUT-2, GLUT-4, and caspase-3 levels but did not show any significant effect on PPAR-γ protein expressions. Additionally, the extract positively regulated mitochondrial membrane potential and succinate dehydrogenase (SDH) activity in diabetic rats. The findings justified the antidiabetic effect of H. cordata which is attributed to an upregulation of GLUT-4 and potential antioxidant activity, which may play beneficial role in resolving complication associated with diabetes.
Highlights
Diabetes mellitus (DM) is a disease that results in chronic inflammation and apoptosis in pancreatic islets in patients with either type 1 or 2 DM and is characterized by abnormal insulin secretion [1]
Glucose transporter 4 is mainly expressed in skeletal muscle, heart, and adipose tissues which plays critical role in insulin stimulated glucose transport in these tissues, with glucose uptake occurring when insulin stimulates the translocation of glucose transporters (GLUTs)-4 from the intracellular pool to the plasma membrane [3]
Glucose and lipid metabolism are largely dependent on the mitochondrial functional state and physiology which, on excessive reactive oxygen species (ROS) formation, leads to mitochondrial oxidative damage and reduced mitochondria biogenesis that contributes to insulin resistance and associated diabetic complications [6, 7]
Summary
Diabetes mellitus (DM) is a disease that results in chronic inflammation and apoptosis in pancreatic islets in patients with either type 1 or 2 DM and is characterized by abnormal insulin secretion [1]. Insulin-resistant glucose use in peripheral tissues such as muscle and adipose tissues is a universal feature of both insulin-dependent DM and noninsulin-dependent DM. In this process, glucose transporters (GLUTs) play crucial role [2]. Glucose transporter 4 is mainly expressed in skeletal muscle, heart, and adipose tissues which plays critical role in insulin stimulated glucose transport in these tissues, with glucose uptake occurring when insulin stimulates the translocation of GLUT-4 from the intracellular pool to the plasma membrane [3]. Glucose and lipid metabolism are largely dependent on the mitochondrial functional state and physiology which, on excessive ROS formation, leads to mitochondrial oxidative damage and reduced mitochondria biogenesis that contributes to insulin resistance and associated diabetic complications [6, 7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
