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. 2018 Mar;34(3):142-149.
doi: 10.1016/j.kjms.2017.11.003. Epub 2017 Nov 29.

Eugenosedin-A improves glucose metabolism and inhibits MAPKs expression in streptozotocin/nicotinamide-induced diabetic rats

Affiliations

Eugenosedin-A improves glucose metabolism and inhibits MAPKs expression in streptozotocin/nicotinamide-induced diabetic rats

Kuo-Ping Shen et al. Kaohsiung J Med Sci. 2018 Mar.

Abstract

This study examined the effects of eugenosedin-A (Eu-A) in a streptozotocin (STZ)/nicotinamide-induced rat model of type II diabetes mellitus (T2DM). Six-week-old Sprague-Dawley rats were randomly divided into three groups: (1) RD group, normal rats fed a regular diet (RD), (2) DM group, T2DM rats fed a high-fat diet, and (3) Eu-A group, T2DM rats fed a high fat diet plus oral Eu-A (5 mg/kg/day). After 30 days, the DM group had higher body weight, higher blood glucose and lower insulin levels than the RD group. The DM group also had increased protein expression of glycogen synthase kinase (GSK) in liver and skeletal muscle and decreased protein expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), IRS-2, AMP-activated protein kinase (AMPK), glucose transporter-4 (GLUT-4), glucokinase (GCK), and peroxisome proliferator-activated receptor γ (PPAR-γ). STZ/nicotinamide-induced T2DM increased the expression of mitogen-activated protein kinases (MAPKs: p38, ERK, JNK) and inflammatory p65 protein. In the Eu-A treated T2DM rats, however, blood glucose was attenuated and the insulin concentration stimulated. Changes in IR, IRS-1 and IRS-2 proteins as well as AMPK, GLUT-4, GCK, GSK, PPAR-γ, MAPKs, and inflammatory p65 proteins were ameliorated. These results suggested that Eu-A alleviates STZ/nicotinamide-induced hyperglycemia by improving insulin levels and glucose metabolism, and inhibiting the MAPKs- and p65-mediated inflammatory pathway.

Keywords: Eugenosedin-A; Glucose metabolism; Insulin; MAPKs pathway; Type II diabetes mellitus.

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Figures

Figure 1
Figure 1
Effects of eugenosedin‐A (Eu‐A) on IR, IRS‐1, IRS‐2, AMPK, GLUT‐4, GCK, GSK, PPAR‐γ proteins in SD rat liver. Rats were fed a standard regular diet (RD group), STZ/nicotinamide injected and then fed a high‐fat diet (DM group), or STZ/nicotinamide and HFD treated rats were supplemented with Eu‐A (5 mg/kg) (Eu‐A group) for 30 days. Each value represents the mean ± S.E. (n = 8). #p < 0.05 vs. RD group; *p < 0.05 vs. DM group.
Figure 2
Figure 2
Effects of eugenosedin‐A (Eu‐A) on IR, IRS‐1, IRS‐2, AMPK, GLUT‐4, GCK, GSK, and PPAR‐γ proteins in skeletal muscle of SD rats. Rats were fed a standard regular diet (RD group), STZ/nicotinamide injected and then fed a high‐fat diet (DM group), or treated STZ/nicotinamide and HFD treated rats were supplemented with Eu‐A (5 mg/kg) (Eu‐A group) for 30 days. Each value represents the mean ± S.E. (n = 8). #p < 0.05 vs. RD group; *p < 0.05 vs. DM group.
Figure 3
Figure 3
Effects of eugenosedin‐A (Eu‐A) on p38, ERK, JNK, and p65 proteins in SD rat liver. Rats were fed a standard regular diet (RD group), STZ/nicotinamide injected and then fed a high‐fat diet (DM group), or STZ/nicotinamide treated HFD rats were supplemented with Eu‐A (5 mg/kg) (Eu‐A group) for 30 days. Each value represents the mean ± S.E. (n = 8). #p < 0.05 vs. RD group; *p < 0.05 vs. DM group.
Figure 4
Figure 4
Proposed mechanism of action of eugenosedin‐A (Eu‐A) in STZ/nicotinamide‐induced type 2 diabetes mellitus (T2DM). Eu‐A reduces STZ/nicotinamide‐induced inflammatory proteins (MAPKs and p65) in skeletal muscle and liver tissues, suggesting that it can prevent T2DM impairment of insulin receptor and insulin secretion, glucose metabolism and glycogen synthesis.

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