Diabetes & Metabolism Journal

Original Article

Fracture Incidence and Risk of Osteoporosis in Female Type 2 Diabetic Patients in Korea: Jong Kwan Jung, Hyo Jeong Kim, Hong Kyu Lee, Sang Soo Kim, Chan Soo Shin, Jin Taek Kim; Diabetes Metab J. 2012;36(2):144-150. Published online April 17, 2012; DOI: https://doi.org/10.4093/dmj.2012.36.2.144

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Background

There are no published data regarding fracture risk in type 2 diabetic patients in Korea. In this study, we compared the fracture incidence and risk of osteoporosis of type 2 diabetic female patients with those in a non-diabetic hypertensive cohort.

Methods

The incidence of fracture in a type 2 diabetic cohort was compared with that in a non-diabetic hypertensive cohort over the course of 7 years. Female type 2 diabetic and non-diabetic hypertensive patients who visited Eulji General Hospital outpatient clinic from January 2004 to April 2004 were assigned to the diabetic cohort and the non-diabetic hypertensive cohort, respectively. Surveys on fracture event, use of anti-osteoporosis medications, and bone mineral density were performed.

Results

The number of fractures was 88 in the female diabetic cohort (n=1,268, 60.6±11.5 years) and 57 in the female non-diabetic hypertensive cohort (n=1,014, 61.4±11.7 years). The RR in the diabetic cohort was 1.38 (P=0.064; 95% confidence interval [CI], 0.98 to 1.94) when adjusted for age. Diabetic patients with microvascular complications (61.0%) showed a higher RR of 1.81 (P=0.014; 95% CI, 1.13 to 2.92) compared with those without these complications. The prevalence of osteoporosis was comparable between the groups, while use of anti-osteoporosis medication was more common in the diabetic cohort (12.8%) than in the hypertensive cohort (4.5%) (P<0.001).

Conclusion

In our study, a higher fracture risk was observed in female type 2 diabetics with microvascular complications. Special concern for this risk group is warranted.

Citations

Citations to this article as recorded by

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婷玉牛
Advances in Clinical Medicine.2022; 12(02): 1178. CrossRef
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Jiaqing Dou, Jing Wang, Qiu Zhang
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Tatiane Vilaca, Marian Schini, Susan Harnan, Anthea Sutton, Edith Poku, Isabel E. Allen, Steven R. Cummings, Richard Eastell
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Hao Wang, Ying Ba, Qian Xing, Jian-Ling Du
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Stephan Scharla
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Joanna Dytfeld, Michał Michalak
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Risk of low-energy fracture in type 2 diabetes patients: a meta-analysis of observational studies
P. Jia, L. Bao, H. Chen, J. Yuan, W. Liu, F. Feng, J. Li, H. Tang
Osteoporosis International.2017; 28(11): 3113. CrossRef
Comorbidity and its relationship with health service use and cost in community-living older adults with diabetes: A population-based study in Ontario, Canada
Kathryn Fisher, Lauren Griffith, Andrea Gruneir, Dilzayn Panjwani, Sima Gandhi, Li (Lisa) Sheng, Amiram Gafni, Patterson Chris, Maureen Markle-Reid, Jenny Ploeg
Diabetes Research and Clinical Practice.2016; 122: 113. CrossRef
Type 2 diabetes mellitus and bone fragility: Special focus on bone imaging
Yong Jun Choi, Yoon-Sok Chung
Osteoporosis and Sarcopenia.2016; 2(1): 20. CrossRef
Epidemiology of fractures in type 2 diabetes
Ann V. Schwartz
Bone.2016; 82: 2. CrossRef
Efficacy and Safety of Weekly Alendronate Plus Vitamin D35600 IU versus Weekly Alendronate Alone in Korean Osteoporotic Women: 16-Week Randomized Trial
Kwang Joon Kim, Yong-Ki Min, Jung-Min Koh, Yoon-Sok Chung, Kyoung Min Kim, Dong-Won Byun, In Joo Kim, Mikyung Kim, Sung-Soo Kim, Kyung Wan Min, Ki Ok Han, Hyoung Moo Park, Chan Soo Shin, Sung Hee Choi, Jong Suk Park, Dong Jin Chung, Ji Oh Mok, Hong Sun Ba
Yonsei Medical Journal.2014; 55(3): 715. CrossRef
Increased Risk of Fracture and Postfracture Adverse Events in Patients With Diabetes: Two Nationwide Population-Based Retrospective Cohort Studies
Chien-Chang Liao, Chao-Shun Lin, Chun-Chuan Shih, Chun-Chieh Yeh, Yi-Cheng Chang, Yuan-Wen Lee, Ta-Liang Chen
Diabetes Care.2014; 37(8): 2246. CrossRef
Aortic Calcification and Bone Metabolism: The Relationship between Aortic Calcification, BMD, Vertebral Fracture, 25-Hydroxyvitamin D, and Osteocalcin
Kwang Joon Kim, Kyoung Min Kim, Kyeong Hye Park, Han Seok Choi, Yumie Rhee, Yong Ho Lee, Bong Soo Cha, Myong Jin Kim, Sun Min Oh, J. Keenan Brown, Sung Kil Lim
Calcified Tissue International.2012; 91(6): 370. CrossRef

Case Report

Two Cases of Autoantibody Negative Fulminant Type 1 Diabetes Mellitus.: Hwa Young Cho, Young Min Cho, Myoung Hee Park, Mi Yeon Kang, Ki Hwan Kim, Yun Hyi Ku, Eun Kyung Lee, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee; Korean Diabetes J. 2007;31(4):372-376. Published online July 1, 2007; DOI: https://doi.org/10.4093/jkda.2007.31.4.372

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Abstract PDF: Autoantibody negative fulminant type 1 diabetes mellitus is a novel subtype of type 1 diabetes, which is characterized by a remarkably abrupt onset, metabolic derangement such as diabetic ketoacidosis at diagnosis, low HbA1c level at onset and a negative islet-related autoantibodies. The prevalence of fulminant type 1 diabetes has large difference between Japan and other countries. The precise reason for this regional variation remains to be clarified. One of the possible explanations is genetic background such as genotype of class II HLA molecule. In addition, environment factors including viral infection are suggested as possible pathogenesis of the disease. Only a few cases with fulminant type 1 diabetes have been reported outside Japan, and most of these cases with definite diagnosis have been reported in Korea. We report here on two Korean patients that met the criteria for diagnosis of fulminant type 1 diabetes in accordance with their HLA genotypes.

Original Article

The Association of Aldose Reductase Gene Polymorphisms with Neuropathy in Patients with Type 2 Diabetes.: In Kyong Jeong, Kyong Soo Park, Min Kyong Moon, Jae Hyeon Kim, Chan Soo Shin, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2007;31(3):274-283. Published online May 1, 2007; DOI: https://doi.org/10.4093/jkda.2007.31.3.274

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Abstract PDF

BACKGROUND
Previous studies have suggested that polymorphisms in and around the aldose reductase (AR) gene are associated with the development of diabetic microvascular disease. This study explored the hypothesis that the polymorphisms of the (A-C)n dinucleotide repeat sequence, located at 2.1 kilobase (kb) upstream of the transcription start site of AR gene, modulate the risk of diabetic neuropathy (DN). METHODS: 66 patients with DN, 30 without microvascular complications (MC) after 20 years of diabetes, and 87 normal healthy controls were studied. To test highly polymorphic microsatellite marker 2.1 kb upstream of the initiation site of the AR gene, we performed polymerase chain reaction using the primer labeled with fluorescent dye and GeneScan by ABI prism 377 automated DNA sequencer and ABI Genotyper software 2.0. RESULTS: Seven alleles (Z-6, Z-4, Z-2, Z, Z+2, Z+4 and Z+6) were identified. Z-2 allele was more frequently observed in patients with DN (77.3%) than in those without MC (43.3%, P = 0.007). The subgroup of patients who developed DN within 5 years after the diagnosis of diabetes also had higher frequency of Z-2 allele (91.7%) compared to those without MC (43.3%, P = 0.028). On the contrary, Z+6 allele tended to be more frequent in patients without MC (10.0%) than in those with DN (0%, P = 0.063). CONCLUSION: These results support the hypothesis that environmental-genetic interactions may modulate the risk of neuropathy in patients with diabetes. Particularly, the Z-2 allele, in the presence of diabetes, may be associated with the development of DN.

Citations

Citations to this article as recorded by

The Association between Serum GGT Concentration and Diabetic Peripheral Polyneuropathy in Type 2 Diabetic Patients
Ho Chan Cho
Korean Diabetes Journal.2010; 34(2): 111. CrossRef

Randomized Controlled Trial

The Effects of Insulin Sensitizers on the Plasma Concentrations of Adipokines in Type 2 Diabetic Patients.: Hye Seung Jung, Young Min Cho, Kyung Won Kim, Byung Soo Youn, Kang Yeol Yu, Hong Je Park, Chan Soo Shin, Seong Yeon Kim, Hong Kyu Lee, Kyong Soo Park; Korean Diabetes J. 2003;27(6):476-489. Published online December 1, 2003

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Abstract PDF: BACKGROUND
Resistin, leptin and adiponectin are proteins secreted from adipose tissue, and have been suggested to play roles in insulin sensitivity. The effects of the circulating levels of two different types of insulin sensitizer, rosiglitazone and metformin, in type 2 diabetic patients were examined to elucidate the relationship between adipokines and insulin resistance. METHODS: Thirty type 2 diabetic patients, who showed poor glycemic control when administered 4 mg glimepiride a day, without severe diabetic complications or medical illness, were randomized to receive an additional 4mg rosiglitazone or 1000 mg metformin a day. The plasma resistin, leptin and adiponectin concentrations were measured at the baseline and after 6 months of treatment. The anthropometric parameters, fasting plasma glucose, HbA1C, total cholesterol, triglyceride, HDL-cholesterol and free fatty acids were also measured. Certain single nucleotide polymorphisms of adipokine genes were also identified. RESULTS: There were no significant differences in the reductions of the plasma glucose and HbA1C levels, after 6 months of treatment, between the two groups. The plasma resistin concentrations decreased, the adiponectin significantly increased and the leptin showed a tendency to increase in the rosiglitazone group. In the metformin group, only the resistin concentration significantly increased. However, the changes in the adipokines did not correlate with the HOMA-IR in either group. The reduction in the HbA1C due to rosiglitazone was greater if the initial leptin level was high, if there was a G allele on the -420th locus of the resistin gene, or the 45th locus of the APM1 (adiponectin gene) was the T-homozygote or there was a T allele on the 276th locus of the APM1. Those due to metfromin were greater with high initial adiponectin levels. CONCLUSION: In type 2 diabetic patients, showing poor glycemic control with sulfonylurea therapy, rosiglitazone or metformin treatment changed some of the adipokine concentrations, but these changes were not clearly related with insulin resistance. Polymorphisms of certain adipokine genes seem to have a relation to the susceptibility of rosiglitazone.

Original Articles

Association between Type 2 Diabetes and Genetic Variations in Uncoupling Protein 2, beta3-Adrenergic Receptor, and Peroxisome Proliferator-Activated Receptor gamma in Korean.: Min Kyong Moon, Young Min Cho, Hye Seung Jung, Tae Yong Kim, Yun Yong Lee, Joong Yeol Park, Ki Up Lee, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Hyoung Doo Shin; Korean Diabetes J. 2002;26(6):469-480. Published online December 1, 2002

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Abstract PDF: BACKGROUND
Type 2 diabetes mellitus is a multifactorial disease influenced by numerous genetic and environmental factors. The uncoupling proteins, 2 (UCP2), beta3-adrenergic receptor ADRB3, and peroxisome proliferator-activated receptor gamma PPAR gamma, are genes involved in energy expenditure and fatty acid metabolisms, ans are therefore regarded as candidate genes for type 2 diabetes. In this study, we examined whether the known polymorphisms of UCP2, ADRB3 and PPAR gamma are associated with type 2 diabetes in the Korean population. METHODS: We studied 516 type 2 diabetic patients and 147 control subjects. The enrollment criteria for the control subjects were as follows; age > 60 years, no family history of diabetes in their first-degree relatives, a fasting plasma glucose (FPG) < 6.1 mmol/L, and a HbA1C < 5.8%. Height, weight, waist and hip circumference, FPG, 2 hour-plasma glucose after 75g-glucose load (2h-PG), blood pressure, lipid profile, and fasting insulin level were measured. The Ala55Val polymorphism of the UCP2, Trp64Arg polymorphism of the ADRB3, and Pro12Ala polymorphism of the PPAR gamma were determined by single base extension method. RESULTS: The allele frequency of the Ala55Val variant of the UCP2 tended to be higher in the control subjects than in the type 2 diabetic patients (0.497 vs. 0.456, p=0.064). The allele frequencies of the Trp64Arg polymorphism of the ADRB3, and the Pro12Ala polymorphism of the PPAR gamma, were comparable between the diabetic patients and the control subjects (0.141 vs. 0.152 and 0.033 vs. 0.041, respectively). In the control subjects, the Ala55Val polymorphism of the UCP2 was associated with a significantly lower 2h-PG compared to the wild type (6.0 +/- 0.8 mmol/L vs. 6.6 +/- 0.7 mmol/L, p=0.002). The female control subjects, with the ADRB3 Trp64Arg variant, had a significantly lower triglyceride level than those without the variant (1.36 +/- 0.53 mmol/L vs. 1.74 +/- 0.82 mmol/L, p=0.020). The type 2 diabetic patients, with the ADRB3 Trp64Arg variant showed a significantly lower body mass index (23.6 +/- 2.6 kg/m2vs. 24.6 +/- 3.0 kg/m2, p=0.001). The PPAR gamma Pro12Ala variant, was not associated with any of the features of insulin resistance. The combined genotype of the Val allele of UCP2, Trp allele of ADRB3 and Ala allele of PPAR gamma was less frequent among the type 2 diabetes patients than the control subjects (0.020 vs. 0.056, p=0.039). CONCLUSION: The Ala55Val variant of the UCP2, the Trp64Arg variant of the ADRB3 and the Pro12Ala variant of the PPAR gamma, were not associated with type 2 diabetes in the Korean population. However, the Ala55Val variant of the UCP2 was associated with a lower 2h-PG in the control subjects and the Trp64Arg variant of the ADRB3 was associated with a lower triglyceride level in the female control subjects. Further study may be required to elucidate if the combined genotype of Val allele of UCP2, Trp allele of ADRB3 and Ala allele of PPAR gamma would be protective against type 2 diabetes.

Expression of ghrelin and its receptor according to feeding state in rats.: Min Seon Kim, Cho Ya Yoon, Young Joo Park, Hyung Kyu Park, Chen Ji Jin, Kyong Han Park, Chan Soo Shin, Kyong Soo Park, Seong Youn Kim, Bo Youn Cho, Hong Kyu Lee; Korean Diabetes J. 2002;26(3):169-178. Published online June 1, 2002

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Abstract PDF: BACKGROUND
Ghrelin is a newly discovered gut peptide, produced mainly in the stomach, which is secreted into the circulating blood and acts on the hypothalamus and the pituitary gland. Although ghrelin was originally identified as an endogenous growth hormone secretagogue, recent studies have suggested its role is in the regulation of food intake and energy homeostasis. The aim of this study was to investigate changes in the expression of ghrelin in the stomach, and of its receptors in the hypothalamus and the pituitary gland in relation to the feeding state. METHODS: Sprague Dawley male rats, divided into 3 groups, freely fed, fasted for 48 hrs and fasted for 48 hrs followed by feeding for 24 hrs, were investigated. The stomach fundus, the hypothalamus and the pituitary glands were collected. The gastric ghrelin mRNA expression was determined by Northern blot analysis and the ghrelin protein by immunohistochemistry. The ghrelin receptor mRNA levels in the hypothalamus and anterior pituitary gland were determined by real time PCR. RESULTS: The ghrelin mRNA levels in the stomach were increased by fasting but reduced again by allowing feeding. The number of ghrelin-immunoreactive gastric epithelial cells tended to increase with fasting. Moreover, the ghrelin receptor mRNA levels increased fold in the hypothalamus, and about 3 fold in the anterior pituitary gland harvested from the rats that had fasted for 48 hrs compared to those that were freely fed. CONCLUSION: Our data demonstrate that expression of both ghrelin in stomach and its receptor in target organs increased in the fasted state, which would be helpful for magnifying the orexigenic effect of ghrelin in the negative energy balance state. Dynamic changes in ghrelin and ghrelin receptor according to altered metabolic state may suggest a physiologic role of ghrelin in the regulation of energy homeostasis.

Pancreatic beta-cell Function and Development in Male Offspring of Protein-Malnourished Rats.: Hyeong Kyu Park, Cheng Ji Jin, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2002;26(1):21-30. Published online February 1, 2002

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Abstract PDF: BACKGROUND
Nutritional deprivation of the fetus and infant may be associated with susceptibility to impaired glucose tolerance or type 2 diabetes in adult life. This association has been interpreted as a long-term effects of nutritional factors that reduce fetal growth and impair the development of tissues that regulate glucose metabolism. This study aimed to investigate the effect of protein malnutrition in a fetus and early life on the pancreatic beta-cell function and development. METHODS: Sprague-Dawley rats were fed a low-protein (8% casein) diet during pregnancy and lactation. Their male offspring were weaned onto either a control (18% casein) diet (recuperated group, R) or a low-protein diet (low-protein group, LP). The offspring of the rats fed control diet were weaned onto control diet (control group, C). Glucose tolerance tests and morphometry of the pancreas were performed to evaluate the pancreatic beta-cell function and development at the 25th week of age. RESULTS: Offspring of the protein-malnourished rats had a significantly lower body weights than the controls. The R and LP showed no major impairment in glucose tolerance, but the plasma insulin concentrations in the R (0.24+/-.03 nmol/L) and LP (0.28+/-.02 nmol/L) groups were lower at 20 min during IVGTT than the C (0.43+/-.05 nmol/L) groups. The areas under the curve for insulin (AUC insulin) during IVGTT were significantly lower in R and LP (0.39+/-.03 nmol/L/min, 0.43+/-.02 nmol/L/min) groups than the C (0.54+/-.03 nmol/L/min) group. In particular, the rats with fetal protein malnutrition showed severe impairment in late-phase insulin secretion to a glucose load. Both the pancreas weight and the proportion of the pancreas weight to the body weight were significantly lower in the R and LP groups than the C group. The proportion of beta-cells to pancreatic cells was lower in the LP (0.91+/-.14%) group than the C (2.19+/-.23%) and R (1.79+/-.25%) group. The relative beta-cell mass was significantly lower in the LP (by 62%) group that the C group. CONCLUSION: Rats with fetal protein malnutrition showed persistently impaired pancreatic beta-cell development and reduced insulin secretion capacity. These findings suggest that in utero protein malnutrition can contribute to the development of type 2 diabetes in adult life along with other deleterious environmental or genetic conditions.

Editorial

Pathophysilolgy and Epidemiology of Diabetes in Elderly.: Chan Soo Shin; Korean Diabetes J. 2001;25(2):110-112. Published online April 1, 2001

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Abstract PDF: No abstract available.

Original Articles

Comparison of Clinical Characteristics of Impaired Fasting Glucose with Impaired Glucose Tolerance in Yonchon County.: In Kyong Jeong, Min Kyong Moon, Sang Wan Kim, Young Joo Park, Sun Yuk Kim, Chan Soo Shin, Do Joon Park, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Noe Kyeong Kim, Hong Kyu Lee; Korean Diabetes J. 2000;24(1):71-77. Published online January 1, 2001

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Abstract PDF: BACKGROUND
To compare the clinical characteristics of 1997 American Diabetes Association (ADA) impaired fasting glucose (IFG) based on fasting plasma glucose (FPG) with World Health Organization (WHO) impaired glucose tolerance (IGT) based on oral glucose tolerance test (OGTT) in a Korean population. METHODS: The analyses were based on the data of 2,251 subjects aged 30-80 years obtained from the surveys of Yonchon County in Korea in 1993, and the data of 1084 subjects participated in the follow-up survey in 1995. Prevalence of glucose tolerance categories was obtained by using WHO and ADA criteria, and the level of agreement was estimated by index. Cardiovascular risk profile and the incidence of diabetes based on the ADA criteria after 2 years were compared by focusing on the discordant ctiagnostic categories namely IGT/NFS in which the subjects were diagnosed as IGT by WHO criteria but normal fasting glucose(NFG) by ADA criteria and NGT/IFG diagnosed as normal glucose tolerance(NGT) by WHO but IFG by ADA. Results The ADA criteria failed to diagnose 69% of IGT patients, that is 62% of them were considered normal and 7% as diabetes. The overall agreement was poor (x statistics = 0.32, p<0.05). Subjects classified into IGT/NFG or NGT/IFG showed the worse cardiovascular risk profile and higher incidence of diabetes than NGT/NFG. Especially, subjects with NGT/IFG exhibited higher incidence of diabetes than those with IGT/NFG. CONCLUSION: Although IFG predicts subsequent development of diabetes much better than IGT, the vast majority of the subjects with IGT will be missed according to ADA criteria based on FPG only. Consequently FPG alone could be an inadequate substitute for the OGTT.

Relationship of Insulin-like Growth Factor(IGF)-1, IGF-2, IGF Binding Protein(IGFBP)-3, and Mitochondrial DNA Amount in the Umbilical Cord Blood to Birth Weight.: Yun Yong Lee, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Hong Kyu Lee, Jong Kwan Jun, Boh Yun Yoon, Jih Yeun Song, Bong Sun Kang; Korean Diabetes J. 1999;23(1):36-45. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Reaven proposed a syndrome (syndrome X), consisting of glucose intolerance, hypertension, hyperinsulinemia, dyslipidemia, as a clinical entity. The fundamental metabolic defect of this syndrome was recognized as insulin resistance, but the pathophysiology of insulin resistance is not clarified as of yet. Recent evidence, suggests that non-insulin dependent diabetes mellitus (NIDDM) ancl lipid and cardiovascular abnormalities-syndrome X-are associated with intrauterine growth retar- dation (IUGR). Recently Shin reported that the amounts of mitochondrial DNA (mtDNA) in a given amount of genomic DNA were lower in NIDDM patients than in healthy controls, and the amount of mtDNA is negatively correlated with blood pressure ancl waist-hip ratio. Birth weight is known to be correlated with levels of insulin-like growth factors (IGFs). The purpose of this study was to identify the correlation of low birth weight with reduced mtDNA and syndrome X. We investigated the relationship of birth weight to IGFs and the amount of mtDNA METHODS: 72 singleton pregnancy babies and their mathers admitted in Seoul National University Hospital from March to May, 1997 were studied. After delivery, the cord blcxxl and maternal venous blood sampling was done. Using the imnnmoradiometric assay (IRMA) the IGF-l, IGF-2, IGFBP-3 was measured from cord and maternal plasma. Among them only 27 pairs samples were measured mtDNA amount with competitive PCR method in their buffy coat. Then statistical analysis was done within these paratneters. RESULTS: Birth weight is correlated significantly with cord plasma IGF-1 (r=0.32, p<0.01), IGFBP-3 (r=0.44, p<0.01), prepregnancy maternal body weight (r=0.45, p<0.01), maternal mtDNA amount (r=0.63, p<0.01). Cord blood mtDNA is correlated with maternal mtDNA amount (r=0.55, p<0,01). In multiple regression analysis, the maternal mtDNA was found to be the only independent factor related to birth weight (p<0.01). COMCLUSION: We have found the correlation between birth weight and maternal prepregnancy body weight and mtDNA amount. The clinical implications of this result remain yet to be deiermined.

Evaluation of Fasting Plasma Glucose to Diagnose Diabetes in Yonchon County.: Young Joo Park, In Kyoung Chung, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Sun Ja Kwon; Korean Diabetes J. 1998;22(3):372-380. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Recently, many studies were performed to evaluate the diagnostic value of fasting plasma glucose to diagnose diabetes, and the diagnostic criteria were revised by ADA in 1997 to avoid discrepancy between the fasting plasma glucose (FPG) and 2 hour post-load plasma glucose(2hPG) cutpoint values after 75g oral glucose loading and to alsc facilitate and encourage the use of test for diagnosing diabetes. This study was performed to assess the performance of different cutpoint of fasting plasma glucose in the diagnosis of diabetes and to compare the prevalence and incidence of diabetes using revised 1997 ADA FPG criterion with those using 1985 WHO criteria in Yonchon County of Korea. METHODS: Two thousand three hundred fifty-six subjects who participated in population based cross-sectional study in Yonchon County in 1993. We have also analysed the data from 1141 subjects who were non-diabetic in 1993 and participated in the follow-up survey in 1995. The relationship between FPG and 2hPG were determined using sensitivity, specificity and the prevalence of diabetes according to FPG and/or 2hPG values. We have determined the prevalence and the incidence of diabetes using the ADA criterion. RESULTS: Based on WHO criteria, a FPG of 6.1 mmol/L(110mg/dL) was determined to yield optimal sensitivity(83.6%) and specificity(82.4%), but it showed low positive predictive value(27.2%) and high prevalence(24.5%). The FPG cutpoint which showed same prevalence with the criterion ot the 2hPG >11.1mmol/L(87 in 2251) was 7.4mmol/L (133mg/dL, 87 in 2251), The crude prevalence of diabetes and impaired fasting glucose by ADA criterion were 9.6% and 14.9%, respectively, where as the crude prevalence of diabetes and IGT were 9.4% and 11.5% by WHO criteria. The crude incidence of diabetes was 5.1% as defined by ADA criterion and 34.4% of subjects who showed impaired fasting glucose in 1993 converted to diabetes in 1995, whereas the incidence was 2.5% by WHO criteria and 13% of IGT subjeets converted to diabetes in 2 years. Conclusions: The adequate cutpoint for FPG seems to lie between 6.1mmol/L and 7.4mmol/L. The 1997 ADA criterion of the FPG > 7.0mmol/L produced similar prevalence and higher incidence than those obtained from 1985 WHO criteria and the former seems to be better to detect the risk group who may progress to diabetes.

NcoI Restriction Fragment Length Polymorphism(RFLP) on the TNF-beta gene in Korean Patients with Type 1(insulin-dependent) Diabetes Mellitus.: Suk Kyeong Kim, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Hun Ki Min, Tae Gun O; Korean Diabetes J. 1998;22(2):155-163. Published online January 1, 2001

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Abstract PDF: BACKGROUND
To investigate whether a TNF-g gene polymorphism is associated with the development of insulin-dependent diabetes mellitus, we analyzed the TNF-g gene polymorphism with restriction enzyme Ncol in 38 Korean patients with insulin -dependent diabetes mellitus(IDDM) and in 150 healthy controls. METHODS: Genomic DNA was extracted from white blood cells, and amplified by polymerase chain reaction(PCR) on 735 base pairs fragment of TNF-g gene with NcoI polymorpnic site. 735 bp PCR product was digested with NcoI restriction endonuclease, then analyzed by agarose gel electrophoresis to detect the NcoI restriction fragment length polymorphism(RFLP). The TNF-g alleles were divided into two types according to the electrophoresis patterns. TNF-b*1 allele, which contains the Ncol restriction site(CCATGG), should be digested 539 bp and 196 bp fragments. On the other hand, TNF-g*2 allele, which lacks the restriction site, only showed 735 bp fragment. RESULTS: Six out of 38(15.8%) IDDM patients were homozygous for the TNF-b*1 allele, 11(28.9%) were homozygous for the TNF-b*2 alleie, and 21 (55.3%) were TNF-b*1/*2 heterozygous compared to 21.7%, 30.7% and 49.3%(p=0.83), respectively, in control subjects. CONCLUSION: The TNF-b gene polymorphism was not associated with insulin-dependent diabetes mellitus in Korean subjects.

The Characteristics of Insulin-resistance Syndrome in the Korean Population.: Jin Sung Kim, Gun Sang Park, Yun Yong Lee, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hyeon Kyu Kim, Yong Soo Park, Soon Ja Kwon; Korean Diabetes J. 1998;22(1):84-92. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Insulin-resistance syndrome or syndrome X which includes diabetes mellitus, hypertension, dyslipidemia, and obesity has been regarded as one of the mechanisms involved in the atherosclerotic disease. This study was performed to evaluate the prevalence of each camponent of insulin-resistance syndrome. We have also analyzed the clustering of insulin-resistance syndrome according to fasting insulin levels in subjects who participated in the Younchon county diabetes prevalence study in 1993. METHOD: One thousand, eight hundred and eleven subjects among 2520 subjects over 30 years-old were enrolled, We investigated the prevalence of 5 metabolic syndromes: glucose intolerance(impaired glucose tolerance and diabetes mellitus by WHO criteria), hypertension(diastolic blood pressure >95 mmHg), Hypertriglyceridemia(triglyceride >2.26 mmol/L), low HDL cholesterolemia(HDL cholesterol <0.91 mmol/ L) and obesity(body mass index >25 kg/m) according to fasting serum insulin level. RESULTS: The prevalence of glucose intolerance (diabetes mellitus and impaired glueose tolerance), hypertension, hypertriglyceridemia, low HDI, cholesterolemia and obestiy were 18.2%, 21.3%, 10.9%, 45.6% and 36.3%, respectively. According to the four quartiles(quartile 1, 2, 3, 4) of fasting serum insulin level, the prevalence rate of each metaboic syndrome was as follows: 9.5%, 15.6%, 22.8% and 25.0% for glucose intolerance; 18.7%, 17.5%, 21.1% and 27.9% for hypertension; 5.0%, 8.1%, 13 8% and 16.9% for hypertriglyceridemia; 37.9%, 46.6%, 46.5% and 51.6% for low HDL cholesterolemia; 19.2%, 30.1%, 40.8% and 55.4% for obesity. As the fasting insulin levels increase, the clustering of 2 or more disease increase. CONCLUSION: Metabolic syndromes associated with insulin-resistance are relatively common disorders in the Korean population. The prevalence and clustering of metabolic abnormalities also increase as serum insulin level increases in Korean population.

Decreased Mitochondrial DNA Content in Peripheral Blood Leukocyte procedes the Development of Type 2 Diabetes Mellitus.: Jae Joon Koh, Jong Ho Ahn, Soon Ja Kwon, Ji Hyun Song, Chan Soo Shin, Do Joon Park, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 1998;22(1):56-64. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Mitochondrial mutations and deletions, have been implicated in the pathogenesis of diabetes mellitus. This can explain only a very small proportion of the patients with diabetes mellitus. Mitochondrial DNA(mtDNA) is vulnerable to oxidative stress, resulting in both qualitative and quantitative changes. We reported that the amount of mtBNA decreased in the peripheral blood leukocyte of patients with NIDDM. In this study, we examined that decreased mtDNA content preceded the development of NIDDM{Non-insulin dependent diabetes mellitus) and correlated with various insulin resistance parameters.In this study, we demonstrated that the amount of mtDNA decreased in peripheral blood leukocyte of patients with NIDDM. Furthermore, we found that lower mtDNA levels preceded the development of diabetes mellitus. METHODS: We utilized the stored blood samples from two community-based survey conducted in Yonchon County, Korea in 1993 and 1995. We selected 23 newly diagnosed diabetic patients and 22 age- and sex-matched control subjects. The buffy coats of peripheral blood samples were used for the competitive PCR and the products pairs were separated by gel EP. The content of mtDNA was calculated with the densitometry. RESULTS: There were no difference in the initial anthropometric parameters, blood pressure and lipid profiles between subjects who became diabetic converters and non converters. The mean quantity of mtDNA was lower in the converters, with 102.8+ 41.5 copies/pg template DNA compared to 137.8+ 67.7 copies/pg template DNA of the controls(p 0.05). The significant inverse correlations were noted between mtDNA content and WHR(r=0.31, p<0.05) in the first, and fasting glucose level(r=-0.35, p<0.05), diastolic blood pressures(r=-0.36, p<0.05), and WHR(r=-0.40, p<0.01) in the second survey. The correlations with the serum levels of total and high density cholesterol, triglyceride, insulin and proinsulin were not statistically significant. CONCLUSION: Although a relationship between diabetes and mitochondrial dysfunction has been suspected. This study showed that decreased mtDNA content in peripheral blood proceded the development of NIDDM. This is the first study to demonstrate that quantitative changes in mtDNA precede the development of NIDDM.

Randomized Controlled Trial

The Effect of Acarbose as an Adjuvant Therapy in Sulfonylurea-Treated NIDDM Patients.: Yun Yong Lee, Geon Sang Park, Jin Seong Kim, Byeong Sool Mun, Do Joon Park, Chan Soo Shin, Kyeong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 1997;21(4):484-492. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Acarbose-an aglucosidase inhibitor-is known to have a glucose lowering effect by delaying the digestion of complex carbohydrates in the small intestine. Acarbose especially prevents the abnormally high increment of postprandial blood glucose, reduces postprandial hyperinsulinemia and probably, alleviates insulin resistance. The aim of this study is to evaluate the glucose lowering effect of acarbose as an adjunt with a sulfonylurea in the treatment of NIDDM patients who have been poorly controlled with the use of sulfonylurea alone. METHODS: Forty NIDDM patients, who were poorly controlled with sulfonylurea alone, were randomly selected frorn outpatient diabetic clinic for study. For 16 weeks, they recieved either acarbose or placebo in additian to sulfonylurea under double blind method. RESULTS: 1) The metabohc parameters measured before initiation of either treatment regimen were similiar. 2) The HbAlc in placebo group increased from 8.9% to 9.0%. In contrast, in the acarbose group, HbAlc value decreased from 9.3% to 8.1%(p<0.05). 3) Mean fasting plasma glucose and 1-h postprandial glucose levels were reduced significantly in the acarbose group(p<0.001), especially in I-h postpandial glucose level in comparison with placebo group(p <0.0001). 4) Mean fasting, 1-h postprandial insulin levels decreased with time in the acarbose group in comparison with placebo group, but the decrease was not statistically significant. 5) Lipid profiles did not change during 16weeks of treatment period. 6) Adverse effects were observed in 3 patients on acarbose and 2 patients on placebo. CONCLUSION: Acarbose can be used as an effective adjuvant therapy to sulfonylurea in NIDDM patients who are poorly controlled with sulfonylurea alone.

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