Abstract
Nypa fruticans Wurmb. vinegar, commonly known as nipa palm vinegar (NPV) has been used as a folklore medicine among the Malay community to treat diabetes. Early work has shown that aqueous extract (AE) of NPV exerts a potent antihyperglycemic effect. Thus, this study is conducted to evaluate the effect of AE on postprandial hyperglycemia in an attempt to understand its mechanism of antidiabetic action. AE were tested via in vitro intestinal glucose absorption, in vivo carbohydrate tolerance tests and spectrophotometric enzyme inhibition assays. One mg/mL of AE showed a comparable outcome to the use of phloridzin (1 mM) in vitro as it delayed glucose absorption through isolated rat jejunum more effectively than acarbose (1 mg/mL). Further in vivo confirmatory tests showed AE (500 mg/kg) to cause a significant suppression in postprandial hyperglycemia 30 min following respective glucose (2 g/kg), sucrose (4 g/kg) and starch (3 g/kg) loadings in normal rats, compared to the control group. Conversely, in spectrophotometric enzymatic assays, AE showed rather a weak inhibitory activity against both α-glucosidase and α-amylase when compared with acarbose. The findings suggested that NPV exerts its anti-diabetic effect by delaying carbohydrate absorption from the small intestine through selective inhibition of intestinal glucose transporters, therefore suppressing postprandial hyperglycemia.
Highlights
Diabetes mellitus (DM) is a chronic metabolic disorder caused by impairment of insulin production by pancreatic β cells and/or defects in insulin action [1]
Clinical studies have indicated that postprandial hyperglycemia is an independent and direct risk factor for cardiovascular disease in nondiabetic and diabetic individuals [17]
Once glucose is available in the brush membrane border, enterocytes mediate the expression of a Na+ /glucose co-transporter, SGLT1, and glucose is actively transported into absorptive epithelial cells
Summary
Diabetes mellitus (DM) is a chronic metabolic disorder caused by impairment of insulin production by pancreatic β cells and/or defects in insulin action [1]. Such abnormalities lead to chronic hyperglycemia, which, in turn, deranges the metabolism of carbohydrates, proteins and fats, and results in several macro- and micro-vascular complications. Postprandial hyperglycemia is one of the earliest detectable abnormalities signaling type 2 diabetes mellitus [2]. To prevent or slow the manifestation of diabetes-related complication, good management of postprandial hyperglycemia is critical early in the treatment of diabetes mellitus. One way to achieve controlled postprandial blood glucose levels is to slow down glucose absorption in the intestines by inhibition of the action of certain carbohydrate-hydrolyzing enzymes, namely pancreatic α-amylase, and intestinal α-glucosidase and glucose transporters like SGLT 1 and GLUT 2 [5]
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