Chitosan Oligosaccharide Alleviates Abnormal Glucose Metabolism without Inhibition of Hepatic Lipid Accumulation in a High-Fat Diet/Streptozotocin-Induced Diabetic Rat Model

Abstract

This study investigated the effects of chitosan oligosaccharide (COS) on glucose metabolism and hepatic steatosis in a high-fat (HF) diet/streptozotocin-induced diabetic rat model. Male Wistar rats were divided into: (1) normal control (NC group), (2) HF diet (HF group), (3) streptozotocin (STZ)-induced diabetes with HF diet (DF group), and DF group supplemented with (4) 0.5% COS (D0.5F group), (5) 1% COS (D1F group), and (6) 5% COS (D5F group) for 4 weeks. COS supplementation significantly decreased the plasma glucose, BUN, creatinine, uric acid, triglyceride (TG), and total cholesterol (TC) levels, and hepatic glucose-6-phosphatase activity, and significantly increased hepatic hexokinase activity and glycogen content in diabetic rats; but the increased hepatic TG and TC levels could not be significantly decreased by COS supplementation. Supplementation of COS increased superoxide dismutase activity and decreased lipid peroxidation products in the diabetic rat livers. COS supplementation significantly increased phosphorylated AMP-activated protein kinase (AMPK) protein expression, and attenuated protein expression of hepatic phosphoenolpyruvate carboxykinase (PEPCK) and phosphorylated p38 and renal sodium-glucose cotransporter-2 (SGLT2) in diabetic rats. These results suggest that COS may possess a potential for alleviating abnormal glucose metabolism in diabetic rats through the inhibition of hepatic gluconeogenesis and lipid peroxidation and renal SGLT2 expression.

Attenuation of diabetes-mediated muscle atrophy in rats by fish oil enriched omega-3 polyunsaturated fatty acids supplementation

“…In this study, the fasting glucose levels in NC rats was 226.4 mg/dL, which seems a little bit too high in contrast to existing literature data. Nonetheless, the observation is consistent with our prior studies that the fasting glucose levels of control rats typically fell within 170~220 mg/dL range [ 30 , 31 , 46 ]. Moreover, the HOMA-IR value in DF group was slightly lower than in the DM group, however, there was no significant difference between the two groups, which was likely due to the fact that the fasting insulin levels did no differ between DM and DF groups, as HOMA-IR is calculated based on the fasting blood glucose and insulin levels.…”

“…Control rats were administered with saline injection and continued on a normal diet (NC group). The STZ-injected, high fat-fed rat model, with lower mortality rates compared to a single high dose of STZ injection model, provides a good animal model of T2DM that mimics insulin resistance syndrome and is suitable for evaluating the antidiabetic activity of test compound [ 31 , 34 ]. The composition of these diets and the fatty acid composition of fish oil were performed as previously described [ 35 ].…”

Chitosan and Chitooligosaccharide: The Promising Non-Plant-Derived Prebiotics with Multiple Biological Activities

“…Likewise, the study in C57BL/6 mice indicated that COS ameliorated hepatic oxidative stress by activating the nuclear factor E2-related factor 2 (Nrf2) pathway and upregulating gene expressions of antioxidant enzymes, including GSH peroxidase (GSH-Px), superoxide dismutase (SOD), NADPH quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), and glutathione S-transferase alpha 1 (GSTA1) [ 53 ]. The results from Liu et al showed that supplementation of COS increased superoxide dismutase activity and decreased lipid peroxidation products, which contributed to alleviating abnormal glucose metabolism in the HFD/streptozotocin-induced diabetic rat livers [ 54 ].…”

Normal fat intake with high MUFA content and an appropriate SFA/MUFA/PUFA ratio improved the health of rats

“…Glucose metabolism is closely associated with lipid metabolism. Indeed, the anabolic and catabolic pathways involved in the metabolism of lipids and glucose in the liver are difficult to distinguish [ 33 ] and several links between glucose and lipid abnormalities have been recognized. [ 34 ] For example, hypertriglyceridemia is both a consequence and cause of disturbances in glucose metabolism, [ 34 ] and the fatty acid content of the diet influences glucose homeostasis.…”