Polysaccharide from Okra (Abelmoschus esculentus (L.) Moench) Improves Antioxidant Capacity via PI3K/AKT Pathways and Nrf2 Translocation in a Type 2 Diabetes Model

Abstract

Polysaccharide extracted from okra (Abelmoschus esculentus (L.) Moench), a traditional functional food, is a biologically active substance reported to possess hypoglycemic and anti-oxidative qualities. However, it is unknown which polysaccharides play a role and have the potential mechanism. This present study is to assess the possible impacts of a novel polysaccharide isolated from okra (OP) on mice fed with a high-fat diet (HFD) combined with an intraperitoneal injection (i.p.) of 100 mg/kg streptozotocin (STZ) twice, to induce type 2 diabetes mellitus (T2DM). We found that an eight-week administration of OP at 200 or 400 mg/kg body weight significantly alleviated the symptoms, with elevations in blood glucose, triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), as well as reducing high-density lipoprotein cholesterol (HDL-C), body weight, food, and water consumption. The OP treatment increased the hepatic glycogen and decreased the mussy hepatic cords and liver fibrosis in the T2DM mice. The decreases of ROS and MDA and the increases of SOD, GSH-Px and CAT in liver were observed after administration of OP. OP alleviated the T2DM characteristics through the activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase 3 beta (GSK3β) pathway, and enhanced the nuclear factor erythroid-2 (Nrf2) expression and promoted Nrf2-medicated heme oxygenase-1(HO-1) and superoxide dismutase 2 (SOD2) expression. OP also relieved mitochondrial dysfunction by inhibiting NOX2 activation. Taken together, these findings suggest that a polysaccharide isolated from okra exerts anti-T2DM effects partly by modulating oxidative stress through PI3K/AKT/GSK3β pathway-medicated Nrf2 transport. We have determined that a polysaccharide possesses hypoglycemic activity, as well as its underlying mechanism.

Physicochemical Characterization of Hizikia fusiforme Polysaccharide and Its Hypoglycemic Activity via Mediating Insulin‐Stimulated Blood Glucose Utilization of Skeletal Muscle in Type 2 Diabetic Rats

“…[28] Specifically, activation of PI3K/ Akt signaling pathway further stimulated conveyance of blood glucose into the cytoplasm of muscle cells via GLUT4, then, glucose converted to glycogen. [25] Furthermore, relative expression levels of PI3K and Akt at mRNA level were shown in Figure 7, the current data demonstrated that the expression of PI3K and Akt in skeletal muscle of diabetic rats from DC group were markedly down-regulated compared with those of NC group (P < 0.05), reducing approximately by 45.54 % and 61.90 %, separately. Oral administration with metformin or HFP was certificated a remarkable extremely up-regulation in the expression of PI3K and Akt in skeletal muscle of diabetic rats compared to DC group (P < 0.05).…”

Consumption of Terpenoids-Rich Padina pavonia Extract Attenuates Hyperglycemia, Insulin Resistance and Oxidative Stress, and Upregulates PPARγ in a Rat Model of Type 2 Diabetes

“…HbA1c is a valuable indicator for the diagnosis and management of hyperglycemia in diabetes and levels lower than 7% indicate good glycemic control [65]. Previous work from our lab [15] as well as others [66,67] have shown hyperglycemia, elevated HbA1c% and altered insulin secretion, and sensitivity in HFD/STZ-induced rodents. In addition, the values of HOMA-IR suggested the development of IR in HFD/STZ-induced rats.…”

Anti-Diabetic Effects and Mechanisms of Dietary Polysaccharides

“…In addition, these polysaccharides improved SOD, CAT, and GSH-Px activities in liver and kidney tissue of diabetic mice. Tea polysaccharides increased the expressions of PI3K/AKT p-AKT and GLUT4 signaling pathway [27,88,152]. All these above findings proved that administration of polysaccharides remarkably inhibited the expression of GSK-3 β and elevated expressions of the insulin receptor, IRS1, PI3K, and AKT in type 2 diabetic animal models.…”

“…Sea cucumber polysaccharide (MW: 21.53 kDa) purified from Acaudina Molpadioides (MW: 20.53 kDa,) and pumpkin polysaccharides (MW: 749.3, 727.0, and 607.6 kDa) and sulfated rhamnose polysaccharides (MW: 4.57 kDa) from Enteromorpha prolifera increased insulin-stimulated glucose uptake, GLUT4 translocation, and Akt/ERK activation in TNF-α-induced insulin-resistant 3T3-L1 adipocytes. This finding strongly suggested that polysaccharide enhanced glucose uptake by activating the PI3K/Akt pathway and MAPK–ERK pathway [90,150,151,152]. Another in vitro study connected with active polysaccharides on LPS-induced RAW 264.7 cells; polysaccharides derived from Agaricus blazei Murill decreased the expression of JNK, ERK, and p38 [132,153,154].…”