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Biomedical subjects

Choon Hee Chung

Publications and source records attributed to Choon Hee Chung.

9 recordsLinked to original sources
PubMed2007

Effects of rosiglitazone and metformin on inflammatory markers and adipokines: decrease in interleukin-18 is an independent factor for the improvement of homeostasis model assessment-beta in type 2 diabetes mellitus.

OBJECTIVE: We examined the individual pharmacological effects of the addition of rosiglitazone and metformin to glimepiride on inflammatory markers and adipokines in patients with type 2 diabetes mellitus. We analysed the relationships between these variables, the measurements of insulin sensitivity and beta-cell function in patients treated with rosiglitazone plus glimepiride. DESIGN AND PATIENTS: One hundred twenty (120) patients with type 2 diabetes mellitus were randomized and treated with glimepiride plus rosiglitazone or glimepiride plus metformin for 12 weeks. The plasma concentrations of the inflammatory markers and adipokines were measured at baseline and after 12 weeks. MEASUREMENTS: Markers of insulin sensitivity and beta-cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of beta-cell function (HOMA-beta), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-18 (IL-18) were measured using ELISA. RESULTS: Improvements in fasting insulin level, QUICKI and HOMA-beta were noted in the rosiglitazone-treated group. Only the QUICKI value improved in the metformin-treated group. Adiponectin concentrations significantly increased in the rosiglitazone-treated group after 12 weeks. Significant decreases in resistin, C-reactive protein, TNF-alpha, IL-6 and IL-18 were seen in the rosiglitazone-treated patients but not in the metformin-treated patients. The independent risk factor for the HOMA-beta change according to stepwise multivariate regression analysis was a change in IL-18. CONCLUSIONS: Rosiglitazone, but not metformin, improved the plasma concentrations of inflammatory markers and adipokines in patients with type 2 diabetes mellitus. A decrease in IL-18 is an independent factor for the improvement of HOMA-beta in type 2 diabetes mellitus.

Adiponectin↗
PubMed2006

Recurrent acute pancreatitis in a patient with type IIb hyperlipoproteinemia: a case report and review of the literature in Korea.

Hyperlipidemia is a rare cause of pancreatitis. It has been believed that free fatty acids released from hydrolyzed serum chylomicrons or triglycerides and chylomicrons induce hyperlipidemic pancreatitis by damaging acinar cells and capillaries. Type I, IV or V hyperlipidemic (Fredrickson's classification) pancreatitides have distinctive features of increased and heightened serum chylomicron and triglyceride levels. In contrast, type IIb hyperlipidemia usually doesn't have increased chylomicrons. It is a dominant inherited genetic disorder and doesn't manifest the subjective symptom before combining vascular complications such as coronary artery disease. Only a few cases of type IIb hyperlipidemic pancreatitis have been reported. We experienced a male patient with recurrent hyperlipidemic pancreatitis combined with type IIb hyperlipidemia. We present the case report and a review of the literature of hyperlipidemic pancreatitis, especially cases in Korea.

Adult↗
PubMed2006

Antioxidants ameliorate the expression of vascular endothelial growth factor mediated by protein kinase C in diabetic podocytes.

BACKGROUND: The increased production of reactive oxygen species (ROS) may be involved in the onset or development of diabetic vascular complications. The release of ROS from podocytes plays a role in the pathogenesis of glomerular damage in various experimental glomerular diseases. Although it is assumed that the podocyte injury also plays an important role in diabetic nephropathy, the mechanism is still unknown. METHODS: Using a differentiated mouse podocyte cell line, we investigated: (1) whether a high level of ambient glucose increases the level of ROS, (2) whether the protein kinase C (PKC) pathway is involved in a high-glucose-induced generation of ROS and vascular endothelial growth factor (VEGF) and (3) whether antioxidants ameliorate PKC-mediated VEGF expression in diabetic milieu. RESULTS: Intracellular ROS generation was significantly higher in high glucose than in control conditions in cultured podocytes. High ambient glucose also increased VEGF mRNA and protein expression. The high-glucose-induced increases in ROS and VEGF mRNA and protein by podocytes were effectively inhibited by pretreatment with various antioxidants and were completely restored by PKC inhibition. The results show that cultured mouse podocytes produce ROS in response to high glucose, and that PKC is involved in high-glucose-induced ROS and VEGF production by podocyte. CONCLUSION: Increased ROS in podocytes may play a role in the pathogenesis of podocyte injury in diabetic nephropathy.

Animals↗
PubMed2006

Anti-diabetic effect of alkaline-reduced water on OLETF rats.

Alkalin-reduced water (ARW) is known to exert several anti-cancer effects, as well as to scavenge reactive oxygen species (ROS) and reduce blood-glucose levels. This study was performed in order to determine the effects of ARW on the control of spontaneous diabetes in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. We assigned 16 male OLETF rats (4 wk) to two groups: an experimental group, which was given ARW, and a control group, which received laboratory tap water. From week 6 to 32, the body weight, lipid composition, and glucose levels in the blood of the rats were measured. The glucose levels of both groups tended to increase. However, the ARW group's glucose levels were significantly lower than those of the control group after 12 weeks (p<0.05). The total cholesterol and triglyceride levels in the ARW group were found to be significantly lower than those of the control group during the experimental period. These results suggest that ARW spurred the growth of OLETF rats during the growth stage, and that long-term ingestion of ARW resulted in a reduction in the levels of glucose, triglycerides, and total cholesterol in the blood.

Alanine Transaminase↗
PubMed2005

Limited effect of CpG ODN in preventing type 1 diabetes in NOD mice.

Type 1 diabetes is considered as Th1 cell mediated autoimmune disease and the suppression of Th1 cells or the activation of Th2 cells has been regarded as a plausible immunologic intervention for the prevention of type 1 diabetogenesis in a rodent model. CpG ODN is an immunostimulatory sequence primarily present in bacterial DNA, viral DNA and BCG. CpG ODN is conventionally classified as a Th1 cell activator, which has been clinically applied to cancer, allergy and infectious disease. Recently, there was a promising report of that CpG ODN administration suppressed the development of type 1 diabetes in NOD mice by inducing Th2 cell mediated cytokine. However, the antidiabetogenic effect of CpG ODN on NOD mice is controversial. Thus, two studies were serially undertaken with various kinds of CpG motif to find a more optimal sequence and administration method. In the first study, CpG ODN was vaccinated four times and pancreatic inflammation and the quantity of serum insulin subsequently evaluated. In the second study, the amounts of IFN gamma and IL-4 in sera were measured as representative cytokines of Th1 and Th2 cells, respectively. As a result, vaccination or continuous injection of CpG ODN failed to show a preventive effect on type 1 diabetogenesis in NOD mice. Structural differences of CpG ODN also had no affect on the result. CpG ODN also consistently showed affect on the pancreatic pathology. The productions of IFN gamma and IL-4 were detected only in the K and D type CpG ODN administration groups. Comparison of the two cytokines leads to the conclusion that CpG ODN generated a Th1-weighted response in both study groups. It was assumed that CpG ODN failed to produce Th2-weighted cytokine milieu, which can overcome the genetically determined phenotype of NOD mice. Given these results, it was concluded that the immunotherapeutic application of CpG ODN on Type 1 diabetes had clear limitations.

Animals↗
PubMed2004

Angiotensin II receptor blocker attenuates overexpression of vascular endothelial growth factor in diabetic podocytes.

VEGF expressed in glomerular podocytes, is known to increase vascular permeability to macromolecules. Angiotensin II can stimulate the release of VEGF, and the protective effects of angiotensin II antagonist against diabetic glomerular injury suggest that the angiotensin II-induced VEGF is an important pathogenetic mechanism in the development of proteinuria during diabetic nephropathy although this mechanism is not fully understood. In this study, the changes of VEGF expression was examined in the experimental diabetic nephropathy to determine whether these changes were modified by renoprotective intervention by blockers of angiotensin II receptors. The streptozotocin- induced diabetic rats were treated with L-158,809, a blocker of angiotensin II receptors, for 12 weeks. Age-matched rats with L-158,809 served as controls. RT-PCR and immunohistochemistry were used to assess and quantify gene and protein expression of VEGF. A progressive increase in urinary protein excretion was observed in diabetic rats. Glomerular VEGF expression was significantly higher in diabetic rats than in the control groups, with a significant reduction in glomerular VEGF expression and proteinuria in L-158,809- treated diabetic rats. VEGF mRNA was also significantly higher in diabetic kidneys than in the control groups, with a significant reduction in VEGF mRNA in L-158,809-treated diabetic kidneys. These results demonstrates that VEGF expression is significantly increased in diabetic podocytes, and angiotensin II receptor antagonist attenuated these changes in VEGF expression and prevented the development of proteinuria in vivo. Attenuation of increased VEGF expression in podocytes could contribute to the renoprotective effects of angiotensin II receptor antagonists in diabetic nephropathy.

Angiotensin II↗
PubMed2004

A case of autoimmune hypoglycemia complicated with diabetic ketoacidosis.

Autoimmune hypoglycemia is characterized by hyperinsulinemia, fasting hypoglycemia, and the presence of insulin auto- antibodies without previous exposure to exogenous insulin. We experienced a case of autoimmune hypoglycemia without diabetes mellitus or any evidence of insulinoma. The insulin auto-antibody and insulin receptor auto-antibody were present. We diagnosed the patient as having autoimmune hypoglycemia and treated with glucocorticoid. After treatment, the hypoglycemic symptoms were resolved. However, four months later, the patient was readmitted with transient diabetic ketoacidosis. After recovery, he showed no signs of diabetes mellitus. We believe that insulin auto-antibodies may play a role in autoimmune hypoglycemia and diabetic ketoacidosis, but its role and mechanism are not precisely known. Further studies are needed to define the action mechanisms and the functions of insulin auto-antibodies: here we present case with a relevant literature.

Diabetic Ketoacidosis↗
PubMed2003

Effect of chronic alcohol ingestion on bone mineral density in males without liver cirrhosis.

BACKGROUND: Osteoporosis in men is an important public health problem. Because of the tendency of the numbers of the elderly population to increase, and age-specific incidence of fractures, it is inevitable that the health burden due to fractures will increase. Chronic alcoholism is associated with other risk factors, such as poor nutrition, leanness, liver disease, malabsorption, vitamin D deficiency, hypogonadism, hemosiderosis, parathyroid dysfunction and tobacco use, and these may contribute to the pathogenesis of bone disease related to alcoholism. Chronic alcohol intake may reduce bone density, but can also increase bone density. It is well established that liver disease also induces bone density changes, thus it is difficult to distinguish the role of liver disease from that of alcohol itself in the bone alterations occurring in patients with chronic alcohol consumption. Chronic male alcoholics, not having liver cirrhosis were studied to assess the effect of chronic alcohol consumption on their bone mineral density. METHODS: The study subjects comprised of 18 chronic heavy drinkers of more than 40 g of alcohol per day for at least 3 years and 18 age-matched controls who drank less than 20 g of alcohol per day. The serum and urinary parameters of bone and mineral metabolism were determined. The bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry at four axial sites (lumbar spine, femoral neck, Ward's triangle and trochanter). RESULTS: The alcoholic and control patients drank an average of 97.6 g and 7.2 g of alcohol per day. Osteocalcin, a marker of bone formation, was slightly decreased in alcoholic patients, and deoxypyridinoline, a marker of bone resorption, was slightly increased, but the difference was not statistically significant (p > 0.05). There were no differences between the two groups in the levels of free testosterone, estradiol, 25(OH) vitamin D and parathyroid hormone. The Ward's triangle and trochanter BMDs of the femur were significantly lower in the alcoholics than the controls, and lumbar spine BMD was decreased in proportion to the total alcohol intake in the alcoholics (r = -0.625, p = 0.01). CONCLUSION: We suggest that chronic alcohol consumption induces low bone density in the femur Ward's triangle and trochanter. There was also a significant inverse correlation between the lumbar spine BMD and the total amount of alcohol consumed. Large scaled randomized and prospective studies are needed to clarify the pathogenesis of alcohol-induced osteoporosis.

Absorptiometry, Photon↗