Abstract

The prevention of postprandial hyperglycemia and diabetic complications is crucial for diabetes management. Inhibition of α-glucosidase to slow carbohydrate metabolism is a strategy to alleviate postprandial hyperglycemia. In addition, suppression of non-enzymatic glycation can diminish the advanced glycation end products and reduce the oxidative stress and inflammation, thereby preventing the diabetic complications. In this study, an anti-oxidative proteoglycan (namedFYGL) extracted fromGanoderma lucidumwas investigated in vitro for its inhibitory effect on α-glucosidase and non-enzymatic glycation using molecular kinetics, intrinsic fluorescence assay, and bovine serum albumin glycation models. The molecular kinetics and fluorescence assay revealed thatFYGLdecreases α-glucosidase activity by forming aFYGL–α-glucosidase complex. To evaluate the anti-glycation effect, fructose-glycated and methylglyoxal-glycated BSA models were analyzed by spectroscopic and SDS-PAGE methods. Results showed thatFYGLinhibited the glycation at every stage and suppressed glycoxidation, possibly due to its anti-oxidative capacity andFYGL–BSA complex formation. Furthermore, we demonstrated in vivo thatFYGLcould alleviate postprandial hyperglycemia indb/dbmice as well as AGE accumulation and vascular injury in diabetic rats. Overall,FYGLpossesses anti-postprandial hyperglycemia and anti-glycation functions and would be potentially used in clinic for diabetes and related complication management.Keywords:Ganoderma lucidum;postprandial hyperglycemia;α-glucosidase;non-enzymatic glycation;advanced glycation end products (AGEs)