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Metabolic Risk/Epidemiology
Sex Differences in the Effects of CDKAL1 Variants on Glycemic Control in Diabetic Patients: Findings from the Korean Genome and Epidemiology Study
Hye Ah Lee, Hyesook Park, Young Sun Hong
Diabetes Metab J. 2022;46(6):879-889.   Published online February 8, 2022
DOI: https://doi.org/10.4093/dmj.2021.0265
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  • 182 Download
  • 1 Web of Science
  • 1 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Using long-term data from the Korean Genome and Epidemiology Study, we defined poor glycemic control and investigated possible risk factors, including variants related to type 2 diabetes mellitus (T2DM). In addition, we evaluated interaction effects among risk factors for poor glycemic control.
Methods
Among 436 subjects with newly diagnosed diabetes, poor glycemic control was defined based on glycosylated hemoglobin trajectory patterns by group-based trajectory modeling. For the variants related to T2DM, genetic risk scores (GRSs) were calculated and divided into quartiles. Risk factors for poor glycemic control were assessed using a logistic regression model.
Results
Of the subjects, 43% were in the poor-glycemic-control group. Body mass index (BMI) and triglyceride (TG) were associated with poor glycemic control. The risk for poor glycemic control increased by 11.0% per 1 kg/m2 increase in BMI and by 3.0% per 10 mg/dL increase in TG. The risk for GRS with poor glycemic control was sex-dependent (Pinteraction=0.07), and a relationship by GRS quartiles was found in females but not in males. Moreover, the interaction effect was found to be significant on both additive and multiplicative scales. The interaction effect was evident in the variants of cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like (CDKAL1).
Conclusion
Females with risk alleles of variants in CDKAL1 associated with T2DM had a higher risk for poor glycemic control than males.

Citations

Citations to this article as recorded by  
  • Hepatic Cdkal1 deletion regulates HDL catabolism and promotes reverse cholesterol transport
    Dan Bi An, Soo-jin Ann, Seungmin Seok, Yura Kang, Sang-Hak Lee
    Atherosclerosis.2023; 375: 21.     CrossRef
Clinical Care/Education
Increased Epicardial Adipose Tissue Thickness in Type 2 Diabetes Mellitus and Obesity
Do Kyeong Song, Young Sun Hong, Hyejin Lee, Jee-Young Oh, Yeon-Ah Sung, Yookyung Kim
Diabetes Metab J. 2015;39(5):405-413.   Published online October 22, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.5.405
  • 3,868 View
  • 62 Download
  • 53 Web of Science
  • 50 Crossref
AbstractAbstract PDFPubReader   
Background

Epicardial adipose tissue (EAT) is suggested to play an important role in the progression of metabolic syndrome. We aimed to establish a simple method to measure EAT and examine the differences in EAT thickness according to the presence of type 2 diabetes mellitus or obesity.

Methods

A total of 94 patients (42.6% type 2 diabetes mellitus, 53.2% obese, mean age 61±13) who underwent multidetector computed tomography were enrolled. Thickness of EAT was measured on the parasternal short and horizontal long axis view. Epicardial fat area (EFA) was measured at the level of left main coronary artery (LMCA).

Results

All EAT thicknesses were correlated with EFA at the LMCA level (r=0.235 to 0.613, all Ps<0.05), and EAT thickness in the left atrioventricular groove (LAVG) had the highest correlation coefficient (r=0.613). EFA, and EAT thicknesses in the LAVG and the left ventricular apex were higher in the group with type 2 diabetes mellitus than in the group without type 2 diabetes mellitus when adjusted only for body mass index. When adjusted only for type 2 diabetes mellitus, EFA, and EAT thicknesses in the LAVG and the right atrioventricular groove were higher in obese group than in nonobese group.

Conclusion

In conclusion, EAT thickness can be easily measured and represent EFA. EAT thickness, especially in LAVG, was higher in groups with type 2 diabetes mellitus and obesity independently. These findings implicate that EAT thickness may be a useful indicator for type 2 diabetes mellitus and obesity.

Citations

Citations to this article as recorded by  
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FTO Gene Variants Are Associated with PCOS Susceptibility and Hyperandrogenemia in Young Korean Women
Do Kyeong Song, Hyejin Lee, Jee-Young Oh, Young Sun Hong, Yeon-Ah Sung
Diabetes Metab J. 2014;38(4):302-310.   Published online August 20, 2014
DOI: https://doi.org/10.4093/dmj.2014.38.4.302
  • 4,122 View
  • 44 Download
  • 25 Web of Science
  • 24 Crossref
AbstractAbstract PDFPubReader   
Background

The fat mass and obesity-associated (FTO) gene is associated with obesity and type 2 diabetes mellitus. Obesity and insulin resistance are also common features of polycystic ovary syndrome (PCOS). Therefore, the FTO gene might be a candidate gene for PCOS susceptibility. The aim of the present study was to evaluate the effects of FTO gene variants on PCOS susceptibility and metabolic and reproductive hormonal parameters.

Methods

We recruited 432 women with PCOS (24±5 years) and 927 healthy women with regular menstrual cycles (27±5 years) and performed a case-control association study. We genotyped the single nucleotide polymorphisms rs1421085, rs17817449, and rs8050136 in the FTO gene and collected metabolic and hormonal measurements.

Results

Logistic regression revealed that the G/G genotype (rs1421085, 1.6%), the C/C genotype (rs17817449, 1.6%), and the A/A genotype (rs8050136, 1.6%) were strongly associated with an increased risk of PCOS (odds ratio, 2.551 to 2.559; all P<0.05). The strengths of these associations were attenuated after adjusting for age and BMI. The women with these genotypes were more obese and exhibited higher free androgen indices (P<0.05) and higher free testosterone levels (P=0.053 to 0.063) compared to the other genotypes. However the significant differences disappeared after adjusting for body mass index (BMI). When we analyzed the women with PCOS and the control groups separately, there were no significant differences in the metabolic and reproductive hormonal parameters according to the FTO gene variants.

Conclusion

The rs1421085, rs17817449, and rs8050136 variants of the FTO gene were associated with PCOS susceptibility and hyperandrogenemia in young Korean women. These associations may be mediated through an effect of BMI.

Citations

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    Do Kyeong Song, Yeon-Ah Sung, Hyejin Lee, Wan-Xi Yang
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  • Haplotyping strategy highlights the specificity of FTO gene association with polycystic ovary syndrome in Tunisian women population
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Long Menstrual Cycle Is Associated with Type 2 Diabetes Mellitus in Korean Women
Unjin Shim, Jee-Young Oh, Hye Jin Lee, Young Sun Hong, Yeon-Ah Sung
Diabetes Metab J. 2011;35(4):384-389.   Published online August 31, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.4.384
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AbstractAbstract PDFPubReader   
Background

Long menstrual cycle is a risk factor for developing type 2 diabetes and cardiovascular disease in women. We aimed to evaluate the association between existing type 2 diabetes and oligomenorrhea before diagnosis of diabetes, and to observe the differences in this association among obese and non-obese Korean women.

Methods

Patients with type 2 diabetes (n=118) and without any clinical evidence of abnormal glucose regulation (n=258) who attended the outpatient clinic of a university hospital and were over age 30. Patients self-reporting a menstrual cycle over 40 days during their 20s were defined as oligomenorrhea before diagnosis of diabetes. Obesity was defined as having a body mass index (BMI) over 25 kg/m2.

Results

The frequency of oligomenorrhea before diagnosis of diabetes was almost two-fold higher in women with type 2 diabetes than in the control group (16.1% vs. 8.5%, P=0.03). Oligomenorrhea was associated with type 2 diabetes after adjusting for age, BMI, systolic blood pressure, triglycerides, and high density lipoprotein cholesterol (odds ratio, 3.89; 95% confidence interval, 1.37 to 11.04). Among women with oligomenorrhea before diagnosis of diabetes, the frequency of type 2 diabetes was significantly higher in obese subjects than in their non-obese counterparts (90.9% vs. 30.0%, P=0.03).

Conclusion

Having a long menstrual cycle could be a risk factor for the development of type 2 diabetes, especially in obese women.

Citations

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Peroxisome Proliferator-activated Receptor-gamma (PPARgamma) Polymorphism in Korean Women with Polycystic Ovary Syndrome.
Jee Young Oh, Hyejin Lee, Young Sun Hong, Yeon Ah Sung, Hye Won Chung
Korean Diabetes J. 2007;31(6):480-487.   Published online November 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.6.480
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AbstractAbstract PDF
BACKGROUND
Polycystic ovary syndrome (PCOS) is a common endocrine disease affecting 5~10% of women with reproductive age. Familial aggregation suggests the evidence supporting a genetic basis for PCOS. The mode of inheritance of PCOS is not yet clear, however, probably polygenic and might be related to insulin resistance. Polymorphism of peroxisome proliferator-activated receptor (PPAR)-gamma gene is a susceptible gene for the development of obesity and diabetes. In this study, we examined the frequency and genetic effect of PPAR-gamma polymorphism on insulin resistance or hyperandrogenemia in Korean women with PCOS. METHODS: One-hundred twenty five Korean women with PCOS were evaluated for their metabolic and reproductive hormonal status. PPAR-gamma polymorphism was analyzed. RESULTS: Genetic frequency of PPAR-gamma was not significantly different between women with PCOS (n = 125) and those with regular menstrual cycles (n = 344). PCOS with Pro12Ala polymorphism had significantly higher levels of waist circumference and subcutaneous fat area compared with those with Pro12Pro genotype. They also had tendency of higher levels of fasting glucose concentration, body mass index (BMI) and visceral fat area. After BMI adjustment, this polymorphism was related to lower fasting insulin and higher insulin sensitivity index, and higher sex hormone binding globulin and lower free testosterone levels. CONCLUSION: Pro12Ala polymorphism of PPAR-gamma gene might be associated with obesity. However, after BMI adjustment, it may have favorable effect on insulin resistance and hyperandrogenemia. Because this study has limitations to conclude the genetic causality, further study is needed to support these findings.
Insulin Resistance in Normal Weight Women with Polycystic Ovary Syndrome.
Eun Kyung Byun, Hye Jin Lee, Jee Young Oh, Young Sun Hong, Hye Won Chung, Yeon Ah Sung
Korean Diabetes J. 2004;28(4):315-323.   Published online August 1, 2004
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AbstractAbstract PDF
BACKGROUND
Insulin resistance is considered a regular component of polycystic ovary syndrome (PCOS). However, several studies have failed to confirm insulin resistance in non-obese women with PCOS. The aim of the study was to identify whether insulin resistance is present in normal weight women with PCOS and the factors associated with insulin sensitivity. METHODS: Twenty-two normal weight (body mass index, BMI < 25 kg/m2) women with PCOS, and 16 age and BMI comparable control women with regular menstrual cycles were examined during their early follicular phase. The levels of serum hormones and lipids were measured. The visceral fat area was assessed by computed tomography at umbilical level. The standard 75g oral glucose tolerance test was performed to determine the glucose tolerance status. The insulin sensitivity was measured using the euglycemic hyperinsulinemic clamp technique (target glucose 90 mg/dL, insulin~1 mu/kg/min). RESULTS: The levels of free testosterone (1.9+/-0.6 pg/mL vs. 0.8+/-0.3 pg/mL, p<0.001), androstenedione (14.5+/-3.7 nmol/L vs. 8.8+/-1.3 nmol/L, p<0.001), LH (10.7+/-4.5 IU/L vs 4.6+/-4.8 IU/L, p<0.001) and FSH (5.8+/-1.7 IU/L vs. 4.2+/-2.4 IU/L, p<0.05) of the women with PCOS were significantly higher than those of the control subjects. The fasting plasma glucose (4.92+/-0.31 mmol/L vs. 4.42+/-0.61 mmol/L, p<0.01) and post glucose load plasma insulin (233.2+/-119.5pmol/L vs. 109.0+/-46.4 pmol/L, p<001) levels of women with PCOS were significantly higher than those of the control subjects. The glucose disposal rate (M value) was significantly lower in women with PCOS compared to the controls (5.3+/-1.2 mg/kg min vs. 6.7+/-1.6 mg/kg min, p<0.05), even after adjusting for age and BMI. There was no significant correlation of the M value with the anthropometric and a metabolic indices, and a multiple regression analysis of the M value showed no significant variables. CONCLUSION: Our non-obese women with PCOS showed significant insulin resistance compared to their age and BMI comparable control subjects, and-their insulin resistance may be an intrinsic defect not associated with other features, such as hyperandrogenemia or body fat distribution patterns.
Association of High Intracellular Calcium Levels with Insulin Resistance in Women with Polycystic Ovary Syndrome.
Jee Young Oh, Hye Jin Lee, Young Sun Hong, Hye Won Chung, Yeon Ah Sung
Korean Diabetes J. 2004;28(2):101-110.   Published online April 1, 2004
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AbstractAbstract PDF
BACKGROUND
Insulin resistance is an intrinsic defect of polycystic ovary syndrome (PCOS), and elevated levels of cytosolic free calcium in insulin target cells may cause insulin resistance. To our knowledge, the relationship between intracellular calcium and insulin resistance in PCOS has not been investigated. The purpose of this study was to determine whether the levels of intracelluar calcium are changed and if they have any association with insulin resistance in women with PCOS. METHODS: The intracellular calcium levels in the platelets and the insulin sensitivity were measured by fluorescent spectrophotometry and the euglycemic hyperinsulinemic clamp technique, respectively, in 16 women with PCOS and 6 normal cycling women. A 2h, 75 g oral glucose tolerance test was performed to determine the glucose tolerance. RESULTS: The insulin sensitivity measured by the glucose disposal rate(the M-value), was significantly lower in women with PCOS(4.6+/-1.5mg/kg/min vs. 7.0+/-1.3mg/kg/min, p<0.01), but the intracellular calcium levels were significantly higher in women with PCOS compared to the controls(122.7+/-36.7 vs 59.1+/-29.3mmol/L, p<0.01). When the women with PCOS were divided into the overweight or obese(n=9, BMI ?23kg/m2) and lean(n=7, BMI<23kg/m2) groups, both groups had significantly lower M values compared to the control subjects(3.9+/-1.3, 5.5+/-1.2 vs. 7.0+/-1.3mumg/kg/min, p<0.001), and these levels between the overweight/obese and lean PCOS groups showed a significant difference(p<0.001). The overweight/ obese and lean women with PCOS had significantly higher levels of intracellular calcium compared to the control subjects(131.3+/-39.6, 111.7+/-31.8 vs. 59.1+/-29.3nmol/L, p<0.01), but these levels did not differ significantly between the overweight/obese and lean women with PCOS. The intracellular calcium levels showed a significant positive correlation with age, and a negative correlation with the M value(r=-0.55, p<0.05). The BMI-adjusted partial correlation showed marginal significance between elevated levels of intracellular calcium and insulin sensitivity (r=-0.47, p=0.07). CONCLUSION: Women with PCOS showed both insulin resistance and increased levels of intracellular calcium compared to the control subjects. Increased levels of intracellular calcium were associated with insulin resistance in women with PCOS.
Association between Hyperleptinemia and Metabolic Syndrome in an Urban Korean Community.
Jee Young Oh, Young Sun Hong, Yeon Ah Sung
Korean Diabetes J. 2003;27(4):313-322.   Published online August 1, 2003
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BACKGROUND
To determine whether hyperleptinemia is a principal component of metabolic syndrome in a Korean population using factor analysis. METHODS: Metabolic syndrome was defined by the NCEP-ATP III guideline. An oral glucose tolerance test was performed, and plasma samples for leptin and lipid profiles were collected from 199 men and 426 women who had no history of diabetes, hypertension, dyslipidemia, or of taking lipid-lowering, antihypertensive, or antihyperglycemic medications. RESULTS: Leptin level was correlated with overall and central obesity, blood pressure, and glucose or insulin levels in men and women aged 30 to 83. Before and after adjustment for BMI, leptin level was significantly and positively correlated, in women only, with insulin and with insulin resistance, as assessed by a homeostasis model assessment (HOMA) (Ps<0.0001). Factor analysis identified the following four factors from among the metabolic syndrome variables; an obesity/hyperinsulinemia factor, a glucose intolerance factor, a hypertension factor, and a dyslipidemia factor in men. Leptin was clustered as an obesity/ hyperinsulinemia and a dyslipidemia factor in men. In women, four different groups were found: an obesity/hypertension factor, a glucose intolerance factor, an obesity/dyslipidemia factor, and an obesity/hyperinsulinemia factor. Leptin was clustered as an obesity/hyperinsulinemia factor in women. CONCLUSION: Our research suggests that leptin level is associated with metabolic syndrome in relation to obesity and hyperinsulinemia. Moreover, obesity, as opposed to hyperinsulinemia, is related to hypertension or dyslipidemia in women only, and this gender differences may reflect different roles of central adiposity on metabolic abnormalities.
The Prevalence and Incidence of Diabetes in Mokdong, Seoul.
Jee Young Oh, Hye Jin Lee, Eun Soon Hong, Young Sun Hong, Yeon Ah Sung, Sun Hee Lee
Korean Diabetes J. 2003;27(1):73-83.   Published online February 1, 2003
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AbstractAbstract PDF
BACKGROUND
Diabetes has recently become a major public health problem due to the socioeconomic changes in Korea. Epidemiological data for diabetes are needed to establish disease control and health improvement programs in the community. Considering the tendency for larger concentrations of the population in the urban areas of Korea, epidemiological studies in these areas are essential. This this was performed to determine the epidemiologic characteristics, prevalence, and incidence of diabetes in Korean urban communities. METHODS: The target cohort of this study was randomly selected from 20,222 residents living in the Mokdong apartment areas one, two, five and six, Yangcheon-Gu, Seoul. Of the 20,222 residents, 1,011 were residents, of which 766 (male 264, female 502) subjects participated and 372 subjects without diabetes at baseline examination followed up for 2 years. At the baseline and follow-up examination, all subjects underwent a 75g oral glucose tolerance test (OGTT) and anthropometric measurements (height, weight, waist to hip ratio, pulse rate, blood pressure, and subcutaneous skin fold thickness) were performed. RESULTS: There was an 8.5% prevalence of diabetes and 7.8% with impaired glucose regulation (IGR), including impaired glucose tolerance (IGT) and impaired fasting glucose (IFG). The age-adjusted prevalence of diabetes IGR were 8.4% and 7.1%, respectively. The prevalence of diabetes or IGR increased with increasing age. The prevalence of diabetes was associated with aging, family history of diabetes, and high levels of waist to hip ratio. The age-adjusted annual incidence rate of diabetes for subjects over 40 years of age at the baseline was 1.3%. The risk factors for the development of incident diabetes, from a multiple logistic regression analysis, were the waist to hip ratio and the 2-hour postload serum glucose concentrations. CONCLUSION: The prevalence of diabetes in the Mokdong apartment area was slightly higher than in Yonchon, Jungup, or Beijing. The annual incidence of diabetes was lower than that found in the studies in Yonchon or in Pima Indian, but higher than those of Caucasians or American Hispanics.
Sex Hormone Binding Globulin, Body Fat Distribution and Insulin Resistance in Premenopausal Women.
Young Sook Lee, Hye Jin Lee, Jee Young Oh, Young Sun Hong, Yeon Ah Sung
Korean Diabetes J. 2003;27(1):63-72.   Published online February 1, 2003
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AbstractAbstract PDF
BACKGROUND
Low levels of sex-hormone binding globulin (SHBG), an indirect index of androgenicity, have been reported to be associated with obesity, especially central obesity. In women, increased androgenicity is related to hyperinsulinemia, impaired glucose tolerance and the development of type 2 diabetes mellitus. Recent studies have suggested that the relationship between SHBG and insulin resistance was mediated by the change in total or visceral adiposity, and that ethnical differences in the relationship between sex hormone and body fat distribution might exist. METHODS: We examined the associations of SHBG to the body fat distribution and insulin resistance in Korean premenopausal women. The fasting serum level of SHBG was measured by RIA, and the insulin sensitivity by the minimal model derived sensitivity index (SI), using the insulin modified intravenous glucose tolerance test. The amount of body fat, and its distribution, were assessed by anthropometric measurement, bioelectric impedance analyses, and computed tomography at the level of the umbilicus. RESULTS: 1. SHBG was significantly inversely correlated with the body mass index (BMI), waist circumference, visceral fat area, and fasting insulin levels, and was significantly positively correlated to the SI. 2. SHBG was significantly lower in premenopausal women with an impaired glucose tolerance, compared to those with a normal glucose tolerance, and significantly lower in those with hypertension (systolic BP> or =140 mmHg or diastolic BP> or =90 mmHg), compared to those with normal blood pressure. SHBG was also significantly lower in persons with central obesity(waist circumference > or = 80 cm) compared to those without. 3. In a multiple linear regression analysis, the SI was significantly associated with SHBG, after adjustment for age, BMI, systolic blood pressure, triglycerides, HDL- cholesterol, and percentage body fat, but this association disappeared after additional adjustment for visceral fat area. 4. In a multiple linear regression analysis, the fasting plasma insulin, BMI and percentage body fat were significant independent factors associated with SHBG. CONCLUSION: Increased androgenicity as assessed by decreased serum SHBG concentrations, is strongly associated with an unfavorable body fat distribution, hypertension, glucose intolerance, hyperinsulinemia, and insulin resistance.
Impaired Insulin Secretion in Normoglycemic Offspring of Patients with Type 2 Diabetes.
Eun Kyung Byun, Young Sun Hong, Jee Young Oh, Yeon Ah Sung, Yeon Jin Jang
Korean Diabetes J. 2003;27(1):39-48.   Published online February 1, 2003
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AbstractAbstract PDF
BACKGROUND
Although it is well known that insulin secretory defects and insulin resistance are major pathogenetic factors of type 2 diabetes, their relative importance still remains controversial in various ethnic groups. Increased levels of proinsulin, and the proinsulin/insulin (PI/I) ratio, are considered markers of pancreatic dysfunction, and predictors for the development of type 2 diabetes. To reveal which pathogenetic abnormality is most prominent in Koreans with type 2 diabetes, we measured the insulin sensitivity and secretory capacity in the normal glucose tolerant offspring of patients with type 2 diabetes. METHODS: Sixty-two offspring, with normal glucose tolerance (mean age 40.4+/-6.5 BMI 23.4+/-2.7 kg/m2), of type 2 diabetes parents, were compared with and 20, age and BMI-matched control subjects, with on family history of diabetes. We measured the serum levels of proinsulin (PI), specific insulin (I), and C-peptide(C) and calculated the PI/I and C/I ratios, as parameters of hepatic insulin clearance. The insulin sensitivity index (SI) was measured by the intravenous glucose tolerance test (IVGTT) using the MINMOD program, as a marker of insulin sensitivity. The acute insulin response to glucose (AIRg), AIRg by product, SI and the area under the insulin curve (AUCinsulin) were measured by IVGTT, and used as a marker of the insulin secretory capacity. We also evaluated the association between the proinsulin and insulin secretory capacities. RESULTS: Offspring of the type 2 diabetic patients had significantly lower AIRg SI and AUCinsulin (p<0.05), and tended to have lower AIRg (p=0.06), than the control subjects. However, there was no significant difference in the SI between the two groups. However, with the proinsulin, and the insulin, PI/I and C/I ratios, not significant differences were found between the offspring and the control subjects, and the PI/I ratio was not correlated with AIRg, AIRg x SI or SI. CONCLUSION: Insulin secretory defect could be a more prominent factor in the development of type 2 diabetes in Koreans, with no change in the proinsulin secretion.
Pospartum Assessment of Insulin Secretion and Sensitivity in Women with Gestational Diabetes Mellitus (GDM).
Eun Soon Hong, Hye Jin Lee, Young Sun Hong, Eon Ah Sung, Yeon Jin Jang
Korean Diabetes J. 2002;26(5):319-327.   Published online October 1, 2002
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AbstractAbstract PDF
BACKGROUND
Gestational diabetes mellitus (GDM) affects 2~4% of all pregnant women. Women with a history of GDM are at high risk of developing type 2 DM, in the future; with a cumulative incidence is 40~60%. Therefore, the assessment of insulin secretion and sensitivity in women with a history of GDM should help in the elucidation of some of the underlying defects of insulin secretion or action in the evolution of type 2 DM. This study was performed to evaluate the characteristics of insulin secretory capacity and sensitivity in women with gestational diabetes following child birth. METHODS: Oral glucose tolerance tests were carried out at 6~8 weeks postpartum in 22 women with a history of GDM, and 20 age and weight matched non- pregnant controls. Frequently sampled intravenous glucose tolerance test (FSIGT) were done at 10~14 weeks postpartm, and insulin secretion was measured as the acute insulin response to glucose (AIRg) and insulin sensitivity as minimal model derived sensitivity index (SI). AIRg*SI was used as an index for beta-cell function because AIRg can be modulated by SI. RESULTS: According to the results of OGTT, the subjects with a history of GDM were classified into 2 groups, one of normal glucose tolerance (postpartum-NGT) (n=11) and the other of an impaired glucose tolerance (postpartum-IGT)(n=11). There were no significant differences in WHR (waist to hip ratio), blood pressure, and serum lipid concentrations among the controls, postpartum-NGT and postpartum-IGT group. The fasting glucose level was significantly higher in the postpartum-IGT group compared to the postpartum-NGT and control groups (p<0.05). The fasting serum insulin level was significantly lower in the postpartum-NGT and -IGT groups than in the control group (p<0.05). The AIRg and AIRg*SI were significantly lower in the postpartum-NGT and -IGT groups compared to the control group (p<0.05), however the SI was lower in the postpartum-NGT and -IGT groups compared to the control group, but the difference did not reach statistical significance. The percentage of parental with history of type 2 diabetes was significantly greater in the postpartum-IGT group compared to the postpartum-NGT group (p<0.05). No significant predictive factors for subsequent IGT were found inform a logistic regression analysis. CONCLUSION: The insulin secretory capacity of women previously having suffered GDM was impaired, even though their glucose tolerance was restored to normal following child birth. Our results suggest that impaired insulin secretion may be a major path-ophysiological factor in the development of type 2 DM in women with a previous history of GDM.
The Changes in Insulin Secretion and GTPase Activity after the Exposure to High Glucose in Rat Pancreatic Islets.
Young Sun Hong, Yeon Ah Sung, Nan Ho Kyung
Korean Diabetes J. 2000;24(5):515-523.   Published online January 1, 2001
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AbstractAbstract
BACKGROUND
Type 2 diabetes mellitus is characterized by defective glucose- induced and glucose-potentiated insulin secretion. Chronic elevation of glucose levels are considered to be a cause of impaired insulin secretion. It has been suggested that such defects in insulin secretion can be related to the alteration in stimulus-secretion coupling. Recent studies have provided evidences for the existence of guanine nucleotide-binding protein (G protein), and the regulatory role of G protein and GTPase activity in stimulus-secretion coupling in pancreatic islets. This study was performed to determine whether the exposure to high glucose concentration alters GTPase activity with decreased insulin secretion in pancreatic islets isolated from normal rats. METHODS: Pancreatic islets isolated from normal Sprague-Dawley rats were incubated in high (20 mM) and low (5 mM) glucose concentration for 48 hours. After incubation, glucose (20 mM) induced insulin secretion was measured. Then subcellular fractions of islets by homogenization and differential centrifugation were obtained and glucose induced inhibition of GTPase activities in each fraction was measured. RESULTS: 1) After 48 hour exposure to 5 mM and 20 mM glucose, insulin secretion in response to 20 mM glucose were 134.4+/-16.8 fmol/10 islets/hr and 90.0+/-10.2 fmol/10 islets/hr, respectively. After the exposure to high glucose, glucose-induced insulin secretion significantly decreased (p<0.05). 2) In each subcellular fraction, there was no significant difference between the islets exposed to 5 mM and 20 mM glucose in the degree of inhibition of GTPase activities by high glucose. CONCLUSION: The exposure to high glucose for 48 hours decreased insulin secretion without any significant differences in the degree of inhibition of GTPase activities. This results suggest that impaired insulin secretion by high glucose is not associated with the change in GTPase activity.
Mechanism of the lnsulin Secretory Defect by Chronically Elevated Glucose Leveis in Pancreatic lslets: Depletion of lnsulin Content due to Hyperstimulation by Glucose.
Yeon Ah Sung, Young Sun Hong
Korean Diabetes J. 2000;24(1):1-9.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is characterized by impaired insulin secretion and decreased insulin sensitivity, although the exact relationship between these two derangements during the development of the disease has not been fully established. Hyperglycemia per se impairs insulin secretion in pancreatic B-cell and the mechanism of impaired insulin by chronic hyperglycemia could be the clue to clarify pathogenesis of type 2 diabetes, and possibly identify the treatments. This study was performed to elucidate the mechanism of impairment of glucose induced insulin secretion by chronic hyperglycemia in pancreatic islets. METHODS: Pancreatic islets were isolated from Sprague-Dawley rats. After incubation of islets in high glucose (20mM) and low glucose (5mM) media for 10 days, glucose (16.7 mM) induced insulin secretion and insulin and DNA content in the islets were measured. Then subcellular distribution of low molecular and heterotrimeric G-proteins were assessed by ADP-ribosylation and radiolabeled GTP binding. RESULTS: 1) Glucose-induced insulin secretion of the islets cultured for 10 days in high glucose media was significantly lower when compared with that in islets cultured in low glucose media (p<0,05) 2) Subcellular distributions of low and heterotrimeric G-protein was not different in the islets cultured in low glucose when compared to those cultured in high glucose. 3) lnsulin content was significantly lower in the islets cultured in high glucose media compared with that in islets cultured in low glucose media (p<0.05) 4) DNA content was not significantly different between the islets cultured in low and high glucose media, and insulin content to DNA ratio was significantly lower in the islets cultured in high glucose media compared with that in islets cultured in low glucose media (p<0.05). CONCLUSION: Impaired insulin secretion to glucose in pancreatic islets exposed to high glucose is caused by depletion of insulin stores affer hyperstimulation.
Prevalence and Risk Factors of Erectile Dysfunction in Diabetic Men by Self-Reported Questionnaires.
Jin Hwa Lee, Jee Young Oh, Young Sun Hong, Yeon Ah Sung, Nan Ho Kyung, Woo Sik Chung, Eun Young Choi
Korean Diabetes J. 1998;22(4):538-545.   Published online January 1, 2001
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BACKGROUND
Erectile dysfunction is the consistent inability to achieve or sustain an erection of suffieient rigidity for sexual intercourse. Erectile dysfunction is an important cause of decreased quality of life in diabetic men. The prevalence of ereciile dysfunction has been reported to be three times higher in diabetic men than nondiabetics. Erectile dysfunction in diabetic men has been associated with increased age, poor glycemic control, smoling, alcohol intake, depression, and microvascular diabetic complication. Our purpose was to determine the prevalence of erectile dysfunction in diabetic men and to assess risk factors re]ated to erectile dysfunction in diabetes mellitus. METHODS: From l53 diabetic men visiting Ewha Womans University Hospital from March, 1997 to March, 1998, we analyzed the self-reported questionnaires. Three questions about erection and one question about overall sexual satisfaetion were given and the answer to each question was categorized into 5 degrees according to the severity of sexua] dysfunction. Erectile dysfunction was diagnosed when any answer for erection showed a degree lower than 4. We obtained the history of smoking, alcohol and hypertension, and measured the current weight and height. Fasting glucose, HBA 1c and lipid profile were me measured. We also evaluated for the presence of diabetic retinopathy, nephropathy and neuropathy. RESULTS: 1) The self-reported prevalence of erectile dysfunction in diabetic men was 75.5 % in this study. 2) In the patients with erectile dysfunction, age, duration of diabetes mellitus, HbAlc, and systolic blood pressure were significantly higher, and BMI and triglyceride significantly lower than in the patients without erectile dysfunction. 3) The prevalence of erectile dysfunction was increased with aging and increasing duration of diabetes mellitus, HBA. was significantly positively related and BMI was inversely related to erectile dysfunction. 4) Age and HbA 1c were independently and positively related to erectile dysfunction by multiple logistic regression. 5) The erectile dysfunction was significantly associated with diabetic autonomic neuropathy and retinopathy. CONCLUSION: The prevalence of self-reported erectile dysfunction in diabetic men was 75.5 % in this study, and it was significantly related to aging and the degree of the glycemic control.

Diabetes Metab J : Diabetes & Metabolism Journal
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