It can be concluded from the above-mentioned experimental results that a high-fructose diet can cause hyperinsulinaemia, while a high-fat diet can result in impaired pancreatic function of insulin secretion and glucose intolerance, indicating that high-fructose diet and a high-fat diet may exert divergent effects on glucose metabolism in rats.
Thin silicate platelets in a dimension of approximately 80 × 80 × 1 nm 3 are isolated for the first time by a newly developed process involving one-step exfoliation of natural montmorillonite clay and toluene/aqueous NaOH extraction. The platelets are observed to be polygon shape by transmission electron microscopy (TEM) and round bent-leaf shape by dynamic force microscopy (DFM). Individual platelets possessing high-aspectratio dimension and ionic character are able to self-assemble into microscale fiber bundles after water evaporation. The self-stacking mechanism indicated strong face-to-face ionic charge stacking propensity in triggering a vertical growth. Regularity of fibrous bundles in an average 5 µm length has been observed.
Chitosan is a natural and versatile biomaterial with a blood-glucose-lowering effect in diabetic animals, but the mechanism of action is still unknown. This study was designed to investigate the possible mechanisms involved in the hypoglycemic activity of chitosan in rats with streptozotocin (STZ)-induced diabetes. Male Sprague−Dawley (SD) rats were divided into non-diabetic with cellulose (control), diabetic with cellulose (DM), and diabetic with low- (DM + LCS) and high- (DM + HCS) molecular-weight chitosan groups. After a 4 week feeding study, plasma glucose and fructosamine levels were increased while plasma leptin was decreased in the DM group when compared to the control group. These alternations caused by diabetes could be effectively reversed by both chitosan treatments. The increased gluconeogenesis-related signals including phosphoenolpyruvate carboxykinase (PEPCK) expression and phosphorylations of p38 and AMP-activated kinase (AMPK) in the livers of diabetic rats were attenuated by chitosans. Moreover, chitosan significantly increased muscle glucose uptake-related signals including Akt phosphorylation and glucose transporter-4 (GLUT4) translocation from the cytosol to membrane in the soleus muscles of diabetic rats. These results indicate that chitosan may possess a potential for alleviating type-1 diabetic hyperglycemia through the decrease in liver gluconeogenesis and increase in skeletal muscle glucose uptake and use.
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