Methods: In this study, type 2 diabetes model mice were induced by streptozotocin and high-fat diet (HFD) and used to evaluate the antihyperglycemic and anti-inflammatory effects of FFP. Mice were fed with HFD and challenged with 30 mg/kg body weight (BW) of streptozotocin for 1 month followed by 6 weeks of supplementation with 0.1 and 1.0 g/kg BW of FFP. Metformin was used as positive control treatment.
Results: Xeniji™-supplemented hyperglycemic mice were recorded with lower glucose level after 6 weeks of duration. This effect was contributed by the improvement of insulin sensitivity in the hyperglycemic mice indicated by the oral glucose tolerance test, insulin tolerance test, and end point insulin level. In addition, gene expression study has shown that the antihyperglycemic effect of FFP is related to the improvement of lipid and glucose metabolism in the mice. Furthermore, both 0.1 and 1 g/kg BW of FFP was able to reduce hyperglycemia-related inflammation indicated by the reduction of proinflammatory cytokines, NF-kB and iNOS gene expression and nitric oxide level.
Conclusion: FFP potentially demonstrated in vivo antihyperglycemic and anti-inflammatory effects on HFD and streptozotocin-induced diabetic mice.
METHODS: AE was administered to streptozotocin (STZ)-induced diabetic rats twice daily at three doses (1000, 500, and 250 mg/kg b.w.) for 12 days p.o. Several biochemical analyses and a histological study of the pancreas and liver were performed, accompanied by a cell culture assay.
RESULTS: As compared to diabetic control (DC), AE at the doses of 500 and 1000 mg/kg b.w. caused significant reduction (p < 0.05) of blood glucose, total cholesterol and triglycerides levels, with positive improvement of serum insulin levels. Interestingly, immunohistochemical staining of the pancreas suggested no β-cell regeneration, despite significant increase in insulin production. AE-treated groups, however, showed overall restoration of the hepatic histoarchitecture of STZ-induced liver damage, suggesting a possible hepatoprotective effect. The pancreatic effect of AE was further studied through RIN-5F cell culture, which revealed a positive stimulatory effect on insulin release at a basal glucose concentration (1.1 mM).
CONCLUSION: Nypa fruticans Wurmb. vinegar's aqueous extract exerts its antihyperglycaemic activity, at least in part, through insulin stimulatory and hepatoprotective effects.
AIM OF THE STUDY: To investigate the anti-hyperglycemic potential of AE through in-vitro enzymatic activities and streptozotocin-nicotinamide (STZ-NA) induced diabetic rat models using proton-nuclear magnetic resonance (1H-NMR)-based metabolomics approach.
MATERIALS AND METHODS: Anti-α-amylase and anti-α-glucosidase activities of the hydroethanolic extracts of AE were evaluated. The absolute quantification of bioactive constituents, using ultra-high performance liquid chromatography (UHPLC) was performed for the most active extract. Three different dosage levels of the AE extract were orally administered for 4 weeks consecutively in STZ-NA induced diabetic rats. Physical assessments, biochemical analysis, and an untargeted 1H-NMR-based metabolomics analysis of the urine and serum were carried out on the animal model.
RESULTS: Type 2 diabetes mellitus (T2DM) rat model was successfully developed based on the clear separation observed between the STZ-NA induced diabetic and normal non-diabetic groups. Discriminating biomarkers included glucose, citrate, succinate, allantoin, hippurate, 2-oxoglutarate, and 3-hydroxybutyrate, as determined through an orthogonal partial least squares-discriminant analysis (OPLS-DA) model. A treatment dosage of 250 mg/kg body weight (BW) of standardized 70% ethanolic AE extract mitigated increase in serum glucose, creatinine, and urea levels, providing treatment levels comparable to that obtained using metformin, with flavonoids primarily contribute to the anti-hyperglycemic activities. Urinary metabolomics disclosed that the following disturbed metabolism pathways: the citrate cycle (TCA cycle), butanoate metabolism, glycolysis and gluconeogenesis, pyruvate metabolism, and synthesis and degradation of ketone bodies, were ameliorated after treatment with the standardized AE extract.
CONCLUSIONS: This study demonstrated the first attempt at revealing the therapeutic effect of oral treatment with 250 mg/kg BW of standardized AE extract on chemically induced T2DM rats. The present study provides scientific evidence supporting the ethnomedicinal use of Ardisia elliptica and further advances the understanding of the fundamental molecular mechanisms affected by this herbal antidote.
MATERIALS AND METHODS: Six control and five DM Wistar rats were evaluated. DM was induced at 11 weeks of age using streptozotocin (STZ; 60 mg/kg, intraperitoneal). Animals were monitored up to 38 weeks of age, when plasma glucose, lipid profile, and markers specific for systemic inflammation, endothelial dysfunction, and oxidative stress were measured. The amount of fat within the aortic wall was assessed semiquantitatively using Oil Red O staining.
RESULTS: Diabetic rats presented significantly higher plasma glucose (p < 0.001), total cholesterol and triglycerides (both p = 0.02), high-sensitivity C-reactive protein (p = 0.01), and vascular endothelial growth factor (p = 0.04) levels, and significantly lower interleukin-10 (p = 0.04), superoxide dismutase (p < 0.01), and glutathione peroxidase (p = 0.01) levels than the control rats. Mild (grade 1) atherosclerotic lesions were observed in the aortic wall of 80% of the diabetic rats and in none of the control rats.
CONCLUSIONS: This study presents a STZ-induced type 1 DM rat model with one of the longest follow-ups in the literature. In this model, long-term DM created a highly pro-atherogenic environment characterised by hyperglycemia, dyslipidemia, systemic inflammation, endothelial dysfunction, and oxidative stress that resulted in the development of early aortic atherosclerotic lesions.
METHODS: Forty female rats were randomly assigned into five groups (n = 8/group) i.e. non-DM (non-diabetes), DM (diabetes), DM + Propolis (diabetes on propolis orally); DM + Insulin (diabetes on insulin subcutaneously) and DM + Combined (diabetes on propolis and insulin) groups. Propolis and insulin were given at 300 mg/kg/day orally and 5.0 IU/kg/day subcutaneously, respectively, for 4 weeks.
RESULTS: Fasting blood glucose, conception period, implantation losses, foetal blood glucose and placental oxidative stress markers such as malonaldehyde and protein carbonyl were significantly higher while maternal weight gain, foetal body weight and total antioxidant capacity were significantly lower in DM group compared with non-DM group. These changes were significantly improved in rats treated with propolis or insulin alone with greater significant effects in rats treated with both propolis and insulin.
CONCLUSION: This study may suggest the protective effects of propolis against DM-induced impaired pregnancy outcomes and placental oxidative stress with greater effects when combined with insulin.