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Yeon Jin Jang  (Jang YJ) 11 Articles
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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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.
Relation of Angiotensin Converting Enzyme (ACE) Gene Polymorphism to Insulin Sensitivity and Carotid Atherosclerosis in Female Nondiabetic Offspring of NIDDM Patients.
Jee Young Oh, Yeon Ah Sung, Nan Ho Kyung, Yeon Jin Jang
Korean Diabetes J. 1999;23(6):831-842.   Published online January 1, 2001
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BACKGROUND
Angiotensin converting enzyme (ACE) gene polymorphism has been known to related to atherosclerotic heart disease such as acute myocardial infarction or left ventricular hypertrophy, diabetic nephropathy or retinopathy, as well as, insulin sensitivity. However, an exact relationship between ACE gene polymorphism and aforementioned diseases have not been fully established. It has been suggested that NIDDM and atherosclerosis may have common pathogenesis since some of NIDDM patients already have atherosclerotic changes at the time of the initial diagnosis. Futhermore, offspring of NIDDM patients are considered as a high risk group for both NIDDM and atherosclerosis, and these two disorders are known to be affected by some common genetic factors. Therefore, in the present study, we planned to investigate, by analyzing female offspring of NIDDM patients (offspring), the relationship of ACE gene polymorphism to insulin resistance and atherosclerosis. METHODS: Fifty-three female offspring of patients with NIDDM were participated in this study, and twenty age-BMI matched normal glucose tolerant subjects without a family history of diabetes were selected as the controls. Based on 75-g oral glucose tolerance test, subjects were divided into normal glucose tolerance (n=42) or impaired glucose tolerance (n=ll). We assessed the patterns of body fat distribution by anthropometric measurement, bioelectric impedence analysis and computed tomogram; insulin sensitivity by minimal model analysis using insulin modified frequently sampled intravenous glucose tolerance test; carotid intima-medial thickness by ultrasonography. We investigated the alleles of the ACE gene by PCR. RESULT: 1. ACE genotypes in offspring were distributed as follows; 39.6% for II, 32.0% for ID, 28.4% for DD 55.7% for I al#lele, 44.3% for D allele. This distribution was not significantly different from those in controls (35.0% for II, 55.0% for ID, 10.0% for DD, 62.5% for I allele, and 37.5% for D allele). 2. There was no significant difference in body mass index (BMI), systolic and diastolic blood pressure, and serum lipid concentrations among three genotypes. However, in the subjects with ID genotype, VSR was significantly increased compared to the subjects with DD genotype (p<0.05). In the subjects with ID genotype, percent body fat, visceral fat area, CIMT were increased, and SI and SG were decreased in comparison to II and DD subjects, although the differences between the two groups did not reached the statistical significance. 3. When the subjects were divided into quartiles of CIMT, the frequency of ID genotype of ACE showed the tendency of increment from the lowest to the highest quartile of CIMT. 4. Multiple regression analysis showed that ACE genotypes was significantly associated with visceral obesity, carotid intima-medial thickening and insulin sensitivity. CONCLUSION: ACE genotypes was not significantly associated with visceral obesity, carotid intima- medial thickening and insulin sensitivity. However, to explore the true associations of ACE gene polymorphism with insulin resistance and ather-osclerosis, we further suggest and recommend prospective studies.
Insulin Secretion, Insulin Sensitivity and Body Fat Distribution Patterns in Patients with Impaired Glucose Tolerance.
Jin Hwa Lee, Yeon Ah Sung, Nan Ho Kyung, Yeon Jin Jang
Korean Diabetes J. 1999;23(5):647-660.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes mellitus(DM) is characterized by impaired insulin secretion and decreased insulin sensitivity, and often preceded by impaired glucose tolerance (IGT). To determine the relative importance of impaired insulin secretion and insulin resistance in development of type 2 DM, we evaluated body fat distribution patterns, insulin secretion and sensitivity in patients with IGT. METHODS: Thirty-six patients with IGT and age and weight matched twenty-four control subjects, were recruited from urban diabetes incidence cohort. Fasting serum glucose and insulin were measured. Body fat distribution pattern was assessed by waist to hip ratio (WHR), percent body fat and fat mass measured by bioelectrical impedence analyzer, and visceral to subcutaneous fat ratio (VSR) at the level of umbilicus using the computed tomography. Using insulin modified intravenous glucose tolerance test, insulin sensitivity was measured as minimal model derived sensitivity index (S(I)), and insulin secretion was measured as acute insulin response to glucose (AIR(g)) and beta-cell disposition index (AlR(g) X Sr). RESULT: l) In the patients with IGT, AIR(g)X S(I)(p<0.01) and area under the curve of insulin (AUC(I))(p<0.01) were significantly decreased compared with control subjects and age was greater than control subjects without statistical significance (p=0.17). 2) In the patients with IGT, body fat distribution patterns, indices of insulin secretion and sensitivity were not different according to the presence of family history of DM. AIR, and S(I) were negatively correlated in control subjects (r=-0.38, p=0.08) and the patients with IGT without family history of DM (r=-0.37, p=0.10), but not in the patients with IGT with family history of DM. 3) In the patients with IGT, indices of insulin secretion and sensitivity were not different according to body mass index (BMI). In both obese (BMI>=25 kg/m ) and non-obese (BMI<25 kg/m) patients with IGT, AIR(g)(p<0.05) and AIR(g) X S(I) were significantly decreased compared with control subjects (p<0.01). 4) In control subjects, age (p<0.05) and body fat mass (p<0.05) were significantly associated with AIR(g) X S(I) by multiple regression analysis. In the patients with IGT, body fat mass was significantly associated with AIR(g)(p<0.01) and AUC(I)(p<0.01), and BMI(p<0.01) was significantly associated with S(I). CONCLUSION: In patients with IGT, impaired insulin secretion was more prominent than decreased insulin sensitivity as compared with control subjects regardless of obesity and the presence of family history.
Dehydroepiandrosterone-Sulfate, Sex Hormone Binding Globulin, Body Fat Distribution Pattern and Insulin Resistance in Women.
Young Sun Hong, Jee Young Oh, Yeon Ah Sung, Nan Ho Kyung, Yeon Jin Jang
Korean Diabetes J. 1998;22(3):328-337.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Sex hormone-binding globulin (SHBG) has been known to be associated with obesity, central fat accumulation and insulin resistance and thought to be a indirect marker for androgenicity in women. The relationships between circulating dehydroepiandrosterone(DHEA). dehydroepiandrosterone sulfate(DHEA-S) levels and body fat accumulation are still controversial. We conducted a cross-sectional study to eva]uate the relationships between serum levels of SHBG, DHEA-S, body fat distribution pattern and insulin sensitivity in women. METHODS: We tested 57 women(age 30~65yr; BMI 18.5~32.8kg/m, 45 premenopausal on the 5~10 day of the menstrual cycle, 12 postmenopausal who were not using hormone replacement therapy) with varying degree of glucose tolerance(32 normal glucose tolerance(NGT), 17 impaired glucose tolerance(IGT) and 8 newly diagnosed diabetes). lnsulin sensitivity was measured as minimal model derived sensitivity index(S) using insulin modified IV glucose tolerance test and fasting serum levels of SHBG and DHEA-S were measured by RIA. Body fat distribution pattern was assessed by waist to hip ratio(WHR),% body fat measured by bioelectrical impedance analyzer, subcutaneous fat area(SFA), visceral fat area(VFA) and VFA to SFA ratio(VSR) at the level of umbilicus using the computed tomography. RESULTS: 1) Measured SHBG and DHEA-S levels were not significantly different among subjects with NGT, IGT and diabetes. 2) SHBG was inversely associated with age, BMI, WHR, diastolic blood pressure, VFA, SFA, VSR,% body fat, fasting insulin and positively associated with S, whereas DHEA-S did not show any significant correlation with above variables except diastolic blood pressure. 3) SHBG level was significantly lower(p<0.05) and DHEA-S level was insignificantly lower (p=0.05) in postmenopausal women than in premenopausal women but the significance disappeared after adjustment for age, BMI, WHR and% body fat. 4) BMI was independently and negatively related to S, WHR and fasting insulin to SHBG by multiple regression analysis. CONCLUSION: We confirmed that SHBG was independently associated with central obesity and fasting hyperinsulinemia. However, S was independently associated with BMI only. It suggested that hyperinsulinemia in insulin resistance might cause the decreased level of SHBG even thaugh the directionality of the association was uncertain because of a cross-sectional nature of this study.
Vitamin C causes lung damages in diabetic rats.
Hyoung Sup Park, Hea Nam Hong, Yeon Jin Jang
Korean Diabetes J. 1993;17(2):183-190.   Published online January 1, 2001
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AbstractAbstract PDF
No abstract available.
The oxidative modification of hepatic intracellular proteins in the streptozotocin-induced diabetic rats.
Yeon Jin Jang, Jae Dam Lee, Hyoung Sup Park
Korean Diabetes J. 1993;17(2):175-182.   Published online January 1, 2001
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No abstract available.
The estimation of the variabilities in the estimates of insulinsensitivity from the minimal model method.
Yeon Jin Jang
Korean Diabetes J. 1991;15(2):189-195.   Published online January 1, 2001
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No abstract available.
The role of impaired response of skeletal muscle glycogen synthase activity to insulin in the pathogenesis of insulin resistance instreptozotocin induced diabetic rats.
Sung Woo Park, Kyo Il Suh, Kyung Soo Park, Yeon Jin Jang, Ki Up Lee
Korean Diabetes J. 1991;15(2):183-188.   Published online January 1, 2001
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No abstract available.
Importance of transcapillary insulin transport on dynamics ofinsulin action in the non-steady state.
Yeon Jin Jang
Korean Diabetes J. 1991;15(1):41-51.   Published online January 1, 2001
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No abstract available.
The effect of insulin on glycogen synthase activity in individualskeletal muscle in rat.
Sung Woo Park, Kye Il Suh, Jin Hee Kim, Hae Sun Park, Yeon Jin Jang, Ki Up Lee
Korean Diabetes J. 1991;15(1):35-40.   Published online January 1, 2001
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AbstractAbstract PDF
No abstract available.

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