Abstract
Aims of study. Present study investigated the effect of Ecklonia cava (EC) on intestinal glucose uptake and insulin secretion. Materials and methods. Intestinal Na+-dependent glucose uptake (SGU) and Na+-dependent glucose transporter 1 (SGLT1) protein expression was determined using brush border membrane vesicles (BBMVs). Glucose-induced insulin secretion was examined in pancreatic β-islet cells. The antihyperglycemic effects of EC, SGU, and SGLT1 expression were determined in streptozotocin (STZ)-induced diabetic mice. Results. Methanol extract of EC markedly inhibited intestinal SGU of BBMV with the IC50 value of 345 μg/mL. SGLT1 protein expression was dose dependently down regulated with EC treatment. Furthermore, insulinotrophic effect of EC extract was observed at high glucose media in isolated pancreatic β-islet cells in vitro. We next conducted the antihyperglycemic effect of EC in STZ-diabetic mice. EC supplementation markedly suppressed SGU and SGLT1 abundance in BBMV from STZ mice. Furthermore, plasma insulin level was increased by EC treatment in diabetic mice. As a result, EC supplementation improved postprandial glucose regulation, assessed by oral glucose tolerance test, in diabetic mice. Conclusion. These results suggest that EC play a role in controlling dietary glucose absorption at the intestine and insulinotrophic action at the pancreas contributing blood glucose homeostasis in diabetic condition.
Highlights
Diabetes is one of the most prevalent and serious metabolic diseases worldwide
The results revealed that Ecklonia cava (EC) reduced Na+-dependent glucose transporter 1 brush border membrane vesicles (BBMVs) (SGLT1) activity, assessed by Na+-dependent glucose uptake and SGLT1 protein expression in BBMV
The elevated insulin secretion with EC treatment at high glucose environment agrees with in vivo results in Table 1, strengthening the evidence that the EC acts as a stimulator of insulin secretion
Summary
Diabetes is one of the most prevalent and serious metabolic diseases worldwide. It is characterized by chronic hyperglycemia, impairment of insulin secretion from pancreatic βcells, and insulin resistance in peripheral tissues. One of the therapeutic approaches for decreasing postprandial hyperglycemia is to retard the absorption of glucose by inhibition of carbohydrate-hydrolyzing enzymes such as α-amylase and α-glycosidase. They are not able to prevent glucose absorption when glucose itself has been ingested. Intestinal glucose absorption is thought to be regulated by the Na+-dependent glucose transporter 1(SGLT1) at the apical membrane of the intestinal epithelia [1] It has been shown in diabetic animals and humans that the capacity of the small intestine to absorb glucose increases at the brush border membrane vesicles (BBMVs) due to the enhanced activity and abundance of SGLT1 [2, 3]
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