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1.
Korean Journal of Otolaryngology - Head and Neck Surgery ; : 806-812, 2022.
Article in Korean | WPRIM | ID: wpr-969040

ABSTRACT

Background and Objectives@#The head and neck multidisciplinary team (MDT) approach plays a crucial role in bringing together the ideas of various medical professionals. This study aimed to evaluate the early characteristics of the MDT approach for head and neck cancer and analyzed patients’ satisfaction.Subjects and Method We analyzed 450 head and neck cancer patients who received MDT care from August 2014 to June 2022. Patient satisfaction with MDT care was evaluated by selfadministered questionnaires consisting of 9 questions. @*Results@#Of 450, 298 (66.2%) were male and 152 (33.8%) were female. The mean age was 60.8±14.7 year. The most common primary site was the larynx (17.3%), followed by the oral cavity and oropharynx. A total of 726 cases of the MDT approach were performed in 266 MDT sessions, and the mean number of patients per MDT session was 2.74. The number of medical professionals participating in MDT ranged from a minimum of 3 to a maximum of 9, with a mean of 5.11. The mean running time of MDT meetings per case was 19.51 minutes. The time of the 2nd MDT was significantly shorter than that of the 1st or 3rd MDT. The mean score was close to very satisfactory in each of the 9 patient satisfaction questions. @*Conclusion@#We believe that the MDT approach is feasible and recommend its introduction for the treatment of head and neck cancer as most patients have shown very high satisfaction. Further studies on the role and efficacy of MDT care for head and neck cancer are necessary.

2.
The Korean Journal of Orthodontics ; : 157-169, 2020.
Article | WPRIM | ID: wpr-835182

ABSTRACT

Objective@#The aim of this retrospective study was to evaluate the pre- and postsurgical bone densities at alveolar and extra-alveolar sites following twojaw orthognathic surgery. @*Methods@#The sample consisted of 10 patients (mean age, 23.2 years; range, 18.0–27.8 years; 8 males, 2 females) who underwent two-jaw orthognathic surgery. A three-dimensional imaging program (Invivo 5) was used with multidetector computed tomography images taken preand postoperatively (obtained 32.3 ± 6.0 days before surgery and 5.8 ± 2.6 days after surgery, respectively) for the measurement of bone densities at the following sites: (1) alveolar bone in the maxilla and mandible, (2) extra-alveolar sites, such as the top of the head, menton (Me), condyle, and the fourth cervical vertebrae (C4). @*Results@#When pre- and postsurgical bone densities were compared, an overall tendency of decrease in bone density was noted. Statistically significant reductions were observed in the densities of cancellous bone at several areas of the maxillary alveolar bone; cortical and cancellous bone in most areas of the mandibular alveolar bone; cortical bone in Me; and cancellous bone in C4. There was no statistically significant difference in bone density in relation to the depth of the alveolar bone. In a comparison of the bone densities between groups with and without genioplasty, there was almost no statistically significant difference. @*Conclusions@#Accelerated tooth movement following orthognathic surgery may be confirmed with reduced bone density. In addition, this study could offer insights into bone metabolism changes following orthognathic surgery, providing direction for further investigations in this field.

3.
Nutrition Research and Practice ; : 87-94, 2019.
Article in English | WPRIM | ID: wpr-741711

ABSTRACT

BACKGROUND/OBJECTIVES: Oxidative stress is a major effector of various diseases; accordingly, antioxidants are frequently ingested in order to prevent or alleviate disease symptoms. Kimchi contains various natural antioxidants, and it is known that the functional activity varies depending on the ingredients and fermentation state. Black raspberries (BR) contain various bioactive compounds with antioxidant effects. This study investigated the antioxidant and liver-protection effects of kimchi supplemented with black raspberry juice powder (BJP). MATERIALS/METHODS: BJP-added kimchi (BAK; at 0.5%, 1%, and 2% concentrations of BJP) and control (without BJP) were prepared and fermented at 4℃ for 4 weeks. Changes in the antioxidant effects of BAK during fermentation were investigated. In addition, the protective activity of BAK against oxidative stress was investigated in a liver cirrhosis-induced animal model in vivo. RESULTS: BAK groups showed the acidity and pH of optimally ripened (OR) kimchi at 2 weeks of fermentation along with the highest lactic acid bacterial counts. Additionally, BAK groups displayed a higher content of phenolic compounds and elevated antioxidant activities relative to the control, with the highest antioxidant effect observed at 2 weeks of fermentation of OR 1% BAK. After feeding the OR 1% BAK to thioacetamide-induced liver cirrhosis rats, we observed decreased glutamate oxaloacetate transaminase and glutamate pyruvate transaminase activities and elevated superoxide dismutase activity. CONCLUSIONS: These findings showed that the antioxidant effects of OR BAK and feeding of OR 1% BAK resulted in liver-protective effects against oxidative stress.


Subject(s)
Animals , Rats , Antioxidants , Bacterial Load , Fermentation , Glutamic Acid , Hydrogen-Ion Concentration , Lactic Acid , Liver Cirrhosis , Liver , Models, Animal , Oxaloacetic Acid , Oxidative Stress , Phenol , Pyruvic Acid , Rubus , Superoxide Dismutase
4.
Endocrinology and Metabolism ; : 115-123, 2017.
Article in English | WPRIM | ID: wpr-64568

ABSTRACT

BACKGROUND: Renal tubulointerstitial fibrosis is a common feature of the final stage of nearly all cause types of chronic kidney disease. Although classic peroxisome proliferator-activated receptor γ (PPARγ) agonists have a protective effect on diabetic nephropathy, much less is known about their direct effects in renal fibrosis. This study aimed to investigate possible beneficial effects of lobeglitazone, a novel PPARγ agonist, on renal fibrosis in mice. METHODS: We examined the effects of lobeglitazone on renal tubulointerstitial fibrosis in unilateral ureteral obstruction (UUO) induced renal fibrosis mice. We further defined the role of lobeglitazone on transforming growth factor (TGF)-signaling pathways in renal tubulointerstitial fibrosis through in vivo and in vitro study. RESULTS: Through hematoxylin/eosin and sirius red staining, we observed that lobeglitazone effectively attenuates UUO-induced renal atrophy and fibrosis. Immunohistochemical analysis in conjunction with quantitative reverse transcription polymerase chain reaction and Western blot analysis revealed that lobeglitazone treatment inhibited UUO-induced upregulation of renal Smad-3 phosphorylation, α-smooth muscle actin, plasminogen activator inhibitor 1, and type 1 collagen. In vitro experiments with rat mesangial cells and NRK-49F renal fibroblast cells suggested that the effects of lobeglitazone on UUO-induced renal fibrosis are mediated by inhibition of the TGF-β/Smad signaling pathway. CONCLUSION: The present study demonstrates that lobeglitazone has a protective effect on UUO-induced renal fibrosis, suggesting that its clinical applications could extend to the treatment of non-diabetic origin renal disease.


Subject(s)
Animals , Mice , Rats , Actins , Atrophy , Blotting, Western , Collagen Type I , Diabetic Nephropathies , Fibroblasts , Fibrosis , In Vitro Techniques , Mesangial Cells , Peroxisomes , Phosphorylation , Plasminogen Activator Inhibitor 1 , Polymerase Chain Reaction , Renal Insufficiency, Chronic , Reverse Transcription , Transforming Growth Factor beta , Transforming Growth Factors , Up-Regulation , Ureter , Ureteral Obstruction
5.
Journal of Preventive Medicine and Public Health ; : 143-152, 2016.
Article in English | WPRIM | ID: wpr-11120

ABSTRACT

OBJECTIVES: Metabolic syndrome is a cluster of risk factors for type 2 diabetes mellitus and cardiovascular disease. Associations between metabolic syndrome and several types of cancer have recently been documented. METHODS: We analyzed the sample cohort data from the Korean National Health Insurance Service from 2002, with a follow-up period extending to 2013. The cohort data included 99 565 individuals who participated in the health examination program and whose data were therefore present in the cohort database. The metabolic risk profile of each participant was assessed based on obesity, high serum glucose and total cholesterol levels, and high blood pressure. The occurrence of cancer was identified using Korean National Health Insurance claims data. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models, adjusting for age group, smoking status, alcohol intake, and regular exercise. RESULTS: A total of 5937 cases of cancer occurred during a mean follow-up period of 10.4 years. In men with a high-risk metabolic profile, the risk of colon cancer was elevated (HR, 1.40; 95% CI, 1.14 to 1.71). In women, a high-risk metabolic profile was associated with a significantly increased risk of gallbladder and biliary tract cancer (HR, 2.05; 95% CI, 1.24 to 3.42). Non-significantly increased risks were observed in men for pharynx, larynx, rectum, and kidney cancer, and in women for colon, liver, breast, and ovarian cancer. CONCLUSIONS: The findings of this study support the previously suggested association between metabolic syndrome and the risk of several cancers. A high-risk metabolic profile may be an important risk factor for colon cancer in Korean men and gallbladder and biliary tract cancer in Korean women.


Subject(s)
Female , Humans , Male , Biliary Tract Neoplasms , Blood Glucose , Breast , Cardiovascular Diseases , Cholesterol , Cohort Studies , Colon , Colonic Neoplasms , Diabetes Mellitus, Type 2 , Follow-Up Studies , Gallbladder , Hypertension , Kidney Neoplasms , Larynx , Liver , Metabolome , National Health Programs , Obesity , Ovarian Neoplasms , Pharynx , Proportional Hazards Models , Rectum , Risk Factors , Smoke , Smoking
6.
Journal of Preventive Medicine and Public Health ; : 180-187, 2015.
Article in English | WPRIM | ID: wpr-211247

ABSTRACT

OBJECTIVES: Metabolic syndrome is an important etiologic factor in the development of certain types of cancers. The economic cost of the treatment of cancer has been steadily increasing. We therefore estimated the economic burden of cancers attributable to metabolic syndrome in Korea. METHODS: We reviewed metabolic syndrome-related cancers and relative risk and then calculated population attributable fractions. We analyzed insurance claims data for metabolic syndrome-related cancers in 2012 in order to estimate the direct costs associated with these cancers, including hospitalization, outpatient visits, transportation costs, and caregivers' costs as well as indirect costs such as loss of productivity due to cancer treatment and premature death. RESULTS: In 2012, 18 070 patients in Korea had cancers attributable to metabolic syndrome. The economic burden was USD 199.8 million and the direct and indirect costs were USD 124.5 million and USD 75.3 million, respectively. CONCLUSIONS: We estimated the economic burden of cancers attributable to metabolic syndrome in Korea and the efforts are necessary to reduce this burden.


Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Cost of Illness , Insurance Claim Reporting , Metabolic Syndrome/complications , Neoplasms/economics , Republic of Korea/epidemiology , Risk
7.
Cancer Research and Treatment ; : 583-590, 2015.
Article in English | WPRIM | ID: wpr-43513

ABSTRACT

PURPOSE: This study estimates the socioeconomic cost and burden for breast cancer patients in Korea between 2007 and 2010. MATERIALS AND METHODS: This study used a prevalence-based approach to estimate the cost of breast cancer. Breast cancer patients were defined as those who were hospitalized or have visited an outpatient clinic during the period from 2007 to 2010. The socioeconomic costs of breast cancer were subdivided into two costs: direct and indirect. RESULTS: From 2007 to 2010, the prevalence of treated breast cancer increased from 7.9% to 20.4%. The total socioeconomic costs incurred by breast cancer increased by approximately 40.7% from US $668.49 million in 2007 to US $940.75 million in 2010. The direct medical care costs for 2010 were 1.4 times greater (US $399.22 million) than for 2007 (US $278.71 million). The direct non-medical costs rose from US $50.69 million in 2007 to US $75.83 million in 2010, a 49.6% increase. Regarding the economic burden of breast cancer, the total indirect costs were US $339.09 million in 2007 and increased by 37.3% to US $465.70 million in 2010. In the sensitivity analysis, with the annual discount rate for each year ranging from 0%-5%, the costs increased 1.1-1.2 times. CONCLUSION: Due to the growing incidence of breast cancer, the annual prevalence and related costs are increasing. We must strive to reduce the socioeconomic burden of breast cancer through preventive measures and early screening.


Subject(s)
Humans , Ambulatory Care Facilities , Breast Neoplasms , Breast , Cost of Illness , Health Care Costs , Incidence , Korea , Mass Screening , Prevalence
8.
Journal of Preventive Medicine and Public Health ; : 84-93, 2014.
Article in English | WPRIM | ID: wpr-218977

ABSTRACT

OBJECTIVES: The incidence and survival rate of colorectal cancer in Korea are increasing because of improved screening, treatment technologies, and lifestyle changes. In this aging population, increases in economic cost result. This study was conducted to estimate the economic burden of colorectal cancer utilizing claims data from the Health Insurance Review and Assessment Service. METHODS: Economic burdens of colorectal cancer were estimated using prevalence data and patients were defined as those who received ambulatory treatment from medical institutions or who had been hospitalized due to colorectal cancer under the International Classification of Disease 10th revision codes from C18-C21. The economic burdens of colorectal cancer were calculated as direct costs and indirect costs. RESULTS: The prevalence rate (per 100 000 people) of those who were treated for colorectal cancer during 2010 was 165.48. The economic burdens of colorectal cancer in 2010 were 3 trillion and 100 billion Korean won (KRW), respectively. Direct costs included 1 trillion and 960 billion KRW (62.85%), respectively and indirect costs were 1 trillion and 160 billion (37.15%), respectively. CONCLUSIONS: Colorectal cancer has a large economic burden. Efforts should be made to reduce the economic burden of the disease through primary and secondary prevention.


Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Middle Aged , Young Adult , Colorectal Neoplasms/economics , Cost of Illness , Health Care Costs , Health Expenditures , Prevalence , Republic of Korea
9.
Experimental & Molecular Medicine ; : e73-2014.
Article in English | WPRIM | ID: wpr-36642

ABSTRACT

Hepatic steatosis is common in obese individuals with hyperinsulinemia and is an important hepatic manifestation of metabolic syndrome. Sterol regulatory binding protein-1c (SREBP-1c) is a master regulator of lipogenic gene expression in the liver. Hyperinsulinemia induces transcription of SREBP-1c via activation of liver X receptor (LXR) and specificity protein 1 (Sp1). Cilostazol is an antiplatelet agent that prevents atherosclerosis and decreases serum triglyceride levels. However, little is known about the effects of cilostazol on hepatic lipogenesis. Here, we examined the role of cilostazol in the regulation of SREBP-1c transcription in the liver. The effects of cilostazol on the expression of SREBP-1c and its target genes in response to insulin or an LXR agonist (T0901317) were examined using real-time RT-PCR and western blot analysis on cultured hepatocytes. To investigate the effect of cilostazol on SREBP-1c at the transcriptional level, transient transfection reporter assays and electrophoretic mobility shift assays (EMSAs) were performed. Cilostazol inhibited insulin-induced and LXR-agonist-induced expression of SREBP-1c and its downstream targets, acetyl-CoA carboxylase and fatty acid synthase, in cultured hepatocytes. Cilostazol also inhibited activation of the SREBP-1c promoter by insulin, T0901317 and Sp1 in a luciferase reporter assay. EMSA analysis showed that cilostazol inhibits SREBP-1c expression by repressing the binding of LXR and Sp1 to the promoter region. These results indicate that cilostazol inhibits insulin-induced hepatic SREBP-1c expression via the inhibition of LXR and Sp1 activity and that cilostazol is a negative regulator of hepatic lipogenesis.


Subject(s)
Animals , Humans , Mice , Rats , Cells, Cultured , Hep G2 Cells , Hepatocytes/drug effects , Hydrocarbons, Fluorinated/pharmacology , Insulin/pharmacology , Lipogenesis , Mice, Inbred C57BL , Orphan Nuclear Receptors/agonists , Promoter Regions, Genetic , Protein Binding , Sp1 Transcription Factor/metabolism , Sterol Regulatory Element Binding Protein 1/genetics , Sulfonamides/pharmacology , Tetrazoles/pharmacology
10.
Journal of Preventive Medicine and Public Health ; : 293-299, 2013.
Article in English | WPRIM | ID: wpr-41526

ABSTRACT

OBJECTIVES: The purposes of this study were to evaluate the prevalence of epilepsy and to estimate the cost of epilepsy in Korea, 2010. METHODS: This study used a prevalence based approach to calculate the cost of epilepsy. Claims data from the Korean national health insurance and data from the Korea health panel, the Korea National Statistical Office's records of causes of death, and labor statistics were used to estimate the cost of epilepsy. Patients were defined as those who were hospitalized or visited an outpatient clinic during 2010 with a diagnosis of epilepsy (International Classification of Diseases 10th revision codes G40-G41). Total costs of epilepsy included direct medical costs, direct non-medical cost and indirect costs. RESULTS: The annual prevalence of treated epilepsy was 228 per 100 000 population, and higher in men. The age-specific prevalence was highest for teenagers. The total economic burden of epilepsy was 536 billion Korean won (KW). Indirect cost (304 billion KW) was 1.3 times greater than direct cost (232 billion KW). By gender, the male (347 billion KW) were more burdened than the female (189 billion KW). The estimated cost in young age younger than 20 years old was 24.5% of the total burden of epilepsy. CONCLUSIONS: A significant portion of the economic burden of epilepsy is borne by people in young age. To reduce the economic burden of epilepsy, effective prevention and treatment strategies are needed.


Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Middle Aged , Young Adult , Cost of Illness , Epilepsy/economics , Health Care Costs/statistics & numerical data , National Health Programs/economics , Prevalence , Republic of Korea/epidemiology
11.
Journal of the Korean Medical Association ; : 1226-1236, 2012.
Article in English | WPRIM | ID: wpr-146676

ABSTRACT

Stroke is a disease that causes a substantial economic burden. With the rapidly aging population in Korea, the prevalence of chronic diseases, including stroke, is expected to rise, along with associated health care expenditures. Therefore, we estimated the economic burden of stroke in Korea in 2010 using nationally representative data. We used a prevalence-based approach to estimate the cost of stroke by claims data from the Korean National Health Insurance. Data from the Korea Health Panel, the Korea National Statistical Office's records of causes of death, and Labor Statistics were used to calculate direct non-medical costs and indirect costs. Direct costs included direct medical costs and direct non-medical costs, and indirect costs were opportunity costs lost due to premature death and productivity loss. Total costs were estimated by adding age- and gender-specific costs. The total economic burden of stroke was $3.53 billion: $1.87 billion for hemorrhagic stroke and $1.66 billion for ischemic stroke. The direct costs were $1.74 billion and the indirect costs were $1.79 billion. By gender, males were burdened at $2.19 billion, while females bore $1.34 billion of the total burden. Stroke imposes a huge economic burden, as indicated by the fact that the costs of stroke increased by 4.4% from 2005 to 2010, and the estimated cost was 0.35% of gross domestic product. Therefore, effective prevention programs and treatments are needed to reduce the economic burden of stroke in Korea.


Subject(s)
Female , Humans , Male , Aging , Cause of Death , Chronic Disease , Cost of Illness , Delivery of Health Care , Efficiency , Gross Domestic Product , Health Expenditures , Korea , Mortality, Premature , National Health Programs , Prevalence , Stroke
12.
Korean Circulation Journal ; : 712-717, 2011.
Article in English | WPRIM | ID: wpr-113387

ABSTRACT

BACKGROUND AND OBJECTIVES: The incidence of inflammatory heart diseases is not yet as high as those of other cardiovascular diseases; however, inflammatory heart diseases do have relatively high mortality rate. Therefore, update information on the economic burden of inflammatory heart diseases are necessary in order to appropriate policy making on these diseases. MATERIALS AND METHODS: This study used a number of resources to obtain data, national health insurance statistics, the Korean Health Panel, and the causes of death report by the Korean National Statistical Office. The total costs of inflammatory heart diseases were estimated as the sum of direct medical care costs, direct non-medical care and indirect costs. RESULTS: The total direct cost of inflammatory heart disease was higher in Korean men than that of Korean women and cost due to inpatient was higher than that of outpatients cost. The costs to cover premature death were highest among all of the components used to determine the total costs for inflammatory heart disease, representing 66.3% of these costs in Korea. CONCLUSION: Inflammatory heart disease has a relatively high mortality rate, and the costs that are associated with premature deaths consume the greatest proportion of the costs associated with this disease. In spite of some limitations of study, this could be a reliable evidence of economic burden of inflammatory heart disease.


Subject(s)
Female , Humans , Male , Cause of Death , Cost of Illness , Endocarditis , Health Care Costs , Heart , Heart Diseases , Incidence , Inflammation , Inpatients , Korea , Mortality, Premature , National Health Programs , Outpatients , Policy Making
13.
Experimental & Molecular Medicine ; : 21-29, 2010.
Article in English | WPRIM | ID: wpr-104282

ABSTRACT

Angiotensin II is a major effector molecule in the development of cardiovascular disease. In vascular smooth muscle cells (VSMCs), angiotensin II promotes cellular proliferation and extracellular matrix accumulation through the upregulation of plasminogen activator inhibitor-1 (PAI-1) expression. Previously, we demonstrated that small heterodimer partner (SHP) represses PAI-1 expression in the liver through the inhibition of TGF-beta signaling pathways. Here, we investigated whether SHP inhibited angiotensin II-stimulated PAI-1 expression in VSMCs. Adenovirus-mediated overexpression of SHP (Ad-SHP) in VSMCs inhibited angiotensin II- and TGF-beta-stimulated PAI-1 expression. Ad-SHP also inhibited angiotensin II-, TGF-beta- and Smad3-stimulated PAI-1 promoter activity, and angiotensin II-stimulated AP-1 activity. The level of PAI-1 expression was significantly higher in VSMCs of SHP-/- mice than wild type mice. Moreover, loss of SHP increased PAI-1 mRNA expression after angiotensin II treatment. These results suggest that SHP inhibits PAI-1 expression in VSMCs through the suppression of TGF-beta/Smad3 and AP-1 activity. Thus, agents that target the induction of SHP expression in VSMCs might help prevent the development and progression of atherosclerosis.


Subject(s)
Animals , Humans , Mice , Rats , Adenoviridae/genetics , Angiotensin II/pharmacology , Blotting, Northern , Cells, Cultured , Electrophoretic Mobility Shift Assay , Genetic Vectors/genetics , Muscle, Smooth, Vascular/cytology , Myocytes, Smooth Muscle/drug effects , Plasminogen Activator Inhibitor 1/genetics , Promoter Regions, Genetic/genetics , Receptors, Cytoplasmic and Nuclear/genetics , Reverse Transcriptase Polymerase Chain Reaction , Smad3 Protein/genetics , Transforming Growth Factor beta/pharmacology
14.
Korean Diabetes Journal ; : 312-319, 2010.
Article in English | WPRIM | ID: wpr-23770

ABSTRACT

BACKGROUND: The highly developed endoplasmic reticulum (ER) structure in pancreatic beta cells is heavily involved in insulin biosynthesis. Thus, any perturbation in ER function inevitably impacts insulin biosynthesis. Recent studies showed that the expression of tribbles-related protein 3 (TRB3), a mammalian homolog of Drosophilia tribbles, in various cell types is induced by ER stress. Here, we examined whether ER stress induces TRB3 expression in INS-1 cells and found that TRB3 mediates ER stress-induced suppression of insulin gene expression. METHODS: The effects of tunicamycin and thapsigargin on insulin and TRB3 expression in INS-1 cells were measured by Northern and Western blot analysis, respectively. The effects of adenovirus-mediated overexpression of TRB3 on insulin, PDX-1 and MafA gene expression in INS-1 cells were measured by Northern blot analysis. The effect of TRB3 on insulin promoter was measured by transient transfection study with constructs of human insulin promoter. RESULTS: The treatment of INS-1 cells with tunicamycin and thapsigargin decreased insulin mRNA expression, but increased TRB3 protein expression. Adenovirus-mediated overexpression of TRB3 decreased insulin gene expression in a dose-dependent manner. A transient transfection study showed that TRB3 inhibited insulin promoter activity, suggesting that TRB3 inhibited insulin gene expression at transcriptional level. Adenovirus-mediated overexpression of TRB3 also decreased PDX-1 mRNA expression, but did not influence MafA mRNA expression. CONCLUSIONS: This study showed that ER stress induced TRB3 expression, but decreased both insulin and PDX-1 gene expression in INS-1 cells. Our data suggest that TRB3 plays an important role in ER stress-induced beta cell dysfunction.


Subject(s)
Humans , Blotting, Northern , Blotting, Western , Endoplasmic Reticulum , Endoplasmic Reticulum Stress , Gene Expression , Insulin , Insulin-Secreting Cells , RNA, Messenger , Thapsigargin , Transfection , Tunicamycin
15.
Korean Diabetes Journal ; : 112-120, 2008.
Article in Korean | WPRIM | ID: wpr-61109

ABSTRACT

BACKGROUND: The highly developed endoplasmic reticulum (ER) structure is one of the characteristic features of pancreatic beta-cells. Recent study showed that ER stress causes beta-cell dysfunction. However, little is known about the effects of high glucose concentration on induction of ER stress in pancreatic beta-cells. Therefore, this study was designed to evaluate whether exposure of high glucose concentration in rat insulinoma cell line, INS-1 cell induces ER stress and whether ER stress decreases insulin gene expression. METHODS: The effect of 30 mM glucose on insulin expression and secretion in INS-1 cells was evaluated by Northern blot analysis and glucose-stimulated insulin secretion (GSIS). Cell viability was evaluated by XTT assay. The effect of 30 mM glucose on phosphorylation of eIF2alpha and CHOP expression, which are markers of ER stress were evaluated by Western blot analysis. RT-PCR analysis was performed to determine whether high glucose concentration induces XBP-1 splicing. To investigate whether ER stress decreases insulin gene expression, the effect of tunicamycin on insulin mRNA expression was evaluated by Northern blot analysis. RESULTS: The prolonged exposure of INS-1 cells with the 30 mM glucose concentration decreased insulin mRNA expression in a time dependent manner and impaired GSIS while did not influence on cell viability. 30 mM glucose increased phosphorylation of eIF2alpha, XBP-1 splicing and CHOP expression in INS-1 cells. Tunicamycin-treated INS-1 increased XBP-1 splicing and decreased insulin mRNA expression in a dose dependent manner. CONCLUSION: This study showed that prolonged exposure of INS-1 with high glucose concentration induces ER stress and ER stress decreases insulin gene expression. Further studies about underlying molecular mechanism by which ER stress induces beta-cell dysfunction are needed.


Subject(s)
Animals , Rats , Blotting, Northern , Blotting, Western , Cell Line , Cell Survival , Endoplasmic Reticulum , Endoplasmic Reticulum Stress , Gene Expression , Glucose , Hyperglycemia , Insulin , Insulinoma , Phosphorylation , RNA, Messenger , Tunicamycin
16.
Korean Journal of Fertility and Sterility ; : 111-120, 2001.
Article in Korean | WPRIM | ID: wpr-32731

ABSTRACT

OBJECTIVE: To verify the expression of leptin receptor (OB-R) in oocytes and preimplantation embryos, the involvement of mitogen activated protein kinase (MAPK or Erk1/2) in the leptin signaling, and effect of leptin on the oocyte maturation in mice. METHOD: RT-PCR analysis of OB-R was conducted in germinal vesicle (GV)-intact and MII stage oocytes, and 1, 2, 8-cell embryos and blastocysts. Germinal vesicle breakdown (GVB), polar body extrusion, monitored in the presence or absence of leptin (1 microM). Following the leptin treatment, temporal changes in MAPK activity were verified by immunoprecipitation and in vitro kinase assay in MII oocytes. RESULTS: The expression of OB-R mRNA was found in GV and MII oocyte but not in the embryos. MAPK activity of the MII oocytes was significantly increased by brief incubation in the HTF supplemented with leptin (1 microM). Priming of PD098059, a MEK inhibitor to leptin treatment attenuated the activation of MAPK by leptin in MII oocytes. Following 24 hrs of culture of the GV oocytes, leptin significant increased the GVB and 1st polar body extrusion. CONCLUSION: This result suggested that functional interaction between leptin and OB-R resulted in potentiation of MAPK (Erk1/2) activity in MII oocytes through MEK activation and that leptin might be a local regulator of meiotic maturation of the mouse oocytes.


Subject(s)
Animals , Mice , Blastocyst , Embryonic Structures , Immunoprecipitation , Leptin , Oocytes , Phosphotransferases , Polar Bodies , Protein Kinases , Receptors, Leptin , RNA, Messenger
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