Mi-Hwa Park

Dieckol isolated from Ecklonia cava inhibits α-glucosidase and α-amylase in vitro and alleviates postprandial hyperglycemia in streptozotocin-induced diabetic mice.

This study was designed to investigate whether dieckol may inhibit α-glucosidase and alpha-amylase activities, and alleviate postprandial hyperglycemia in streptozotocin-induced diabetic mice. Dieckol isolated from Ecklonia cava, brown algae, evidenced prominent inhibitory effect against alpha-glucosidase and alpha-amylase. The IC(50) values of dieckol against alpha-glucosidase and alpha-amylase were 0.24 and 0.66 mM, respectively, which evidenced the higher activities than that of acarbose. Dieckol did not exert any cytotoxic effect in human umbilical vein endothelial cells (HUVECs) at various concentrations (from 0.33 to 2.69 mM). The increase of postprandial blood glucose levels were significantly suppressed in the dieckol administered group than those in the streptozotocin-induced diabetic or normal mice. Moreover, the area under curve (AUC) was significantly reduced via dieckol administration (259 versus 483 mmol min/l) in the diabetic mice as well as it delays absorption of dietary carbohydrates. Therefore, these result indicated that dieckol might be a potent inhibitor for α-glucosidase and α-amylase.

Dieckol Isolated from Ecklonia cava Protects against High-Glucose Induced Damage to Rat Insulinoma Cells by Reducing Oxidative Stress and Apoptosis

Pancreatic β cells are very sensitive to oxidative stress and this might play an important role in β cell death with diabetes. The protective effect of dieckol, one of the phlorotannin polyphenol compounds purified from Ecklonia cava (E. cava), against high glucose-induced oxidative stress was investigated by using rat insulinoma cells. A high-glucose (30 mM) treatment induced the death of rat insulinoma cells, but dieckol, at a concentration 17.5 or 70 µM, significantly inhibited the high-glucose induced glucotoxicity. Treatment with dieckol also dose-dependently reduced thiobarbituric acid reactive substances (TBARS), the generation of intracellular reactive oxygen species (ROS), and the nitric oxide level increased by a high glucose concentration. In addition, the dieckol treatment increased the activities of antioxidative enzymes including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) in high glucose-pretreated rat insulinoma cells. Dieckol protected rat insulinoma cells damage under high glucose conditions. These effects were mediated by suppressing apoptosis and were associated with increased anti-apoptotic Bcl-2 expression, and reduced pro-apoptotic cleaved caspase-3 expression. These findings indicate that dieckol might be useful as a potential pharmaceutical agent to protect against the glucotoxicity caused by hyperglycemia-induced oxidative stress associated with diabetes.

Diphlorethohydroxycarmalol isolated from Pae (Ishige okamurae) protects high glucose-induced damage in RINm5F pancreatic β cells via its antioxidant effects

Pancreatic β cells are very sensitive to oxidative stress and this may play an important role in β cell death in diabetes. The protective effect of diphlorethohydroxycarmalol (DPHC), one of phlorotannin polyphenol compound purified from pae (Ishige okamurae) against high glucoseinduced oxidative stress was investigated using RINm5F pancreatic β cells. High glucose (30 mM) treatment induced RINm5F pancreatic β cells cell death, but DPHC, at concentration 10 or 50 μg/mL, significantly inhibited the high glucose-induced glucotoxicity and apoptosis. Furthermore, treatment with DPHC dose-dependently decreased thiobarbituric acid reactive substances (TBARS), intracellular reactive oxygen species (ROS) generation and nitric oxide level increased by high glucose. In addition, DPHC treatment increased activities of antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) in high glucose pretreated RINm5F pancreatic β cells. DPHC treatment improved the secretory responsiveness following stimulation with glucose. These findings indicate that DPHC might be used as potential nutraceutical agent which will protect the glucotoxicity caused by hyperglycemia-induced oxidative stress associated with diabetes.

Phlorofucofuroeckol A isolated from Ecklonia cava alleviates postprandial hyperglycemia in diabetic mice.

This study was designed to investigate whether phlorofucofuroeckol A inhibited α-glucosidase and α-amylase activities and alleviated postprandial hyperglycemia in diabetic mice. Phlorofucofuroeckol A that was isolated from Ecklonia cava (brown algae) demonstrated prominent inhibitory effects against α-glucosidase and α-amylase activities. The IC50 values of phlorofucofuroeckol A against α-glucosidase and α-amylase were 19.52 and 6.34μM, respectively. These inhibitory activities of phlorofucofuroeckol A were higher than those of acarbose, which was used as a positive control. Increases in postprandial blood glucose levels were significantly more suppressed in the group administered phlorofucofuroeckol A compared to the control group in both diabetic and normal mice. Moreover, the area under the curve was significantly lower after phlorofucofuroeckol A administration (2296 versus 2690mmolmin/l) in the diabetic mice. These results suggested that phlorofucofuroeckol A is a potent α-glucosidase inhibitor and can alleviate the postprandial hyperglycemia that is caused by starch.

Bioactive compounds extracted from Gamtae (Ecklonia cava) by using enzymatic hydrolysis, a potent α-glucosidase and α-amylase inhibitor, alleviates postprandial hyperglycemia in diabetic mice

This study was designed to investigate whether the brown alga gamtae (Ecklonia cava) may inhibit α-glucosidase and α-amylase activities, and alleviate postprandial hyperglycemia in streptozotocin-induced diabetic mice. For that purpose, we prepared an enzymatic hydrolysate from gamtae (EHG) by using the carbohydrase, Celluclast. EHG evidenced prominent inhibitory effect against α-glucosidase and α-amylase. The IC50 values of EHG against α-glucosidase and α-amylase were 0.62 and 0.59 mg/mL, respectively, which evidenced the higher activities than that of acarbose. EHG did not exert any cytotoxic effect in human umbilical vein endothelial cells (HUVECs) at various concentrations (from 0.25 to 2 mg/mL). The increase of postprandial blood glucose levels were significantly suppressed in the EHG administered group than those in the streptozotocin-induced diabetic or normal mice. Moreover, the area under curve (AUC) was significantly reduced via EHG administration (6,102 vs. 10,425 mg·min/dL) in the diabetic mice as well as it delays absorption of dietary carbohydrates. These result indicated that EHG might be a potent inhibitor for α-glucosidase and α-amylase.

Anti-hyperglycemic and hypolipidemic effects of baechukimchi with Ecklonia cava in type 2 diabetic db/db mice

Anti-hyperglycemic and hypolipidemic effects of baechukimchi with Ecklonia cava were investigated in type 2 diabetic db/db mice. Baechukimchi with 15% added E. cava (BKE) was fermented at 5°C for 28 days to obtain optimally ripened BKE (pH 4.28, acidity 0.71). BKE was subjected to extraction using 80% methanol. Male db/db mice were divided into groups of db/db-control, db/db-BKE, and db/db-rosiglitazone (db/db-RG). Compounds were orally administered every day for 6 weeks. The db/db-BKE mice had lowered blood glucose and plasma insulin levels. Plasma total cholesterol, triglyceride, and LDL-cholesterol levels in db/db-BKE mice were significantly (p<0.05) decreased, compared with untreated db/db mice, while db/db-BKE mice had significantly (p<0.05) increased HDL-cholesterol levels. The db/db-BKE mice had significantly (p<0.05) decreased levels of liver total cholesterol and triglyceride. BKE significantly (p<0.05) increased antioxidant enzyme activities, and ROS and lipid peroxidation levels were significantly (p<0.05) lower in db/db-BKE mice than in db/db mice.

Gelidium amansii ethanol extract suppresses fat accumulation by down-regulating adipogenic transcription factors in ob/ob mice model

The purpose of this study was to determine the anti-obesity effects of Gelidium amansii extract (GAE) in the C57BL/6J-ob/ob mice. The ob/ob mice were fed GAE at 0.5% for 4 weeks, after which body weight, epididymal adipose tissue weight, plasma triglycerides, and hepatic lipid accumulation were significantly reduced in GAE-fed mice compared with ob/ob control mice. Plasma adiponectin levels were significantly higher in GAE-fed mice than in ob/ob control mice. These findings were supported by the expression levels of enzymes and proteins related to lipid metabolism assessed by western blotting: protein expression levels of the peroxisome proliferator-activated receptor γ and CCATT/enhancer binding protein α decreased significantly, while hormone-sensitive lipase and phospho-AMP-activated protein kinase levels increased in the GAE-fed mice compared with ob/ob control mice. These findings demonstrate that GAE regulates plasma lipid profiles and increasing highdensity lipoprotein cholesterol levels as well as by regulating the expression levels of lipid metabolic factors, resulting in reduced weight gain in ob/ob mice.

The hypoglycemic effect of fermented Pueraria thunbergiana extract in streptozotocin-induced diabetic mice

This study investigated the effect of fermented and non-fermented Pueraria thunbergiana extract (FPE and PE, respectively) on postprandial hyperglycemia in streptozotocin-induced diabetic mice. FPE was prepared by fermentation of P. thunbergiana with Bifidobacterium breve K-111 followed by methanol extraction. FPE’s inhibitory activity against α-glucosidase and α-amylase was significantly higher than that of PE with IC50 values of 0.15 and 0.10 and 0.23 and 0.44 mg/mL for FPE and PE, respectively. The increase in postprandial blood glucose levels was significantly higher in FPE- than in PE-treated diabetic mice. Furthermore, FPE significantly lowered the incremental area under the curve (AUC) in the diabetic mice; the AUC in the normal mice corroborated FPE’s hypoglycemic effect. The results from this study suggest that FPE, more than PE, may help decrease postprandial hyperglycemia by inhibiting α-glucosidase and a-amylase.