Abstract
Ruellia tuberosa L. (RTL) exhibits a wide range of phytochemical activities, for example, on treatment of diabetes mellitus (DM), in Orient. There is, however, few study regarding the effect of RTL on glycemic‐related homeostasis in type 2 DM (T2DM). We investigated the effect of RTL aqueous and ethanolic extracts on hypoglycemia in high‐fat diet (HFD)‐fed plus streptozotocin (STZ)‐induced T2DM rats, and examined the effect of RTL on glucose uptake in tumor necrosis factor‐α‐induced insulin‐resistant mouse C2C12 myoblasts, a mouse skeletal muscle cell line. The administration of 100 or 400 mg kg BW−1 day−1 of RTL aqueous or ethanolic extracts once a day for 4 weeks significantly ameliorated hyperglycemia, hyperinsulinemia, and the insulin resistance (IR) index in diabetic rats. RTL either aqueous or ethanolic extract at a concentration of 25–800 μg/ml significantly improved glucose uptake in insulin‐resistant mouse C2C12 myoblasts, indicating inhibiting the IR in skeletal muscles. These evidences suggest that RTL ameliorates hyperglycemia in HFD/STZ‐induced T2DM rats may be attributed to the alleviation of IR in skeletal muscles.
Highlights
Type 2 diabetes mellitus (T2DM) occurs mainly due to insufficient or a lack of insulin secretion from the pancreatic β cells and insulin insensitivity for a tissue, resulting in insulin cannot effectively be exerted, causing insulin resistance (IR; Boden et al, 2005; Tuncman et al, 2006)
Del Aguila, Claffey, and Kirwan (1999) utilized C2C12 cells induced by tumor necrosis factor-α (TNF-α) at a concentration of 10 ng/ml for 1 hr and found that under these conditions, the activity of IRS-1/2 is inhibited, resulting in a decrease in PI3-kinase activity andThe present study demonstrates inhibition of P42MARK and P44MARK phosphorylation, thereby enabling insulin to stimulate the decrease in glucose uptake of C2C12 cells
We demonstrate that various concentrations of both RTL water extracts (RTLW) and RTL ethanolic extracts (RTLE) enhanced glucose uptake ability in TNF-α-induced insulin- resistant C2C12 cells model
Summary
Type 2 diabetes mellitus (T2DM) occurs mainly due to insufficient or a lack of insulin secretion from the pancreatic β cells and insulin insensitivity for a tissue, resulting in insulin cannot effectively be exerted, causing insulin resistance (IR; Boden et al, 2005; Tuncman et al, 2006). Various factors are involved in the pathogenesis of IR, such as ectopic lipid metabolite accumulation, unfolded protein response activation, and innate immune responses (Samuel & Shulman, 2012) These pathogenic mechanisms may be related to abnormal fat metabolism and synthesis or energy consumption caused by the accumulation of ectopic lipid metabolites (Chang, Shen, & Wu, 2013; Chang et al, 2015; Longato, Tong, Wands, & de la Monte, 2012; McNeilly, Williamson, Sutherland, Balfour, & Stewart, 2011). Previous studies reported that tumor necrosis factor-α (TNF-α) may activate the inhibitor of nuclear factor κ-B kinase and c-Jun N-terminal protein kinase (JNK) pathways, resulting in IR in skeletal muscle cells (Boden et al, 2005; Samuel & Shulman, 2012; Tuncman et al, 2006)
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
