Skip Navigation
Skip to contents

Diabetes Metab J : Diabetes & Metabolism Journal

Search
OPEN ACCESS

Previous issues

Page Path
HOME > Browse > Previous issues
9 Previous issues
Filter
Filter
Article category
Keywords
Authors
Volume 26(4); August 2002
Prev issue Next issue
Reviews
Diagnostic Criteria for Gestational Diabetes in Korean Women: Is New ADA Criteria Appropriate?.
Hak Chul Jang
Korean Diabetes J. 2002;26(4):221-228.   Published online August 1, 2002
  • 676 View
  • 16 Download
AbstractAbstract PDF
No abstract available.
Sex Hormone and Action of Insulin.
Yeon Ah Sung
Korean Diabetes J. 2002;26(4):229-237.   Published online August 1, 2002
  • 723 View
  • 16 Download
AbstractAbstract PDF
No abstract available.
Editorial
Endothelial Dysfunction in Type 2 Diabetes: Role of Alpha-lipoic Acid, an Antioxidant.
Ki Ho Song, Joong Yeol Park
Korean Diabetes J. 2002;26(4):238-241.   Published online August 1, 2002
  • 757 View
  • 16 Download
AbstractAbstract PDF
No abstract available.
Original Articles
The Effect of Alpha-lipoic Acid on Endothelial Dysfunction in Postmenopausal Uncomplicated Type 2 Diabetes.
Ho Chan Cho, Sang Jun Lee, Mi Jung Kim, Hye Sun Kim, Tae Sung Yun, Sung Jae Kim, Sang Hyon Kim, Seung Ho Hur, Kyo Chul Moon, Jae Hoon Bae, In Kyu Lee
Korean Diabetes J. 2002;26(4):242-252.   Published online August 1, 2002
  • 1,370 View
  • 19 Download
AbstractAbstract PDF
BACKGROUND
Recently, increased oxidative stress has been proposed as a major cause of vascular complications of patients with diabetes mellitus. Increased generation of oxygen free radicals in patients with diabetes mellitus could deplete cellular antioxidants and inactivate endothelial dependent vasodilating factor (EDRF), such as nitric oxide (NO). The purpose of this study was to evaluate whether the antioxidant alpha-lipoic acid (ALA) is effective in endothelial dysfunction of brachial artery, which induced by increased oxidative stress in postmenopausal diabetic women using high resolution ultrasound technique and initial reaction time (IRT) measurement. METHODS: We enrolled 11 menopausal women (mean age, 56.5+/-5.1 years) with uncomplicated type 2 diabetes. All patients were taking 1200 mg of ALA (Thioctacid(R), Bukwang, Korea). We measured of superoxide anion (O2-) in neutrophils as a marker of oxidative stress. Flow-mediated dilation (FMD) was measured using a high-resolution ultrasound. RESULTS: After treatment of ALA, fasting blood glucose was decreased significantly, the endothelium-dependent vasodilation of the brachial artery was increased, and O2- production was also decreased significantly. CONCLUSION: These results show that short term ALA treatment could improve the endothelial dysfunction in patients with type 2 diabetes mellitus. This improvement might be related with the antioxidants effect of ALA.
Effect of Leptin on Alteration of beta-cell Mass in Rat Pancreas.
Seong Bin Hong, Yu Mi Han, Young Ju Park, Yun Joo Oe, Sung Ki Kim, Yoe Joo Kim, Moon Suk Nam, Yong Seong Kim, In Sun Park
Korean Diabetes J. 2002;26(4):253-264.   Published online August 1, 2002
  • 1,012 View
  • 16 Download
AbstractAbstract PDF
BACKGROUND
Diabetes mellitus can occur when insulin secretion and action are inadequate in relation to blood glucose level. Several experiments recently reported that leptin and pancreatic beta-cells have functional axis to interact each other. The present study was aimed to investigate the role of leptin on regulation of beta-cell mass during neonatal period when they show a dynamic growth. METHOD: Leptin was injected intraperitoneally to rat neonates for 7 days from the second day after birth. Using the pancreas of the rat pups, immunohistochemical stain, in-situ hybridization and northern blot for insulin were done for analysis of beta-cell mass as well as for insulin synthesis and secretion. In addition, PCNA (proliferating cell nuclear antigen) was examined to assess the effect of leptin on islet cell proliferation. RESULT: 1) The weight gain and blood glucose levels showed no significant difference between leptin injected groups (0.1 mg/kg, 0.5 mg/kg) and control one. 2) The weights of pancreas were not different between both group. 3) Pancreatic islets of rat who received leptin 0.5 mg/kg were reduced in area and number than those of normal pups. They also showed the decreased beta-cell number per islet compared with control as well as leptin 0.1 mg/kg injected groups (59+/-49 vs 47+/-31 vs 31+/-21 per islet, p<0.05). 4) The beta-cell mass of rat who received leptin 0.5 mg/kg decreased but there was no significant difference. 5) The mRNA expressions of insulin were not different among control, leptin 0.1 mg/kg and leptin 0.5 mg/kg group. 6) The expression of PCNA as a proliferation marker showed no difference between control and leptin injected group. CONCLUSION: These results reflected that leptin negatively regulated neonatal islet cell growth occurring in normal rat pups, and resulted to relative decrease of beta-cell number compared to the untreated control. We, therefore, suggest that leptin may play the important role in beta-cell mass during neonatal period.
Effects of Hydrogen Peroxide on Insulin Secretion in Rat Pancreatic Islets.
Chul Hee Kim, Chan Hee Kim, Hyeong Kyu Park, Kyo Il Suh, Ki Up Lee
Korean Diabetes J. 2002;26(4):265-273.   Published online August 1, 2002
  • 1,811 View
  • 59 Download
AbstractAbstract PDF
BACKGROUND
It has been hypothesized that reactive oxygen species (ROS) are involved in the progression of beta cell dysfunction in both type 1 and type 2 diabetes mellitus. On the other hand, recent evidence suggests that ROS might be an integral component of intracellular signaling. This study was undertaken to examine effects of hydrogen peroxide (H2O2) on insulin secretion by various secretagogues in isolated rat pancreatic islets. METHODS: Pancreatic islets from normal Sprague-Dawley rats were isolated by intraductal injection of collagenase and Ficoll-gradient centrifugation. Isolated islets were treated with H2O2 directly added to the culture media or continuously generated by glucose-glucose oxidase system for 24 hours. Insulin secretion stimulated by glucose, arginine, and KCl was measured by radioimmunoassay. RESULTS: Basal insulin secretion was increased after treatment with H2O2. Treatment with low concentration of H2O2 stimulated insulin secretion in response to 27 mM glucose. In contrast, insulin secretion stimulated by 27 mM glucose was significantly decreased after treatment with high concentrations of H2O2. Arginine- stimulated insulin secretion was increased by both low- and high concentrations of H2O2. Insulin secretion stimulated by KCl was not affected by treatment with H2O2. CONCLUSION: These results suggest that the effect of H2O2 is diverse according to its concentration and different insulin secretagogues. In particular, H2O2 has a dual action on glucose-induced insulin secretion. At low concentration, H2O2 can stimulate insulin secretion probably by acting on signaling pathway of stimulus- secretion coupling. In contrast, high concentrations of H2O2 impairs glucose- induced insulin secretion, probably by acting as an oxidative stress.
The Role of Akt-1/PKBalpha on Insulin Action in 3T3-L1 Adipocyte.
Jung Min Lee, Hyun Shik Son, Hyuk Sang Kwon, Seung Ki Kwack, Seung Hyun Ko, Sang Ah Chang, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Prem Sharma
Korean Diabetes J. 2002;26(4):274-285.   Published online August 1, 2002
  • 1,080 View
  • 18 Download
AbstractAbstract PDF
BACKGROUND
S: Akt/PKB as a serine/threonine kinase is stimulated by insulin and other growth factors. And insulin stimulates glucose uptake by promoting the translocation of glucose transporter 4 (GLUT4) to the cell membrane. But, it is not clear that Akt/PKB, a downstream target of PI 3-kinase, is involved in glucose uptake pathway. In this study, we investigated the role of Akt/PKB, especially Akt-1, on insulin action in 3T3-L1 adipocyte. METHODS: We made recombinant Ad5.Akt-1 vector by the insertion of Akt-1 gene to adenoviral vector. And then, we overexpressed Akt-1 proteins(wild type and kinase inactive type) in 3T3-L1 adipocytes by using a adenoviral transfection method. We observed the changes of glucose uptake, glycogen synthesis, activities of mitogen-activated protein kinase (MAPK, also called extracellular signal-regulated kinase), p70 ribosomal s6 protein kinase (p70s6k), and glycogen synthase kinase 3 (GSK3) according to Akt-1 activity and insulin treatment. RESULTS: First, overexpression of Akt-1 did not affect to glucose uptake, whether insulin stimulates or not. Second, overexpression of Akt-1 did not affect the phosphorylation of p44/42-MAPK, either. Third, the glycogen synthesis was increased by overexpression of Akt-1. CONCLUSION: Akt-1 activation is necessary for glycogen synthesis, but is not essential for glucose transport in 3T3-L1 adipocytes.
Effect of Transforming Growth Factor-Induced Gene Product, beta ig-h3 on Proliferation, Migration, and Adhesion of Aortic Smooth Muscle Cells Cultured in High Glucose.
Sung Woo Ha, Gui Hwa Jung, He Jin Yeo, Jong Sup Bae, Soon Hee Lee, Jung Guk Kim, Rang Woon Park, In San Kim, Bo Wan Kim
Korean Diabetes J. 2002;26(4):286-295.   Published online August 1, 2002
  • 915 View
  • 16 Download
AbstractAbstract PDF
BACKGROUND
Diabetes mellitus is associated with a substantial increase in the prevalence of atherosclerotic disease. There are many factors which are involved in development of these processes. Transforming growth factor (TGF-beta) is known to be an important factor in the pathogenesis of diabetic vascular complications. TGF-beta-induced gene-h3 (beta ig-h3) is an adhesive molecule whose expression is induced by TGF-beta. Considering that TGF-beta plays an important role in diabetic complications and that beta ig-h3 is induced by TGF-beta, we hypothesized that beta ig-h3 may also play a role in the development of diabetic angiopathy. Then, we examined the effects of beta ig-h3 on biologic function of vascular smooth muscle cells (VSMCs) and potential roles of beta ig-h3 in the pathognesis of diabetic angiopathy. METHODS: VSMCs were isolated from rat thoracic aorta. We conditioned cells with different concentration of TGF-beta or glucose. We measured TGF-beta and beta ig-h3 protein in cell supernatant by ELISA. We also examined whether TGF-beta involves in high glucose-induced beta ig-h3 expression. Finally, we did proliferation, migration, and adhesion assay to investigate biologic function of beta ig-h3 in VSMCs. RESULTS: Our results demonstrated that TGF-beta induced beta ig-h3 expression in VSMCs in dose dependent manners. High glucose induced TGF expression as well as beta ig-h3 protein. Finally, beta ig-h3 was found to support the proliferation, migration, and adhesion of rat VSMCs. CONCLUSION: These results suggest that high glucose-and TGF-beta-induced beta ig-h3 may play an important role in diabetic angiopathy by regulating proliferation, migration, and adhesion of VSMCs.
Homeostasis Model Assessment In Korean Type 2 Diabetes Patients.
Hyun Ha Chang, Jin Woo Kim, Mee Suk Rhu, Cheol Young Park, Seung Joon Oh, Jeong Taek Woo, Sung Woon Kim, Young Seol Kim, Young Kil Choi
Korean Diabetes J. 2002;26(4):296-305.   Published online August 1, 2002
  • 1,013 View
  • 19 Download
AbstractAbstract PDF
BACKGROUND
Both insulin resistance and decreased insulin secretion have been known to be defects causing type 2 diabetes. However, decreased insulin secretion rather than insulin resistance has been suggested to be a more important factor in development of type 2 diabetes in Korea. Thus, we undertook this study to evaluate insulin resistance and beta cell function in Korean type 2 diabetes patients. METHODS: Retrospectively, we applied HOMA model to 1,233 type 2 diabetes pateints (575 males and 658 females) and assessed HOMA(beta cell) function and HOMA(IR). RESULTS: The HOMA(IR) of Korean male was 2.6 (0.05~39.53) and that of Korean female was 3.1 (0.04~53.54), and the HOMA(beta cell) of male was 22.3 (0.2~873.8)%, and that of female was 30.6 (0.37~1738.3)%. There was no significant difference. There was no significant correlation between HOMA(IR) and age and duration of diabetes, but there was significant correlation between HOMA(beta cell) and BMI, 0 min, 30 min insulin level and 0 min C-peptide level in oGTT. In the group of high HOMA(IR) than lower HOMA(IR), HOMA(beta cell) have more strong correlation with age at dignosis, BMI, duration of diabetes, FBS, 0 min and 60 min insulin, 0 min C-peptide and 24 hour urine C-peptide. CONCLUSION: In comparison with HOMA Model of San Antonio Heart Study, the HOMA(beta cell) and HOMA(IR) of Korean were lower, so the HOMA(beta cell) and HOMA(IR) may be different between ethnic groups. And further prospective analysis for the evaluation of insulin resistance and insulin secretion defect with HOMA model should be done in Korean type 2 diabeties.

Diabetes Metab J : Diabetes & Metabolism Journal
Close layer