Diabetes & Metabolism Journal

Volume 21(2); June 1997

Original Articles

Pathogenesis of Diabetic Retinopathy.: Tae Wha Kim; Korean Diabetes J. 1997;21(2):115-121. Published online January 1, 2001

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Abstract PDF: No abstract available.

Modecular Approach in Vascular Disease.: In Kyu Lee; Korean Diabetes J. 1997;21(2):122-126. Published online January 1, 2001

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Non-Insulin Dependent Diabetes Mellitus andbeta3-Adrenergic Receptor Gene Polymorphism.: Hong Sun Baek; Korean Diabetes J. 1997;21(2):127-129. Published online January 1, 2001

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Abstract PDF: No abstract available.

Thebeta3-adrenergic Receptor Gene Polymorphism in Non-Insulin Dependent Diabetes Mellitus.: Ji Hyun Lee, Hai Ri Li, Sang Won Lee, Su Youn Nam, Young Jun Won, Bong Soo Cha, Moon Suk Nam, Young Duk Song, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh; Korean Diabetes J. 1997;21(2):130-137. Published online January 1, 2001

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Abstract PDF: BACKGROUND
The B3-adrenergic receptor, located mainly in adipose tissue, is known to be involved in the regulation of lipolysis and thermogenesis. Recently studies have shown that the B3-adrenergic receptor gene polymorphism is associated with Non-Insulin Dependent Diabetes Mellitus(NIDDM) and insulin resistance. We investigated the relationship between the B3-adrenergic receptor gene polymorphism and the cli!ical and biochemical features of NIDDM patients. METHODS: Anthropometeric and biochemi al characteristics were determined for 134 NIDDM subjects and 30 nondiabetic controls. All subjects were genotyped for the 0-adrenergic receptor gene mutation using restriction fragment length polymorphism assay. RESULTS: The allelic frequency of the mutated allele was similar in NIDDM subjects and nondiabetic controls(11%, 12% respectively). There was no difference in the Arg64 allelic frequency of the B3-adrenergic receptor gene according to the onset age of diabetes. In diabetic group, the clinical and biochemical characteristics were not statistically different between the B3-adrenergic receptor gene mutation and nonmutation group. In control group, also no clinical differences were found between mutation and non-mutation group. When comparing frequency of obesity according to the B3-adrenergic receptor gene mutation in diabetic patients, we did not find the difference between the two groups. CONCLUSION: These results suggest that the b3-adrenergic receptor gene is not a major determinant for the development of obesity and NIDDM in Korea.

Relationship between Angiotensin I Converting Enzyme Gene Polymorphism and Vascular complications in Non-Insulin Dependent Diabetic Patients.: Byoung Gue Na, Tae Geun Oh, Sang Moo Jung, Sang Woo Oh, Jae Hong Choi, Ji Hyun Lee, Seong Su Koong, Seung Taik Kim; Korean Diabetes J. 1997;21(2):138-146. Published online January 1, 2001

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Abstract PDF: No abstract available.

Mitochondrial DNA point mutations in Korean NIDDM patients.: Suk Kyeong Kim, Kyong Soo Park, Chan Soo Shin, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh; Korean Diabetes J. 1997;21(2):147-155. Published online January 1, 2001

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Abstract PDF: BACKGROUND
There are a few genes with proven potential for causing some form of NIDDM, These include the insulin gene, the insulin receptor gene, a gene linked to the adenosine deaminase gene on chrornosome 20, and the glucokinase gene. Recently, an A to G transition at position 3243 in transfer ribonucleic acid ""' ' was reported in maternally inherited NIDDM patients in Japan, it was reported that approximately 1% of diabetes patients have the 3243 bp point mutation. In this study we examined the positive rate and clinical characteristics of Korean NIDDM patients with mitochondrial DNA point mutation. METHODS: We screened randomly selected 433 NIDDM patients (rnale 221, female 212) from the diabetes clinic of Seoul National University Hospital regardless of age of onset, family history of diabetes, mode of' therapy, or any other clinical characteristics. Genomic DNA was extracted from pheripheral lymphocytes. To detect the 3243 bp mutation, PCR was carried out using mtDNA primers(2928-2947, 3558-3539) and then, PCR products were electro-phoresed on a 2%: agarose gel after digestion with the restriction endonuclease Apa-I. When electrophoretic results showed two or three bands, we confirmed mtl)NA 3243 bp point rnutation by DNA sequencing. RESULTS: Of the 433 Korean NIDDM patients, 5 patiients had mtDNA point mutation digested by restriction endonuclease Apa I. Only two patients (OA6%) had heteroplasmic point mutation at nucleo-tide 3243. The remaining three patients(0.69%) with homoplasmic point mutation at nt 3426 were inciden-tally discovered during procedure in detecting 3243 bp point mutation. This 3426 point rnutation had the same adenine to guanine point mutation as 3243 point mutation digested by Apa I and therefore was confused with 3243 point mutation by RFLP method. Two patients with 3243 points mutation, aged 39 and 32 years, BMI 17.0 and 14.4(kg/m), had neither hearing impairrnent nor family history of diabetes. They required insulin for the control of their hyperglycemia and their C-peptide levels less than 1.Ong/mL showed insulin dependent tendency. On the contrary, three patients with 3426 bp point mutation, aged 71, 70, and 62 years, BMI 28.0, 23.0, and 22.6 (kg/m2 ), showed their C-peptide levels 5.4ng/mL and 3.%g/mL and insulin resistant diabetes mellitus. CONCLUSION: Two kinds of point mutation were found in the mtDNA at position nt 3243 and nt 3426, and their incidence were 0.46%(2/433) and 0.69% (3/433) respectively. 3243 point mutation was associated with insulin deficient diabetes mellitus whereas 3426 point mutation insulin resistant diabetes mellitus. 3426 point mutation has the same adenine to guanine transition as 3243 point mutation restricted by Apa I and so, DNA sequencing is warranted to differentiate with 3426 from 3243 point mutation.

Effect of high glucose on function of cultured rabbit vascular endothelial cells.: Seok Man Son, In Ju Kim, Yong Ki Kim, Chi Dae Kim, Ki Whan Hong; Korean Diabetes J. 1997;21(2):156-167. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Vascular disease accounts for the majority of the clinical complications of diabetes mellitus. Changes in local control of vascular tone such as imbalanced production of relaxing and contracting factors by endothelium may be related to the initiation and maintenance of abnormal vascular reactivity characteristically seen in diabetic vascular complications. Cytokines and growth factors released from injured endothelial cells, T-cells, and macro-phages enhance atherogenesis. In this study, we examined NO and TNF-a released from cultured rabbit aortic endothelial cells(RAECs) under different glucose concentration to investigate the relationship between high glucose and endothelial cell dysfunction. METHODS: The thoracic and abdominal aortae of rabbit(23kg) were isolated and periadventitial connective tissue was carefully removed. Rabbit aortic endothelial cells in primary culture were prepared by the m.ethod of Schwartz with modification. RAECs were grown to confluence in 25 cm2 flask in DMEM supplemented with 20% FBS, 150pg/mL endothelial cell growth supplernent, 90pg/mL heparin, 100 U/mL penicillin and 100pg/mL streptomycin at 37'C in humidified 5% carbon dioxide in air. For experiments, confluent cells were replaced in 1 1 mm, 48 well plate containing same medium composition. Cells were then incubated in the presence or absence of FBS for various times up to 48 hours(time course) to eveluate the NO and TNF-a response to different glucose concentrations(0, 5.5, 11, 22, and 44 mmol/ L). Cells were also incubated with various concentration of ACH and ADP(10, 10', 10 and 10' mol/L) and 10' mol/L of ACH or ADP with different glucose concentrations for 24 hours to evaluate stimulated effect of ACH and ADP on NO release. RESULTS: 1) Total NO release from RAECs was significantly in a time-dependent. After 48 hours incubation, the total secretion of NO was significantly higher in culture medium with FRS than without FBS. 2) Glucose concentration resembling severe hyper-glycemic conditions(22 and 44 mmol/L) significantly inhibited NO release from RAECs, 3) Acetylcholine and ADP induced a clear dose-dependent NO release in RAECs. 4) Stimulation of acetylcholine and ADP on NO release according to different glucose concentration was not significantly higher than NO release in culture medium with glucose alone. 5) The increment in TNF-a levels was associated with a significant increase at higher glucose concentration, 6) There was a negative correlation between NO and TNF-a release in culture medium with FBS but not in culture medium without FBS. CONCLUSION: Our data show that decreased NO release and increased TNF-a release from RAECs were noted under high glucose concentration. Such interaction could play a significant role in the development of diabetic vascular complication in hyperglycernic conditions.

Mechanism of Insulin Resistance : Time Dependence of the Development of Insulin Resistance in High Fat Fed Rats.: Kyong Soo Park, Ki Up Lee, Sung Woo Park, Hong Kyu Lee, Hun Ki Min; Korean Diabetes J. 1997;21(2):168-175. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Increased FFA availability is known to induce insulin resistance by decrease in peripheral glucose utilization and increase in hepatic glucose procluction. However, there are conflicting results about the time dependence of the developrnent of insulin resistance with increased availability of FFA. METHODS: To elucidate the time dependence of the development of insulin resistance associated with increased availability of FFA, peripheral glucose utilization rate and hepatic glucose production rate were measured by euglycemic hyperinsulinemic clamp with 3-3H glucose infusion in rats fed high fat diet (1 week or 3 weeks) or control diet(ordinary chow diet). RESULTS: Basal plasrna FFA levels and steady state plasma insulin levels increased after high fat diet. After 1 week of high fat diet, suppressibility of hepatic glucose production rate by insulin was impaired(p<0.05 vs control). Insulin sensitivity index(glucose utilization rates/steady state plasma insulin concentrmtions X100) was decreased only after 3 weeks of high fat diet(p<0.05 vs control) which was accompanied by decreased glycogen synthase activity. CONCLUSION: High fat diet induces hepatic insulin resistance before peripheral insulin resistance and decreased glycogen synthase activity may contribute to the development of peripheral insulin resistance in rats fed high fat diet.

Urinary albumin excretion, von Willebrand factor and macrovascular disease in patients with NIDDM.: Sin Gon Kim, Soo Mi Kim, Dong Hyun Shin, Nan Hee Kim, Yoon Sang Choi, Ie Byung Park, Sei Hyun Baik, Dong Seop Choi; Korean Diabetes J. 1997;21(2):176-184. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Increased urinary albumin excretion (UAE) is not only an independent predictor of progressive renal disease but also an important marker of atherosclerotic disease in patients with NIDDM. However, the pathaphysiologic basis of this observation is poorly understood. Recently, one interesting hypothesis suggested: UAE rnerely reflects a glomerular manifestation of an otherwise generalized vascular dysfunction(hyperpermeable state), and Stehouwer et al. Reported a strong relationship between plasma von Willebrand factor level(a measure of endothelial dysfunction), UAE and cardiovascular diseases. Therefore, we studied the relationship between UAE, plasma vWF and macrovascular disease in patients with NIDDM. METHODS: We measured UAE and plasma vWF levels in 102 patients with NIDDM, and investigated the telationship between these values and macrovascular diseses. Also, we assesed the risk factars for macrovascular disease. RESULTS: 1) Among total of 102 patients, nonnoalbuminuria, microalbuminuria and macroalbuminuria group were 58 patients(56.9%), 28 patients(27.5%) and 16 patients(15.6%), respectively. 2) The prevalencies of hypertension, diabetic retinopathy and macrovascular diseases were the highest in macroalbuminuria group, followed by microalbuminuria and norrnoalbuminuria group in order of frequency. 3) Plasma vWF and UAE levels were significantly correlated(r=0.44). 4) Plasma vWF concentrations were higher in patients with macrovascular diseases than in those without macrovascular diseases, and also higher in patients with retinopathy compared with those without retinopathy. 5) Multivariate logistic regression analysis showed that age, smoking and vWF were independent risk factors for macrovascular diseases. CONCLUSION: 1) As plasma vWF and UAE values were increased, more macrovascular diseases were observed in patients with NIDDM. 2) Plasma vWF may be used as an indicator of macrovascular disease in patients with NIDDM.

The Effect of Metformin Monotherapy in Patients with NIDDM.: Yu Bae Ahn, Sung Dae Moon, Sang Ah Jang, Jong Min Lee, Hyun Shik Son, Kun Ho Yoon, Moo Il Kang, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang; Korean Diabetes J. 1997;21(2):185-193. Published online January 1, 2001

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Abstract PDF: BACKGROUND
We performed this study to investigate the effect of metformin on glycemia, insulin secretion and body weight in patients with non-insulin-dependent diabetes melltus(NIDDM) who could not aehieve satisfactory glycemic control by sulfonylurea or diet therapy. METHODS: A total of 167 patients with NIDDM were included in this study. At baseline the patients underwent anthropometry and a 75g oral glucose tolerance test. Jn addition, levels of hemoglobin Alc (HbAlc), setum lipids, fasting and postprandial 2hr glucose were measured. Metformin was given in an initial dose of 500mg twice daily and increased by 500mg every month as long as the fasting blood sugar(FBS) concentration exceeded 7.8mmol/L and the side effects were tolerable. After 3 rnonths of metformin therapy we defined a responder as a patient who experienced a FBS of under 7.8 mmol/L or a HbAlc of under 7%. Patients who failed to respond to metformin monotherapy were excluded in the study. Anthrapometric changes and results of a 75 g oral glucose tolerance test were reevaluated in the responder group after 6 months of metformin treatment. RESULTS: I) The overall response rate to metformin mono-therapy was 55.6%(79/142) in the study population. 2) There were significant changes in body weight (64.4+/-8.2 vs 62.9+/-8.4 kg, p(0.01) and body mass index(25.3+/-2.3 vs 24.6+/-2.3kg/m, p<0.01) during metformin treatment. 3) There were significant decreases in the fasting, postprandial 2hr serum glucose(10.1+/-2.8 vs 7.9+1.6, 15,2+/-5.0 vs 12.2+/-3.9 mmol/L, p 0.01) and HbAlc levels(8.4+/-1.7 vs 6.5+/-0.9%, p<0.05) after 6 months of metformin treatment. 4) There were significant decreases in the levels of AUC[g](59.2+/-15.5 vs 49.4+/-9.4mmol L-1. Min-1, p =C0.01) without changes of AUC[I] and AUC[I]/ AUC[g] ratio (558.0+486.0 vs 536.4+374.4 pmol.L-1. Min-1, p=0.71, 11.7+/-13.0 vs 11.8+/-10.0, p=0.89). 5) The incidence of side effects was 25% in the study population, but most of them were mild and fade away with continuous use of metformin, CONCLUSION: Metforrnin monotherapy improved glycemic control in NlDDM patients who failed to respond to diet or sulfonylurea therapy and may be a useful hypoglycemic agent for the treatment of NIBDM.

Prognostic Factors in the Elderly Diabetic Hyperosmolar Non-ketotic Coma.: Min Sook Park, Hyung Joon Yoo, Sun Hwa Jung, Kwon Yeop Lee, Cheol Soo Park, Cheol Hong Kim, Hyun Gyu Kim, Jae Myeog Yoo, Du Man Kim, Sung Hee Ihm, Moon Gi Choi, Sung Woo Park; Korean Diabetes J. 1997;21(2):194-199. Published online January 1, 2001

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Abstract PDF: OBJECTIVES
: The diabetic hyperosmolar non-ketotic coma represents an acute complication of diabetes affecting mostly elderly persons with non-insulin dependent diabetes rnellitus. It is characterized by marked hyperglycemia, hyperosmolarity, severe dehydration, occasional neurologic signs, obtunded sensorium, and absence of ketonemia or acidosis. Most investigators have evaluated the relationship of predisposing conditions with HNKC, to evaluate outcome of the elderly HNKC we studied the prognostic factors in the elderly HNKC. Patients and METHODS: We retrospectively studied 43 patients with HNKC admitted to Hospital of Hallym University during an 6-year period, 1990 through 1995. All medical records of elderly patients (65 years old or more) discharged with the diagnosis of HNKC, were reviewed. To be included as a case, patients had to have a serum glucose level greater than 500mg/dL, measured plasma osmolarity greater than 320mOsm/L, pH greater than 7.30 and disoriented sensorium. 1nformation that was gathered age, glucose, blood urea nitrigen, creatinine, Na+, K+, HCO3-, anion gap, plasma osmolarity, urine osmolarity and whether the patients was discharged alive or died in the hospital. Data were analyzed by one-factor ANOVA and significance of difference between proportions was calculated by Newman-Keuls test. RESULTS: Survivors of 43 elderly HNKC were 22 patients and non-survivors were 21 patients. Mortality was 49%. Analysis revealed that the plasma osmolarity was significantly higher among those who non-survivors (376 +/- 10.8versus 331 +/- 5.0mOsm/L, p 0.01). Non-survivors also had significantly higher serum creatinine level than survivors (2.1+/-0.41versus 1.6 +/- 0.18mg/dL, p = 0.024) Conelusion: These results suggest that the prognostic factors of elderly HNKC were plasma osrnolarity and serum creatinine level.

Case Report

A case of Emphysematous cystitis due to E . coli and Candida albicans ; Successful management by appropriate antibiotics and adequate urinary drainage.: Man Sun Back, Jean Man Hur, Kyoung Keun Jo, Mi Suk Kim, Jong Il Jeon, Kyoung Il Cheun, Suk Kyoung Hung, Seung Chul Lee, Hyun Choi, Moon Jun Na, Kang Seo Park; Korean Diabetes J. 1997;21(2):200-204. Published online January 1, 2001

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Abstract PDF: Emphysematous Cystitis is an uncommon disease in which bacteria produce gas in the bladder wall and surrounding tissues. It is associated with diabetes mellitus, bladder outlet obstruction, chronic urinary tract infection and neurologic bladder dysfunction. The most common bacteria causing emphysematous cystitis are the gas forming bacteria such as E.coli, Enterobacter and klebsiella species. The early diagnosis of emphysematous cystitis is important to improve prognosis and reduced mortalites. Patients should be started an appropriate antimicrobial agent and correction of underlying causes. We report a case of emphysematous cystitis treated successfully with administration of appropriate antibiotics and bladder drainage.

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