Diabetes & Metabolism Journal

Volume 25(4); August 2001

Review

Prevention of Diabetes Mellitus: Including Review of Finnish Diabetes Prevention Study and Diabetes Prevention Program.: Doo Man Kim; Korean Diabetes J. 2001;25(4):251-257. Published online August 1, 2001

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Abstract PDF: No abstract available.

Editorial

Type II Diabetes and Uncoupling Protein.: Woong Hwan Choi; Korean Diabetes J. 2001;25(4):258-261. Published online August 1, 2001

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Abstract PDF: No abstract available.

Original Articles

Polymorphism of the Uncoupling Protein 1 (UCP-1) Gene and Fatty Acid Binding Protein 2 (FABP2) Gene in Korean Type 2 Diabetic Patients.: Sun Gyu Kim, Chul Hee Kim, Seog Ki Yun, Yeo Il Yun, Yong Hyun Kim, Il Song Nam, Ju Young Lee, Ji O Mok, Hyeong Kyu Park, Young Sun Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo; Korean Diabetes J. 2001;25(4):262-272. Published online August 1, 2001

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Abstract PDF: BACKGROUND
It is well known that genetic component plays an important role in developing obesity and type 2 diabetes mellitus. A number of candidate genes have been suggested, but the major gene determining the development of obesity and type 2 diabetes has not yet been uncovered. Previous studies suggest that polymorphisms of the intestinal fatty acid binding protein (FABP2) and uncoupling protein 1 (UCP-1) gene were related with obesity and/or insulin resistance in several populations. METHODS: We examined 76 type 2 diabetic patients (aged 44+/-6 years) and 96 healthy controls (aged 25+/-3 years). Ala54Thr polymorphism of the FABP2 gene and A to G polymorphism (-3826) of the UCP-1 gene were determined by polymerase chain reaction and restriction fragment length polymorphism method. RESULTS: The Thr54 allele of the FABP2 gene was found with a frequency of 0.33 in nondiabetic controls and 0.36 in type 2 diabetic patients. The genotype frequency of the Ala54Thr polymorphism was similar in nondiabetic and diabetic subjects ( 2=0.87, P=0.64). The -3826 G allele of UCP-1 gene was found with a frequency of 0.51 in nondiabetic controls, and 0.46 in type 2 diabetic patients. The genotype frequency of the -3826 A to G polymorphism was also similar in nondiabetic and diabetic subjects ( 2=1.46, p=0.46). When the subjects of each groups were subdivided into nonobese and obese group by BMI of 25 kg/m2, there was no significant difference in genotype frequencies of the UCP-1 and FABP2 gene polymorphisms. CONCLUSION: These results suggest that either the Ala54Thr polymorphism of the FABP2 gene or the A to G polymorphism (-3826) of UCP-1 gene do not play a major role in developing type 2 diabetes mellitus or obesity in Korean.

Effects of Aminoguanidine on Nitric Oxide Production, Insulin Release and Hsp 70 Expression in Cultured Rat Islets Exposed to IL-1betabeta.: Kyu Chang Won, Mi Jung Eun, Jae Hong Kim, Jung Hyun Oh, Sang Yub Nam, Ji Sung Yoon, Hyun Dae Yoon, In Ho Cho, Hyoung Woo Lee; Korean Diabetes J. 2001;25(4):273-285. Published online August 1, 2001

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Abstract PDF: BACKGROUND
IL-1beta has been implicated to play an important role in the autoimmune beta cell lesion of type 1 diabetes because of its inhibition of insulin secretion and direct islet cytotoxicity. Thus, this study evaluated the effect of aminoguanidine on No production, insulin release and hsp 70 expression in cultured rat islets exposed to IL-1beta. METHOD: Islets isolated from Sprague-Dawley rats were cultured with IL-1beta , aminoguanidine AG and GSNO, individually and in combination for 24hours. Accumulated nitrite production, insulin release and islet expression of hsp 70 were measured. RESULTS: IL-1beta increased nitrite production, inhibited insulin release, and increased hsp 70 expression. AG alone had no effect on nitrite production, insulin release and hsp 70 expression. In combination, AG completely blocked IL-1beta but increased nitrite production, reversed IL-1beta inhibited insulin release and reversed IL-1beta increased hsp 70 expression. Moreover, nitric oxide NO donor, GSNO stimulated hsp 70 expression. CONCLUSION: Findings from this study suggest that hsp 70 may be one potential protein that is expressed in response to NO and that participates in islet recovery from NO mediated islet damage.

Effect of Nerve Growth Factor on Cultured Mouse Dorsal Root Ganglion Cells in Hyperglycemic Condition.: Byoung Hyun Park, Chung Gu Cho, Geun Young Jang, Ki Hun Kim, Seung Taeck Park; Korean Diabetes J. 2001;25(4):286-296. Published online August 1, 2001

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Abstract PDF: BACKGROUND
Multiple etiology of diabetic neuropathy has been proposed, including altered polyol metabolism, superoxide radical formation, protein glycation, vascular insufficiency, blunted nitric oxide production and neurotrophic factor (NTF) deficiency. Nerve growth factor (NGF) is a member and family of neurotrophic factors. NGF is produced in tissues innervated by its responsive neurons. In the peripheral nervous system, NGF messenger RNA (mRNA) is produced in target fields of small pain and temperature-mediating dorsal root ganglia (DRG) sensory neurons and sympathetic neurons. NGF has been shown to promote their survival, differentiation, and maintenance. However, the mechanism of neuronal damage in diabetes and the effect of NGF on diabetic neuropathy are not clear. METHODS: In order to clarify the effect of NGF, the changes of cell viability were evaluated by MTT assay on mouse cultured dorsal root ganglion cells which were grown with media containing concentrations of high glucose for inducing hyperglycemic condition. Furthermore, the neuroprotective effect of nerve growth factor (NGF) against hyperglycemia-induced dorsal root ganglion cell changes were also examined. RESULTS: 1. Cell viability of cultured mouse dorsal root ganglion cells treated with hyperglycemic media made with 15, 25 mM glucose was markedly decreased in a dose-dependent manner when compared with control medium (normoglycemic medium) containing concentration of 5.5 mM glucose (p<0.05). 2. Cultured dorsal root ganglion cells exposed to hyperglycemic medium made with 25 mM glucose for 72 hours showed morphological changes such as dissociations, loss of neurites and decrease of cell viability (p<0.05). 3. Pretreatment of 150 ng/mL NGF for 2 hours significantly increased the cell viability of cultured dorsal root ganglion cells which exposed to hyperglycemic medium (25 mM glucose for 72 hours). CONCLUSION: Findings from this study suggested that hyperglycemic condition induces the decrease of cell viability and morphological changes (loss of neurites, dissociation) on cultured dorsal root ganglion cells of mouse. Furthermore, selective neurotrophic factors such as NGF are very effective in preventing dysfunction and morphological changes of DRG cells induced by hyperglycemic condition.

The Efficiency of Routine 99mTc-MIBI Myocardial SPECT for Detecting Silent IHD in Type 2 Diabetic Patients.: Duk Kyu Kim, Mi Kyoung Park, Do Young Kang; Korean Diabetes J. 2001;25(4):297-306. Published online August 1, 2001

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Abstract PDF: No abstract available.

Serum Uric Acid Levels and Insulin Resistance Syndrome in the People Living at Kijang County of Busan City.: Bo Young Yoon, Doo Geun Chai, Sung Mok Kim, Moon Suk Cho, Dong Joon Kim, Jeong Hyun Park, Byung Doo Rhee, Kyung Ho Lim, Chang Il Kang; Korean Diabetes J. 2001;25(4):307-315. Published online August 1, 2001

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Abstract PDF: BACKGROUND
Insulin resistance syndrome is defined as the constellation of central obesity, hypertension, glucose abnormality and dyslipidemia. Other constituents of insulin resistance syndrome have recently been reported including serum uric acid. Causative correlation between serum uric acid and insulin resistance syndrome is still not clear. We performed epidemiologic study to clarify its correlation with insulin resistance syndrome in the people living at Kijang district of Busan City. METHODS: We performed volunteer study of the people living at Kijang district of Busan City from 16th to 19th day of November in 1998 (n=232). Height, body weight, abdominal and hip circumference, and blood pressure were measured. We also measured fasting blood glucose, fasting serum insulin (Linco RIA), HDL-cholesterol, triglyceride, total cholesterol and serum uric acid. Insulin resistance was calculated by HOMA (homeostasis model assessment) method. RESULTS: Total number of subjects were 232 (male 61, female 171), and their mean age was 5.1+/-13.4 (years), BMI (body mass index) 23.4+/-3.2 kg/m2, and WHR (waist to hip ratio) 0.82+/-0.07. Mean HOMA-IR value derived from fasting blood glucose and insulin was 2.5+/-2.4, mean serum uric acid was 270+/-72 mol/L. The serum uric acid level showed positive correlation with BMI (r=.324), WHR (r=.403), log transformed triglyceride value (r=.135), systolic blood pressure (r=.181), diastolic blood pressure (r=.185) and negative correlation with HDL-cholesterol (r=-.185,p<0.01). Stepwise linear regression revealed that only serum creatinine, WHR and natural logarithmic value of triglyceride showed statistically independent correlation with serum uric acid level. CONCLUSION: Serum uric acid level in the people living at Kijang district of Busan City showed statistically significant correlation with other well-known constituents of insulin resistance syndrome. Thus, we may conclude that the level of serum uric acid can be regarded as the component of insulin resistance syndrome in the people living at Kijang district. However, its relationship with insulin resistance syndrome may be indirect.

Prevalence of Diabetes Mellitus in Pancreatic Cancer Patients.: Yu Jeong Park, Kwang Won Kim, Eun Young Oh, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Jong Kyun Lee, Kyu Taek Lee, Yong Il Kim, Yoon Ho Choi; Korean Diabetes J. 2001;25(4):316-322. Published online August 1, 2001

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Abstract PDF: BACKGROUND
Pancreatic cancer is a highly malignant tumor and its incidence has been significantly increased. It has well been known that pancreatic cancer patients had high prevalence of diabetes mellitus. But it is still controversial if diabetes predispose pancreatic cancer or it is an epiphenomenon of pancreatic cancer. Thus, the aims of this study was to investigate the prevalence of diabetes mellitus in pancreatic cancer patients in Korea, to characterize the diabetes mellitus in this situation, and to observe an association between the two conditions. METHOD: 275 pancreatic cancer patients admitted in Samsung Medical Center from January 1998 to December 2000 were selected for this study. We reviewed patients medical record and recorded diabetic history. Subjects who visited our Health Promotion Center in 1999 was used to evaluate the prevalence of diabetes mellitus. RESULT: 30% of pancreatic cancer patients had diabetes mellitus. 60% of diabetic pancreatic cancer patients had detected diabetes within recent two years. 25.6% of them had been known their diabetic state when they detected pancreatic cancer. There were no differences in smoking history, percent of distant metastasis, frequency of curative resection, and BMI between diabetic and nondiabetic pancreatic cancer patients. Significant weight loss was noted in pancreatic cancer patients with diabetes (p<0.01). CONCLUSION: The prevalence rate of diabetes in pancreatic cancer patient was significantly high. Pancreatic cancer patients with diabetes presented with much profound weight loss. Furthermore, more than half of the pancreatic cancer patients with diabetes had recent onset diabetes. Further investigations would be necessary to elucidate causal relation in the pathogenesis of diabetes and pancreatic cancer.

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