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Hye Seung Jung  (Jung HS) 7 Articles
Autophagy in Diabetes.
Hye Seung Jung, Myung Shik Lee
Korean Diabetes J. 2009;33(6):453-457.   Published online December 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.6.453
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AbstractAbstract PDF
Diabetes mellitus is characterized by decreased insulin secretion and action. Decreased insulin secretion results from a reduction in mass and/or function of pancreatic beta-cells. Apoptosis, oxidative stress, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress responses have been suggested as mechanisms for the changes in beta-cells in type 2 diabetes; however, the underlying causes have not been clearly elucidated. Autophagy is an intracellular process that maintains cellular homeostasis through degradation and recycling of organelles. Recently, we reported reduction of beta-cell mass in autophagy-deficient mice. Pancreatic insulin content was also decreased due to the decreased beta-cell mass and the reduced number of insulin granules. Morphological analysis of these beta-cells revealed an accumulation of ubiquitinated proteins, swollen mitochondria, and distended ER. Insulin secretory function ex vivo was also impaired. As a result, autophagy-deficient mice showed hypoinsulinemia and hyperglycemia. These results suggested that autophagy is necessary to maintain the structure, mass and function of beta-cells. In addition, as autophagy may play a protective role against ER stress and rejuvenate organelle function, impaired autophagy may lead to mitochondrial dysfunction and ER stress, which have been implicated as causes of insulin resistance. Therefore, in addition to beta-cell homeostasis, dysregulated autophagy may possibly be involved in insulin resistance.
Effects of Islet Transplantation on Endogenous beta-cell Regeneration after Partial Pancreatectomy in Rodents.
Hye Seung Jung, You Ran Ahn, Seung Hoon Oh, Jung Hwa Jung, Tae Hyun Kim, You Cheol Hwang, Mira Kang, Yongsuk Bae, Young seok Kim, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
Korean Diabetes J. 2007;31(2):113-122.   Published online March 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.2.113
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AbstractAbstract PDF
BACKGROUND
Islet transplantation is one of regimens supplying the deficient insulin in diabetes patients, but the effects of islet grafts on the changes of endogenous beta-cells are not clear. In the present study, we examined the changes of endogenous beta-cell mass after islet transplantation in partially pancreatectomized mice. METHODS: Balb/c mice were 70% pancreatectomized, transplanted with syngeneic islets (group IV), and were compared with pancreatectomized mice treated with insulin (group III) or no insulin (group II). Blood glucose levels and body weight were monitored. Remnant pancreas was obtained at 6 or 10 days after pancreatectomy, and immunohistochemical staining was done for the evaluation of beta-cell mass changes. RESULTS: Hyperglycemia and weight loss were induced after pancreatectomy. After islet transplantation or insulin treatment, blood glucose levels recovered to normal, and body weight started to increase. Plasma insulin levels were higher and beta-cell mass was larger in group IV than in group II (P < 0.05). Especially, the difference of beta-cell mass between them was more evident at 7 days as compared to at 3 day after transplantation. When compared to group III, group IV showed larger individual beta-cell area after 7 days and larger beta-cell mass after 3 days of islet transplantation (P < 0.05). CONCLUSION: These observations indicate that islet transplantation plays a role in enhancing remnant beta-cell regeneration after partial pancreatectomy in rodents.
Adiponectin and Diabetes Mellitus.
Hye Seung Jung, Kyong Soo Park
Korean Diabetes J. 2004;28(4):239-249.   Published online August 1, 2004
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AbstractAbstract PDF
No abstract available.
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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AbstractAbstract 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.
Genetic Association of Adiponectin Polymorphisms with Risk of Type 2 Diabetes Mellitus.
Yun Yong Lee, Nam Seok Lee, Young Min Cho, Min Kyong Moon, Hye Seung Jung, Young Joo Park, Hong Je Park, Byoung Soo Youn, Hong Kyu Lee, Kyong Soo Park, Hyoung Doo Shin
Korean Diabetes J. 2003;27(6):438-448.   Published online December 1, 2003
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AbstractAbstract PDF
BACKGROUND
Adiponectin, an adipocyte-secreted protein, is known to modulate insulin sensitivity, glucose homeostasis and the development of atherosclerosis. Recently, several single nucleotide polymorphisms (SNPs) in the adiponectin gene have been reported to be associated with type 2 diabetes and components of the insulin resistance syndrome. METHODS: The frequencies of SNP T45G and G276T of the adiponectin gene was examined in 493 unrelated type 2 diabetic and 136 non-diabetic control Korean subjects. The clinical characteristics and plasma adiponectin levels of the subjects were compared within these genotypes. RESULTS: The T allele at SNP45 was significantly more frequent in the type 2 diabetes than in the control subjects (71.6 vs. 64.3%, p=0.013). The subjects with the G/G genotype of SNP45 were at reduced risk for type 2 diabetes (OR: 0.495, 95% CI 0.246-0.995, p=0.048) compared with those having the T/T genotype. However, there were no statistically significant differences in allele the frequencies (G frequency in the control vs. the diabetic group 73.9 vs. 68.9%, p=0.106) and genotype frequencies at SNP276 between groups. The subjects with the T/T genotype at SNP45 had higher a body mass index (24.6+/- 3.1 vs. 24.1+/-2.8 kg/m2, p=0.036) and serum triglyceride levels (2.03+/-1.31 vs. 1.87+/-1.38 mmol/1, p=0.041) than the T/G+G/G genotypes in the diabetic group. Those with the T/T genotype also had lower plasma adiponectin levels than those without T/T genotype at SNP45 in the control group (6.11+/-3.10 vs. 8.24+/-4.24 g/mL, p=0.043). There was a similar trend in diabetic group, but this did not reach statistical significance (4.32+/-2.81 vs. 4.96+/-3.26 g/mL, p=0.097). The SNP276 had no association with the clinical features of insulin resistance or plasma adiponectin level. CONCLUSION: The T/T genotype of SNP45 in the adiponectin gene was associated with a low adiponectin level, high body mass index, the serum triglyceride level and risk of type 2 diabetes mellitus. The SNP276 in the adiponectin gene may not be an important determinant of insulin resistance or type 2 diabetes in Korean subjects.
Clinical Characteristics of Post-transplantation Diabetes Mellitus associated with Tacrolimus Therapy after Kidney Transplantation.
Young Min Cho, Hye Seung Jung, Yun Yong Lee, Min Kyong Moon, Suk Kyung Kim, Hyun Jung Jeon, Curie Ahn, Jong Won Ha, Sang Joon Kim, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2002;26(6):509-519.   Published online December 1, 2002
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AbstractAbstract PDF
BACKGROUND
Post-transplantion diabetes mellitus (PTDM) is a major metabolic complication of transplantation and shows a variable incidence among studies with different population or different definition. We examined the incidence and the risk factors of PTDM in the Korean patients with tacrolimus-based immunosuppression following kidney transplantation, and also investigated the change of insulin secretory capacity. METHODS: Twenty-one patients using tacrolimus as primary immunosuppressant were recruited and tested with serial 75-g oral glucose tolerance test (OGTT) at 0, 1, 3, and 6 months after kidney transplantation. RESULTS: According to the American Diabetes Association criteria, the incidence of PTDM was 57.1% (12 of 21). Baseline characteristics of PTDM group were old age (especially > 40 yr), high body mass index, high fasting glucose, high plasma insulin, and increased insulin resistance. The insulin secretory capacity in PTDM group was maximally suppressed 3 months after transplantation and was gradually restored thereafter along with dose reduction of tacrolimus. CONCLUSIONS: Attention should be paid to the patients, especially who are over 40 yr of age, throughout the high dose tacrolimus therapy.
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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AbstractAbstract 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.

Diabetes Metab J : Diabetes & Metabolism Journal