• The Korean Journal of Physiology and Pharmacology
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• v.22 no.3
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• pp.257-267
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• 2018

The present study aimed to evaluate the cinnamic acid effect on memory impairment, oxidative stress, and cholinergic dysfunction in streptozotocin (STZ)-induced diabetic model in mice. In this experimental study, 48 male Naval Medical Research Institute (NMRI) mice (30-35 g) were chosen and were randomly divided into six groups: control, cinnamic acid (20 mg/kg day, i.p.), diabetic, and cinnamic acid-treated diabetic (10, 20 and 40 mg/kg day, i.p.). Memory was impaired by administering an intraperitoneal STZ injection of 50 mg/kg. Cinnamic acid was injected for 40 days starting from the 21st day after confirming STZ-induced dementia to observe its therapeutic effect. Memory function was assessed using cross-arm maze, morris water maze and passive avoidance test. After the administration, biochemical parameters of oxidative stress and cholinergic function were estimated in the brain. Present data indicated that inducing STZ caused significant memory impairment, whereas administration of cinnamic acid caused significant and dose-dependent memory improvement. Assessment of brain homogenates indicated cholinergic dysfunction, increase in lipid peroxidation and reactive oxygen species (ROS) levels, and decrease in glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities in the diabetic group compared to the control animals, whereas cinnamic acid administration ameliorated these indices in the diabetic mice. The present study demonstrated that cinnamic acid improves memory by reducing the oxidative stress and cholinergic dysfunction in the brain of diabetic mice.

• Nutrition Research and Practice
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• v.10 no.5
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• pp.507-515
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• 2016

BACKGROUND/OBJECTIVES: This study was designed to investigate whether Gynura procumbens extract (GPE) can improve insulin sensitivity and suppress hepatic glucose production in an animal model of type 2 diabetes. MATERIALS/METHODS: C57BL/Ksj-db/db mice were divided into 3 groups, a regular diet (control), GPE, and rosiglitazone groups (0.005 g/100 g diet) and fed for 6 weeks. RESULTS: Mice supplemented with GPE showed significantly lower blood levels of glucose and glycosylated hemoglobin than diabetic control mice. Glucose and insulin tolerance test also showed the positive effect of GPE on increasing insulin sensitivity. The homeostatic index of insulin resistance was significantly lower in mice supplemented with GPE than in the diabetic control mice. In the skeletal muscle, the expression of phosphorylated AMP-activated protein kinase, pAkt substrate of 160 kDa, and PM-glucose transporter type 4 increased in mice supplemented with GPE when compared to that of the diabetic control mice. GPE also decreased the expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase in the liver. CONCLUSIONS: These findings demonstrate that GPE might improve insulin sensitivity and inhibit gluconeogenesis in the liver.

• Journal of the Korean Society of Food Science and Nutrition
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• v.41 no.6
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• pp.774-781
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• 2012

This study investigated dose-response effects of chlorogenic acid (CA) on glucose metabolism and the antioxidant system in streptozotocin (STZ)-induced diabetic mice with a high-fat diet (HFD). Male ICR mice were fed with a HFD (37% calories from fat) for 4 weeks prior to intraperitoneal injection with STZ (100 mg/kg body weight). Diabetic mice were supplemented with two doses of CA (0.02% and 0.05%, wt/wt) for 6 weeks. Both doses of CA significantly improved fasting blood glucose level, glucose tolerance and insulin tolerance without any changes in plasma insulin and C-peptide levels. Plasma leptin concentration was significantly higher in the CA-supplemented groups than in the diabetic control group. Both doses of CA significantly increased hepatic glucokinase activity and decreased glucose-6-phosphatase activity compared to the diabetic control group. The ratio of glucokinase/glucose-6-phosphatase was dose-independently higher in CA-supplemented mice than in diabetic control mice. CA supplementation dose-independently elevated superoxide dismutase and catalase activities, whereas it lowered lipid peroxide levels compared to the diabetic control mice in the liver and erythrocyte. These results suggest that low-dose CA may be used as a hypoglycemic agent in a high-fat diet and STZ-induced diabetic mice.

• Journal of Ginseng Research
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• v.36 no.2
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• pp.153-160
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• 2012

Panax ginseng has long been used as a traditional herbal medicine. More recently, it has received attention for its anti-diabetic and anti-obesity effects in humans and in animal models of type 2 diabetes. In the present study, we tested the hypoglycemic effects of ginseng berry extract in beta-cell-deficient mice and investigated the mechanisms involved. Red (ripe) and green (unripe) berry extracts were prepared and administered orally (100 or 200 mg/kg body weight) to streptozotocin-induced diabetic mice daily for 10 wk. The body weight was measured daily, and the nonfasting blood glucose levels were measured after 5 and 10 wk after administration. Glucose tolerance tests were performed, and the serum insulin levels were measured. The proliferation of beta-cells was measured in vitro. The administration of red or green ginseng berry extract significantly reduced the blood glucose levels and improved the glucose tolerance in beta-cell deficient mice, with the higher doses resulting in better effects. Glucose-stimulated insulin secretion was significantly increased in berry extract-treated mice compared with streptozotocin-induced diabetic control mice. Treatment with ginseng berry extract increased beta-cell proliferation in vitro. Both red berry and green berry extracts improved glycemic control in streptozotocin-induced diabetic mice and increased insulin secretion, possibly due to increased beta-cell proliferation. These results suggest that ginseng berry extracts might have beneficial effects on beta-cell regeneration.

• The Korean Journal of Community Living Science
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• v.16 no.1
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• pp.105-111
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• 2005

This study was carried out to investigate the effect of Lentinus edodes which were harvested at different times of maturity on blood glucose and lipid levels in diabetic mice. The diabetic KK mice were fed diets supplemented with Lentinus edodes harvested early (LE) or late (LL) for eight weeks, and control (CO) mice were fed regular diet without Lentinus edodes. Diet intake, body weight, organ weight, blood glucose and serum lipid levels were measured. The mice which were fed diets supplemented with LE and LL showed significantly lower body weights compared to the CO group. There were no significant differences in the diet intake and the weights of different organs including liver, heart, kidneys, and epididymal fat pad among three different groups. Furthermore, the concentrations of serum triglycerides and total cholesterol were significantly lower in LE and LL groups compared to the CO group. These results clearly demonstrate that Lentinus edodes, regardless of their harvested period reduced body weight and serum lipid without affecting blood glucose level in diabetic mice.

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.5
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• pp.952-959
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• 1998

To investigate the effect of sea tangle on macrophage activity in normal and diabetic states, 10week old ICR mice were fed control(C) and sea tangle(S) diet containing 5%(w/w) cellulose and 13.6%(w/w) dry sea tangle for four weeks, after which two thirds of mice(CD and SD) were made diabetic by intramuscular injection of streptozotocin(150mg/kg bw). At 4th day after diabetes was apparent by urinary glucose, one half of diabetic mice(CDM and SDM) were treated with metformin(500mg/kg bw) orally. Peritoneal macrophages obtained from 3%-thioglycollate treated mice were cultured in the presence of lipopolysaccaride from Salmonella abortus equi(10$\mu\textrm{g}$/ml) for 24 hrs and tumor necrosis factor-$\alpha$(TNF$\alpha$), interleukin-1$\beta$(1L-1$\beta$)and prostaglandin E2(PGE2) were measured in culture media. Release of IL-1$\beta$and PGE2 from macrophage were increased in normal mice by sea tangle diet and had the same tedency in diabetic mice with or without metformin treatment although not statistically significant. Release of TNF$\alpha$ tended to be reduced by diabetes but were not changed significantly by sea tangle diet. Fatty acid compositions of macrophage and liver phospholipids showed that diabetes reduced arachidonic acid/linoleic acid ratio and sea tangle diet appeared to increase contentsof polyunsaturated fatty acids.

• Journal of the Korean Society of Food Culture
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• v.30 no.6
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• pp.818-824
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• 2015

Makgeolli is a health beneficial food for diabetes compared to other alcoholic beverages. We examined the effect of Makgeolli on blood glucose level and survival rate in a streptozotocin (STZ)-induced diabetic mouse model. We force fed 30 male STZ-induced diabetic ICR mice Makgeolli consisting of 6% alcohol (DM-MAK), 6% ethanol (DM-EtOH), or distilled water (DM-DW) for 4 weeks. In the DM-MAK group, food intake and water intake were higher than those of other groups after 4 weeks. Body weight, however, was not different among the experimental groups. We also found no significant difference in blood glucose level among the experimental groups. In normal ICR mice fed Makgeolli for 1 week, the area of the blood glucose curve was higher than those of other groups fed 6% ethanol, 2% glucose, or distilled water. Survival rates of STZ-induced diabetic mice fed Makgeolli, 6% ethanol, or DW for 4 weeks were 100%, 25%, and 62.5%, respectively. In conclusion, Makgeolli had no beneficial effect on blood glucose in a STZ-induced diabetic mouse model, although their survival rate was high. These results show that Makgeolli has an effect on type 1 diabetes through other mechanisms than blood glucose control.

• Archives of Pharmacal Research
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• v.29 no.8
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• pp.666-676
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• 2006

Gangliosides are widely distributed in mammalian cells and play important roles in various functions such as cell differentiation and growth control. In addition, diabetes and obesity cause abnormal development of reproductive processes in a variety of species. However, the mechanisms underlying these effects, and how they are related, are not fully understood. This study examined whether the differential expression of gangliosides is implicated in the abnormal follicular development and uterine architecture of streptozotocin (STZ)-induced and db/db diabetic mice. Based upon the mobility on high-performance thin-layer chromatography, mouse ovary consisted of at least five different ganglioside components, mainly gangliosides GM3, GM1, GD1a and GT1b, and diabetic ovary exhibited a significant reduction in ganglioside expression with apparent changes in the major gangliosides. A prominent immunofluorescence microscopy showed a dramatic loss of ganglioside GD1a expression in the primary, secondary and Graafian follicles of STZ-induced and db/db diabetic mice. A significant decrease in ganglioside GD3 expression was also observed in the ovary of db/db mice. In the uterus of STZ-induced diabetic mice, expression of gangliosides GD1a and GT1b was obviously reduced, but gangliosides GM1, GM2 and GD3 expression was increased. In contrast, the uterus of db/db mice showed a significant increase in gangliosides GM1, GD1a and GD3 expression. Taken together, a complex pattern of ganglioside expression was seen in the ovary and uterus of normoglycemic ICR and $db/^+$ mice, and the correspoding tissues in diabetic mice are characterized by appreciable changes of the major ganglioside expression. These results suggest that alterations in ganglioside expression caused by diabetes mellitus may be implicated in abnormal ovarian development and uterine structure.

• Journal of Life Science
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• v.26 no.8
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• pp.921-927
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• 2016

Postprandial hyperglycemia is an early defect of type 2 diabetes and one of primary anti-diabetic targets. The alpha-glucosidase inhibitors regulate postprandial hyperglycemia by impeding the rate of carbohydrate (such as starch) digestion in the small intestine. This study was designed to investigate the inhibitory actions of mulberry fruit extract (MFE) on α-glucosidase and α-amylase activities, and its alleviating effect on postprandial hyperglycemia activities in vitro and in vivo. Male four-week old ICR mice and streptozotocin (STZ)-induced diabetic mice were treated with mulberry fruit extract. MFE showed strong inhibitory effects against α-glucosidase and α-amylase activities, with half-maximal inhibitory concentration (IC₅₀) values of 0.16 and 0.14 mg/ml, respectively, and was more effective than acarbose, which was used as a positive control. The increase in postprandial blood glucose levels was more significantly attenuated in the MFE-administered group mice than in the control group mice of both STZ-induced diabetic and normal mice. Moreover, the area under the glucose response curve significantly decreased following MFE administration in diabetic mice. These results indicate that MFE may be a potent inhibitor of α-glucosidase and α-amylase, and helpful in suppressing postprandial hyperglycemia in diabetic mice. The mulberry fruit extracts may be considered as a potential candidate for the management of diabetes.

• Nutrition Research and Practice
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• v.10 no.1
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• pp.33-41
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• 2016

BACKGROUND/OBJECTIVES: Diabetes mellitus (DM) is a major chronic disease which increases global health problems. Diabetes-induced renal damage is associated with inflammation and fibrosis. Alpha (AT) and gamma-tocopherols (GT) have shown antioxidant and anti-inflammatory effects in inflammation-mediated injuries. The primary aim of this study was to investigate effects of AT and GT supplementations on hyperglycemia induced acute kidney inflammation in alloxan induced diabetic mice with different levels of fasting blood glucose (FBG). MATERIALS/METHODS: Diabetes was induced by injection of alloxan monohydrate (150 mg/kg, i.p) in ICR mice (5.5-week-old, male) and mice were subdivided according to their FBG levels and treated with different diets for 2 weeks; CON: non-diabetic mice, m-DMC: diabetic control mice with mild FBG levels (250 mg/dl ${\leq}$ FBG ${\leq}$ 450 mg/dl), m-AT: m-DM mice fed AT supplementation (35 mg/kg diet), m-GT: m-DM mice with GT supplementation (35 mg/kg diet), s-DMC: diabetic control mice with severe FBG levels (450 mg/dl < FBG), s-AT: s-DM mice with AT supplementation, s-GT: s-DM mice with GT supplementation. RESULTS: Both AT and GT supplementations showed similar beneficial effects on $NF{\kappa}B$ associated inflammatory response (phosphorylated inhibitory kappa B-${\alpha}$, interleukin-$1{\beta}$, C-reactive protein, monocyte chemotactic protein-1) and pre-fibrosis (tumor growth factor ${\beta}$-1 and protein kinase C-II) as well as an antioxidant emzyme, heme oxygenase-1 (HO-1) in diabetic mice. On the other hands, AT and GT showed different beneficial effects on kidney weight, FBG, and oxidative stress associated makers (malondialdehyde, glutathione peroxidase, and catalase) except HO-1. In particular, GT significantly preserved kidney weight in m-DM and improved FBG levels in s-DM and malondialdehyde and catalase in m- and s-DM, while AT significantly attenuated FBG levels in m-DM and improved glutathione peroxidase in m- and s-DM. CONCLUSIONS: the results suggest that AT and GT with similarities and differences would be considered as beneficial nutrients to modulate hyperglycemia induced acute renal inflammation. Further research with careful approach is needed to confirm beneficial effects of tocopherols in diabetes with different FBG levels for clinical applications.