• Biomolecules & Therapeutics
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• v.9 no.4
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• pp.277-281
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• 2001

Chromium is an essential nutrient and participates in glucose and lipid metabolism in human beings and animals. The present study was conducted to assess the effects of chromium picolinate (Cr-pic) on glucose tolerance and insulin sensitivity in type I and ll diabetic rats. The experimental groups were type I diabetic (streptozotocin-induced: 40 mg/kg, i.p.) and type II diabetic (Goto-Kakizaki rats) models. Each group was subdivided into control. low-dose and high-dose of Cr-pic treated groups. The Cr-pic was orally administered with Cr-pic (100 mg/kg for low dose group and 200 mg/kg for high dose group) for 4 weeks. And then we performed intraperitoneal glucose tolerance test (IPGTT) and insulin sensitivity test (ITT). The glucose tolerance test was carried out by inection of glucose (2 g/kg, i.p.). The peripheral insulin sensitivity test was con- ducted by injection of insulin (5 units/kg, s.c.) and glucose. We performed determining of blood glucose concentration at 0, 10, 30, 60, 90, and 120 min using automated glucose analyzer. The plasma insulin concentration was determined by rat insulin EIA kit. Administration of Cr-pic improved weight gain in all group s with higher significant in the low-dose group. There was no significance between the control and the Cr-pic treated groups in the area under the blood glucose curve and serum insulin concentration plots of IPGTT and peripheral ITT in type I diabetic rats. But Cr-pic treated groups showed significantly lower levels of the area under the blood glucose currie during IPGTT and ITT and the high-dose group showed less effects compared with the low-dose group in the type II diabetic rats. The plasma insulin concentration of both diabetic groups was not influenced by Cr-pic supplementation. We can conclude that chromium picolinate may improve the endogenous and exogenous insulin action and peripheral insulin sensitivity in type II diabetic rats.

• Culinary science and hospitality research
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• v.17 no.1
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• pp.238-247
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• 2011

The aim of this study was designed to evaluate the effects of natural functional mixture(FM) on plasma BUN and lipid levels, hepatic lipid levels, hepatic antioxidant enzyme activities and plama aminotransferase activity in streptozotocin (STZ) induced diabe1ic rats. Total cholesterol (TC) level in the diabe1ic rats supplemented with FM(70.69 mg/dL) was reduced comparing to groups without FM(87.12 mg/dL). This results caused the increase of the ratio of HDL-cholesterol to TC (42.60 to 51.49 %). However, superoxide dismutase (SOD), cytosol catalase (CAT), glutathione peroxidase (GSH-Px), GSH and lipoperoxide (LPO) activities were not significantly changed, which indicated the supplementation with FM could not reduce the oxidative stress in diabetic rats. In addition, asperate aminotransferase (AST) activity in FM-diabetic rat was lower than that in diabetic group. This results showed supplementation with FM in rats could improve the hepatic function damaged by STZ-induced diabetes.

• Toxicological Research
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• v.23 no.2
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• pp.127-133
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• 2007

Metformin is a drug used to lower blood sugar levels in patients with type 2 diabetes via activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK). The primary objective of this study was to investigate whether metformin at the pharmacologically effective concentrations affects the expressions of ${\gamma}$-glutamylcysteine synthetase and phase II antioxidant genes in the H4IIE cell. Treatment of the cells with either metformin or 5-aminoimidazole-4-carboxamide riboside (AICAR) abrogated tert-butylhydroxyquinone (t-BHQ) induction of ${\gamma}$-glutamylcysteine synthetase, a rate limiting enzyme of GSH synthesis. The ability of t-BHQ to induce glutathione S-transferases (GSTs), a major class of phase II detoxifying enzymes that playa critical role in protecting cells from oxidative stress or electrophiles, was also inhibited by the agents. Transcriptional gene repression by metformin was verified by the GSTA2 promoter luciferase assay. Moreover, either metformin or AICAR treatment significantly decreased t-BHQ-dependent induction of other GSTs (i.e., $GST{\mu}$ and $GST{\pi}$ forms). Taken together, our data indicate that metformin treatment may result in the repression of ${\gamma}$-glutamylcysteine synthetase and glutathione S-transferase genes possibly via AMPK activation.

• Nutrition Research and Practice
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• v.10 no.1
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• pp.11-18
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• 2016

BACKGROUND/OBJECTIVES: Type 2 diabetes (T2D) is more frequently diagnosed and is characterized by hyperglycemia and insulin resistance. $\small{D}$-xylose, a sucrase inhibitor, may be useful as a functional sugar complement to inhibit increases in blood glucose levels. The objective of this study was to investigate the anti-diabetic effects of $\small{D}$-xylose both in vitro and stretpozotocin (STZ)-nicotinamide (NA)-induced models in vivo. MATERIALS/METHODS: Wistar rats were divided into the following groups: (i) normal control; (ii) diabetic control; (iii) diabetic rats supplemented with a diet where 5% of the total sucrose content in the diet was replaced with $\small{D}$-xylose; and (iv) diabetic rats supplemented with a diet where 10% of the total sucrose content in the diet was replaced with $\small{D}$-xylose. These groups were maintained for two weeks. The effects of $\small{D}$-xylose on blood glucose levels were examined using oral glucose tolerance test, insulin secretion assays, histology of liver and pancreas tissues, and analysis of phosphoenolpyruvate carboxylase (PEPCK) expression in liver tissues of a STZ-NA-induced experimental rat model. Levels of glucose uptake and insulin secretion by differentiated C2C12 muscle cells and INS-1 pancreatic ${\beta}$-cells were analyzed. RESULTS: In vivo, $\small{D}$-xylose supplementation significantly reduced fasting serum glucose levels (P < 0.05), it slightly reduced the area under the glucose curve, and increased insulin levels compared to the diabetic controls. $\small{D}$-xylose supplementation enhanced the regeneration of pancreas tissue and improved the arrangement of hepatocytes compared to the diabetic controls. Lower levels of PEPCK were detected in the liver tissues of $\small{D}$-xylose-supplemented rats (P < 0.05). In vitro, both 2-NBDG uptake by C2C12 cells and insulin secretion by INS-1 cells were increased with $\small{D}$-xylose supplementation in a dose-dependent manner compared to treatment with glucose alone. CONCLUSIONS: In this study, $\small{D}$-xylose exerted anti-diabetic effects in vivo by regulating blood glucose levels via regeneration of damaged pancreas and liver tissues and regulation of PEPCK, a key rate-limiting enzyme in the process of gluconeogenesis. In vitro, $\small{D}$-xylose induced the uptake of glucose by muscle cells and the secretion of insulin cells by ${\beta}$-cells. These mechanistic insights will facilitate the development of highly effective strategy for T2D.

• Archives of Pharmacal Research
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• v.22 no.5
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• pp.437-447
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• 1999

Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic $\beta$ cells by a progressive $\beta$ cell-specific autoimmune process. The pathogenesis of autoimmune IDDM has been extensively studied for the past two decades using animal models such as the non-obese diabetic (NOD) mouse and the Bio-Breeding (BB) rat. However, the initial events that trigger the immune responses leading to the selective destruction of the $\beta$ cells are poorly understood. It is thought that $\beta$ cell auto-antigens are involved in the triggering of $\beta$ cell-specific autoimmunity. Among a dozen putative $\beta$ cell autoantigens, glutamic acid decarboxylase (GAD) has bee proposed as perhaps the strongest candidate in both humans and the NOD mouse. In the NOD mouse, GAD, as compared with other $\beta$ cell autoantigens, provokes the earliest T cell proliferative response. The suppression of GAD expression in the $\beta$ cells results in the prevention of autoimmune diabetes in NOD mice. In addition, the major populations of cells infiltrating the iselts during the early stage of insulitis in BB rats and NOD mice are macrophages and dendritic cells. The inactivation of macrophages in NOD mice results in the prevention of T cell mediated autoimmune diabetes. Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of $\beta$cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. CD4+ and CD8+ T cells are both believed to be important for the destruction of $\beta$ cells. These cells, as final effectors, can kill the insulin-producing $\beta$ cells by the induction of apoptosis. In addition, CD8+ cytotoxic T cells release granzyme and cytolysin (perforin), which are also toxic to $\beta$ cells. In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the $\beta$ cells in conjunction with $\beta$ cell autoantigens and MHC class I and II antigens, resulting in the onset of autoimmune type I diabetes.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.7
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• pp.973-979
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• 2005

To investigate the effect of Pinus densiflora on biochemical parameters in type I diabetic rats, we evaluated the changes of body weight, fasting blood glucose level, oral glucose tolerance test (OGTT) and biochemical parameters after the intraperitoneal injection of distilled solution of Pinus densiflora in streptozotocin (STZ)­induced rats. Thirty-seven male Sprague Dawley rats $(180\pm10g)$ were divided into four groups; diabetic mellitus (DM) group received STZ (50 mg/kg BW, i.v.); low level of pine extract (LP) group received Pinus densiflora (5 mg/kg BW, i.p.), high level of pine extract (HP) group received Pinus densiflora (10 mg/kg BW, i.p.) after the single injection of STZ (50 mg/kg BW, i.v.), respectively. Normal control (NC) group received saline. The change of fasting blood glucose level and OGTT were measured using glucocard II, and the change of biochemical parameter were measured by Automatic Chemistry Analyzer (Hitach-747, Japan). Mean body weight change of DM group was retarded greatly by STZ-exposure. While, body weights of LP and HP groups were progressively increased with some fluctuation, although the increase rates were slower than that of NC group. Fasting blood glucose levels of LP and HP groups were reduced by Pinus densiflora injection, although the fasting blood glucose levels were higher than that of NC group. The results of OGTT was significantly improved in both of LP and HP group compared to DM group. Increases of blood glucose, alanine aminotransferase (ALT), alkaline phosphatase (ALP) and blood urea nitrogen (BUN) levels by STZ-exposure were attenuated by the Pinus densiflora treatment (p<0.05). From the results, it was suggested that Pinus densiflora has a tendency to decrease STZ-induced toxicity in terms of monitoring fasting blood glucose, OGTT and some biochemical parameters of rat.