Diabetes & Metabolism Journal

Volume 28(3); June 2004

Review

Peroxisome Proliferator-activated Receptors (PPARs) in Diabetic Nephropathy.: Cheol Whee Park; Korean Diabetes J. 2004;28(3):149-159. Published online June 1, 2004

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Abstract PDF: No abstract available.

Editorial

Role of Osmotic Stress in the Development of Chronic Diabetic Complications.: Jaetaek Kim, Yeon Sahng Oh, Soon Hyun Shinn; Korean Diabetes J. 2004;28(3):160-163. Published online June 1, 2004

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Abstract PDF: No abstract available.

Original Articles

Alteration of Hypertonic Responses in Hyperglycemic Human Retinal Pigment Epithelial and Placental Cells.: Won Kun Park; Korean Diabetes J. 2004;28(3):164-176. Published online June 1, 2004

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Abstract PDF: BACKGROUND
In mammals, cellular protection from hypertonic damage is achieved by increasing the expression of genes, such as aldose reductase(AR) and Na+/myo-inositol transporter(SMIT). Recent studies have revealed that tonicityresponsive enhancer binding protein(TonEBP) regulates the increased transcription of these genes. Increased AR gene expression leads to hyperglycemiainduced cellular impairment, and the degree of basal aldose reductase gene expression influences the development of diabetic complication. The alteration of cellular protection genes, such as AR, SMIT, HSP(Heat Shock Protein) 70 and TonEBP, from hypertonic stress in the presence of sustained hyperglycemia was examined in human retinal pigment epithelial(hRPE) and placental cells. METHODS: After the cultures became confluent, the hRPE cells were exposed to 25mM glucose, 100mM NaCl or both for 1, 2 and 3 days. The expressions of AR, SMIT and HSP70 were determined by northern blot analysis. Decreased inductions of the hypertonicity in AR and SMIT mRNA were first evident after exposure to 25mM glucose after 1 day, achieving near maximal level after 3 days; however, no significant alteration in the HSP70 mRNA was noted at any time. For these reasons, the alteration of cellular protection genes, such as AR, SMIT and TonEBP, in hRPE and placental cells were examined after 3-days exposure to the various experimental conditions. The cells were incubated in serum-free media, containing 5.5 or 25mM glucose, 100mM NaCl(in hRPE cells) or 75mM NaCl(in placental cells) and 25mM glucose+100mM NaCl(in hRPE cells) or 75mM NaCl(in placental cells), with or without 20muM tolrestat for 72hrs, at which time the expressions of AR, SMIT and TonEBP were determined. To examine the role of cellular ionic strength in hyperglycemic hRPE cells, excess(5mM) betaine was added to the medium to accelerate the accumulation of the compatible osmolyte, which should lead to a strength reduction. RESULTS: In the hRPE and placental cells, incubated in media with 25mM glucose+100mM(in hRPE cells) or 75mM(in placental cells) NaCl, the AR and SMIT mRNA levels were decreased compared to those cells incubated in media with 100mM(in hRPE cells) or 75mM(in placental cells) NaCl alone. Significant prevention of these decreased AR and SMIT mRNA levels were also observed in those cells incubated with tolrestat. The addition of betaine reduced the abundance of AR and SMIT mRNA in hypertonic stress, similar to in hypertonic and hyperglycemic cells. The inhibition of aldose reductase due to tolrestat in hyperglycemic and hypertonic media was complete in the media not containing betaine. CONCLUSION: Under conditions where sorbitol rapidly increases in hypertonic and hyperglycemic medium should be an important new system for exploring the mechanism of cellular impairment to the effects of hyperglycemia. The expressions of AR and SMIT genes that may influence the development of diabetic complication were down-regulated by the intracellular accumulation of sorbitol in sustained hyperglycemia, and the reliable effect of AR inhibitors on the biological improvements were verified in hyperglycemic cells.

Characteristics of the Newly Established Diabetic Model Mice, TallyHo.: Sang Dal Rhee, Won Hun Jeong, Yoon Young Sung, Hye Sung Lee, Kun Bock Lee, Hee Yeon Kim, Sung Don Yang; Korean Diabetes J. 2004;28(3):177-186. Published online June 1, 2004

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Abstract PDF: BACKGROUND
TallyHo(TH) mice are a newly established model for non-insulin dependent diabetes mellitus(NIDDM), for polygenic causative genes that have not yet been identified. It has been reported that TH mice show mild obesity, hyperinsulinemia, hyperlipidemia and male-limited hyperglycemia. The characteristics of these mice were examined. METHODS: Diabetes related physiological data of TH mice, such as body weight, the plasma concentration of biochemical parameters(glucose, triglyceride and nonesterified free fatty acid) and changes in the pattern of the oral glucose tolerance test(OGTT), were obtained up to the age of 35 weeks. The insulin tolerance test(ITT) was performed at 7 weeks of age and the weights of the fat pad and liver were measured at 35 weeks of age. RESULTS: TH mice revealed hyperlipidemia, glucose intolerance and disturbed insulin tolerance, even when prediabetic at 7 weeks of age. Hyperglycemia and hyper- insuline-mia were observed as early as 10 weeks of age; however, individual variations in the blood glucose level were large at this age. Obesity in TH mice seems to be caused by the predominant deposition of visceral fat. CONCLUSION: These results suggest that TH mice are an appropriate rodent model for diabetes with visceral obesity and insulin resistance.

High Carbohydrate Diet Effects on the Development of Diabetes Mellitus and Modification of Pancreatic Islets in OLETF Rats.: Sung Ki Kim, Seong Bin Hong, Hwi Ra Park, Eun A Kim, Kyung Wook Lee, Moon Suk Nam, Yong Seong Kim; Korean Diabetes J. 2004;28(3):187-198. Published online June 1, 2004

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Abstract PDF: BACKGROUND
Diet has long been believed to be an important risk factor for type 2 diabetes. The composition of carbohydrates in the diet was higher in the past, where as now it is considerably reduced in the diet of Korean peoples, which is probably associated with the risk of developing type 2 diabetes. The aim of the present study was to investigate the long-term effect of high carbohydrate/low protein diets on the glucose and lipid metabolism and the pancreatic islet in OLETF(Otsuka Long-Evans Tokushima Fatty) rats, the animal model of type 2 diabetes. METHODS: Seven week old male OLETF rat were fed a high carbohydrate/low protein diet(carbohydrate 71.0%, fat 14.5%, protein 14.5%) as the experimental group, with an ordinary chow diet(carbohydrate 63.5%, fat 14.5%, protein 22%) fed to the controls. The plasma insulin, lipid profiles, free fatty acid and oral glucose tolerance were analyzed at 16 and 32 weeks. After the glucose tolerance test, the pancreas was excised, and immunohistochemical staining was conducted for the islet morphology and insulin mRNA to quantify the insulin secretory capacity. RESULTS: The basal glucose levels tended to be higher in the control group, but with no significant statistical difference. There were no differences in the serum insulin, total cholesterol, triglyceride, HDL-cholesterol and plasma free fatty acid levels between the two groups. The pancreatic islets of the control group showed multilobulation, with fibrotic changes; where as those of the experimental group were maintained normal profiles. A higher expression of insulin mRNA was observed in the experimental than in the control group. CONCLUSION: A high carbohydrate diet induced lower body weight increases, and protected against beta cell injury and decreased the development of abnormal glucose tolerance in OLETF rats. This may explain the growing incidence of diabetes with respect to the change in carbohydrate composition in the diet of Korean peoples. However, whether the protective effect of a high carbohydrate diet, against the development of diabetes in OLETF rats, can be attributed to small weight increases or if the change in food composition itself, or both needs to be determined.

Study on the Methylglyoxal-induced Apoptosis in Bovine Retinal Pericytes.: Jaetaek Kim, Seok Hong Lee, Jang Won Son, Jeong An Lee, Yeon Sahng Oh, Soon Hyun Shinn; Korean Diabetes J. 2004;28(3):199-207. Published online June 1, 2004

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Abstract PDF: BACKGROUND
One of the histopathological hallmarks of early diabetic retinopathy is the loss of pericytes. Evidences suggest that this pericyte loss in vivo is mediated by apoptosis. However, the underlying cause of pericyte apoptosis is not fully understood. This study investigated the influence of methylglyoxal(MGO), a reactive alpha-dicarbonyl compound of glucose metabolism, on the apoptotic cell death in retinal pericytes. METHODS: Primary cultures of retinal pericytes were prepared from isolated bovine retinal microvessels. The cells were incubated under normoglycemic conditions after treatment with 200-800muM methylglyoxal for 6 hours. The cell viability was assessed using the MTT assay. The apoptosis and intracellular reactive oxygen species(ROS) generation were measured using an ELISA kit and flow cytometry, respectively. The NF-kappaB activation was detected by immunocytochemistry. RESULTS: MGO produced a progressive cytotoxic effect on the retinal pericytes. An analysis of the internucleosomal DNA fragmentation by ELISA showed that MGO(200 to 800muM) induced apoptosis in a concentration-dependent manner. ROS were generated earlier and the antioxidant, N-acetyl cysteine, inhibited the MGO-induced apoptosis. The NF-kappaB activation and increased caspase-3 activity were detected. The apoptosis was also inhibited by the caspase-3 inhibitor, Z-DEVD-fmk, or the NF-kappaB inhibitor, pyrrolidine dithiocarbamate. CONCLUSION: These results suggest that the elevated MGO levels observed in diabetes may cause apoptosis in the retinal pericytes through an oxidative stress mechanism, and suggests that the nuclear activation of NF-kappaB is involved in the apoptotic process.

Evaluation of Glycemic Control in Type 2 Diabetic Patients have been Treated in General Hospital.: Joung Ho Park, Kwan Woo Kim, Eun Jin Kang, Tak Young Kim, Sa Ra Lee, Su Chan Bae, Mi Kyung Kim, Sin Yeong Choi, Jeong Hyun Park; Korean Diabetes J. 2004;28(3):208-218. Published online June 1, 2004

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Abstract PDF: BACKGROUND
Good metabolic control is one of the most important parts of managing diabetes. Several studies in western countries have shown glycemic control in type 2 diabetic patients to be poorer than expected. Similar reports in Korea are very limited. Therefore, this study was performed to estimate the degree in glycemic control of type 2 diabetic patients that have been treated in general hospitals in Korea. METHODS: This was a cross-sectional retrospective study conducted on 1012 type 2 diabetic patients treated at the Maryknoll Hospital. Subjects with type 1 diabetes or a treatment duration of less than 6 month were excluded. The glycemic control was estimated by HbA1c and the clinical characteristics, including duration of diabetes, age, height and body weight, checked. The treatment methods were divided into four groups, namely diet, oral hypoglycemic agent, insulin alone, and insulin and oral hypoglycemic agent combination. Data were analyzedsed by SPSS version 11.0. RESULTS: The mean age, BMI, duration of diabetes and HbA1c of the subjects were 61.6+/-9.8 years, 24.6+/-3.2kg/m(2), 12.1+/-6.5 year and 7.6+/-1.3%, respectively, and the percentage of those achieving the goal of glycemic control(HbA1c<7%) was 35.7%. Those who achieved glycemic control were older than those who could not and also had a shorter duration of diabetes(p<0.001). There were no significant differences in the BMI, gender and HbA1c levels before treatment between the four groups. The subjects on diet treatment had a lower mean HbA1c level than those on insulin alone or combined therapy(p<0.05) CONCLUSION: The percentage of type 2 diabetic patients in good glycemic control in our general hospital was less than 40%, which was similar to previous western data. It is our suggestion that a large nationwide study is required to more accurately evaluate the state of glycemic control and find the reasons why certain patients could not reach this goal.

A Case of Renal Subcapsular Abscess Complicated with Psoas Abscess and Femoral Vein Thrombosis in Diabetic Patient.: Eun Ha Chae, Ki Hoon Kang, Byung Soo Lee, Myung Chan Kim, Jae Il Jung, Hee Jong Chang, Sun Hee Park; Korean Diabetes J. 2004;28(3):219-224. Published online June 1, 2004

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Abstract PDF: Psoas abscesses are rarely encountered with various etiologies and nonspecific clinical presentation, frequently resulting in delayed diagnosis, with increased morbidity and mortality. They are divided into primary when the origin is not found and secondary when a focus for infection spreading is detected. Herein, an unusual case of venous thrombosis and a psoas abscess, complicated by a renal subcapsular abscess, is reported in a diabetic patient. A 60-year-old female presented with fever and generalized weakness of 1 week duration. She had been diagnosed with diabetes 6 years earlier, but had only received intermittent oral antidiabetic agents. Abdominal sonography and CT showed a left renal subca-psular abscess and a right psoas abscess. A percutaneous drainage catheter was inserted and IV antibiotic was started immediately. Both cultures of the pus and urine showed K. pneumoniae. During treatment, the patient developed a right femoral vein thrombosis.

A Case of Newly Diagnosed Type 2 Diabetes Mellitus Presenting with Rhinocerebral Mucormycosis.: Jung Hwa Jung, Jong Ryeal Hahm, Mi Yeon Kang, Sung Won Moon, Tae Sik Jung, Deok Ryong Kim, Soon Il Chung; Korean Diabetes J. 2004;28(3):225-230. Published online June 1, 2004

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Abstract PDF: Rhinocerebral mucormycosis(RM) is a rare opportunistic fungal infection that mainly occurs in immunocompromised or diabetic patients, but rarely in healthy indi-viduals. This fungal infection usually begins at the nose and progresses through the paranasal sinuses, and secondarily invading the orbit and central nervous system. Because of its rapid progression and high mortality, early diagnosis and treatment are crucial to increase the patient survival rate. A combination of ampho-tericin B administration and surgery is a standard repertoire of RM treatment. Herein, a case in which a 69-year-old male patient with type 2 diabetes mellitus, presentings as RM, is reported. This patient had never been diagnosed with diabetes mellitus until the diabetes and RM were identified by us using the oral glucose tolerance test, measurement of the glycated hemoglobin level and a paranasal sinus CT scan. The RM was further confirmed by a biopsy of an oral mucosal ulcerative lesion. This case suggests that RM can present in newly diagnosed type 2 diabetes patients.

A Case of MELAS(Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke-like Episodes) Syndrome Manifested by Diabetic Ketoacidosis.: Sung Hoon Jung, Eun Jung Kim, So Hi Im, Kang Ju, Kang hyun Choi, Seung Hyun Ko, Yu Bae Ahn, Ki Ho Song, Ho Young Son, Sung Kyung Park, Jeong Su Jun; Korean Diabetes J. 2004;28(3):231-237. Published online June 1, 2004

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Abstract PDF: MELAS(mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes) syndrome is a rare cause of mitochondrial encephalomyopathy, with variable clinical features, such as encephalomyopathy, lactic acidosis, stroke, diabetes, short stature, sensorineural hearing loss and basal ganglia calci-fication, etc. It can be confirmed by molecular genetic analysis that reveals the mitochondrial A3243G point mutation. Among the clinical manifestations in MELAS syndrome, diabetes mellitus is associated with impaired insulin secretion and often misdiagnosed type 1 diabetes. Herein, a rare case for the MELAS syndrome, with diabetes mellitus that came from ketoacidosis, is introduced. A 21-year-old woman, carried to the emergency department had a stuporous mentality. She was thin(BMI 16.1kg/m(2)), and had difficulty with her hearing capacity. According to the initial laboratory results, she showed the metabolic acidosis, hyperglycemia, ketonemia, and ketonuria. She was diagnosed as diabetic ketoacidosis and treated with insulin and hydration. Brain imaging from MRI, and a CT scan showed basal ganglia calcification, hemorrhagic infarction and diffuse brain atrophy. The markers for beta-cell autoimmunity were negative. Her electromyography suggested proximal myopathy. In addition, a molecular genetic analysis identified A3243G point mutation in the peripheral blood leukocytes from her, her mother and her sister.

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