- A Case of Multifocal Pyomyositis in Diabetes Mellitus.
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Eun Seo Park, Joo Hyun Kim, Bo Yong Jung, Jae Ho Park, Ji Hun Ahn, Jun Young Lee, Soon Ho Hwang, Kyung Wook Lee, Jong Kyu Han, Ji O Mok, Yeo Joo Kim, Hyeong Kyu Park, Chul Hee Kim, Sang Jin Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo
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Korean Diabetes J. 2006;30(2):140-144. Published online March 1, 2006
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DOI: https://doi.org/10.4093/jkda.2006.30.2.140
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- Pyomyositis is an acute bacterial infection of skeletal muscle, usually caused by Staphylococcus aureus. It is common in the tropics but rare in temperate climates. In temperature climate there are predisposing factors, such as diabetes, HIV infection, malignancy. The incidence of reported bacterial pyomyositis is increasing in recently, especially among immunocompromised persons such as HIV infection or diabetes mellitus. We experience multifocal pyomyositis in 49-year-old man with type 2 diabetes mellitus presented with drowsy mental state. Muscular USG and MRI finding shows multifocal abscess in thigh. Blood culture revealed Staphyloccus aureus. And patient received a intravenous broad-spectrum antibiotics, incision and drainage. He was successfully managed with drainage and antibiotics then discharge. Since diabetes or infection with HIV predisposes patients to bacterial infection, pyomyositis will occur more frequently. Increased awareness if the disease will improve management.
- Effect of VRP (Vascular Rab-GAP / TBC Domain Containing Protein) Overexpression on Vascular Endothelial Cell Functions.
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Chul Hee Kim, Hideto Yonekura, Hiroshi Yamamoto
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Korean Diabetes J. 2003;27(6):449-455. Published online December 1, 2003
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VRP (vascular Rab-GAP/TBC domain containing protein) is a recently discovered gene from antisense - display screening of angiogenesis- related genes. However, its function in vascular endothelial cells has not been elucidated yet. This study was performed to examine the effects of overexpression of VRP on the function of vascular endothelial cells. METHODS: VRP cDNA was cloned from polyA+ RNA from human microvascular endothelial cells, and inserted into a mammalian expression plasmid vector under the control of a CMV promotor. The constructed VRP expression vector was transfected into ECV304 cells. Then the proliferation, tube formation, and vascular endothelial growth factor (VEGF) secretion of the VRP-overexpressed cells were examined. RESULTS: The expression of VRP mRNA was about two-fold greater in the VRP-transfected cells than in the control ECV304 cells. There was, however, no significant difference in the proliferation, cord-like structure formation, and VEGF secretion between the two cell groups. CONCLUSION: These results demonstrate that VRP overexpression does not affect the proliferation, tube formation, or VEGF secretion of ECV304 cells. Further studies are needed to elucidate the functional role of VRP in endothelial cells.
- A Case of Acute Multifocal Bacterial Nephritis Associated with Diabetic Autonomic Neuropathy.
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Eun Kyung Park, Jae Hak Lee, Ji Sung Yoon, Ji O Mok, Yeo Joo Kim, Hyeong Kyu Park, Chul Hee Kim, Sang Jin Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo
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Korean Diabetes J. 2003;27(4):379-384. Published online August 1, 2003
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- Acute multifocal bacterial nephritis is a severe form of acute renal infection in which a heavy leukocytic infiltrate occurs throughout the kidney. It is also an early phase of renal corticomedullary abscess. Clinically, patients have evidence of a severe urinary tract infection secondary to a gram-negative organism and there are frequently signs of sepsis. About half of the reported patients have been diabetics. Urinary tract infections are more common in diabetic women than in non-diabetic women. A variety of factors may contribute. The most important predisposing factor may be bladder dysfunction as a result of diabetic neuropathy and cystopathy. Diabetic cystopathy begins as decreased bladder sensation and decreased reflex detrusor activity caused by neuropathy affecting sympathetic and parasympathetic afferent fibers. Impaired bladder sensation results in bladder distention and increased residual urine volume. Long-term effects may eventually be vesicoureteral reflux and recurrent upper urinary tract infection. However, until now no diabetic patient with acute multifocal bacterial nephritis has been reported in Korea. Acute multifocal bacterial nephritis can be diagnosed by clinical manifestations and on radiologic grounds, including abdominal computed tomography showing multiple, wedge shaped, poorly defined areas of decreased contrast enhancement in multiple renal lobes. Therefore, we report the first Korean case of acute multifocal bacterial nephritis associated with diabetic autonomic neuropathy and review the literatures.
- A Case of Invasive Aspergillosis of the Nasal Septum in a Patient with Diabetes Mellitus.
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Tae Hoon Kim, Ji Sung Yoon, Ji O Mok, Yeo Joo Kim, Hyeong Kyu Park, Chul Hee Kim, Sang Jin Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo, Jang Mook Kim, Yoon Jung Kim
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Korean Diabetes J. 2003;27(4):373-378. Published online August 1, 2003
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- Invasive aspergillosis of the nasal cavity and paranasal sinuses is characterized by invasion and destruction of the bony sinus walls, the orbit, and other soft tissues of the face. It occurs particularly in patients with severe immune deficits, and less frequently in patients with diabetes mellitus. The therapeutic outcome of invasive aspergillosis is unsatisfactory. Mortality rates range from 50 to 80%, depending primarily on the underlying disease. In general, the prognosis depends on making a prompt diagnosis of infection and providing early treatment. However the diagnosis of invasive aspergillosis is difficult because there is no specific symptom, nor any rapid diagnostic method for confirmation. We report a case of a 64-year old woman with diabetes mellitus and invasive aspergillosis of the nasal septum. She was diagnosed by biopsy of the nasal septum and treated with systemic antifungal agent and surgical debridement. (Ed- paragraphs combined here) In conjunction with this case we review the previous literatures and suggest that prompt antifungal therapy with glycemic control is an important element in the treatment of invasive aspergillosis in a diabetic patient.
- A Case of Endogenous Endophthalmitis in a Patient with Diabetic Retinopathy.
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Chang Hee Han, Ji Sung Yoon, Ji O Mok, Yeo Joo Kim, Hyeong Kyu Park, Chul Hee Kim, Sang Jin Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo, Jun Sun Kim
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Korean Diabetes J. 2003;27(4):367-372. Published online August 1, 2003
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- Infectious endogenous endophthalmitis can occur by entrance of a pathogenic microorganism into the eye from various primary infection sites other than the eye. Although relatively rare, it results in visual loss frequently in spite of early diagnosis and treatment. It occurs in the process of systemic infection and its underlying conditions are diabetes, advanced liver disease, and immune suppressive state or drug abuse. We report a case of a 51-year old man with proliferative diabetic retinopathy and endogenous endophthalmitis caused by S. aureus from a skin infection. The ocular symptoms improved after systemic and intravitreal antibiotic therapy but visual loss could not be prevented. In conjunction with this case, we review the available literatures and stress the seriousness of this disease when concurrent in diabetic patients.
- Impairment of Insulin Secretion by Fat Overload in Rat Pancreatic Islets and Effects of Antioxidants.
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Chul Hee Kim, Chan Hee Kim, Hyeong Kyu Park, Kyo Il Suh, Ki Up Lee
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Korean Diabetes J. 2002;26(5):347-356. Published online October 1, 2002
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It has recently been suggested that fat overload on pancreatic beta cells is responsible for the abnormal pattern of insulin secretion in type 2 diabetes mellitus. Antioxidant treatment was reported to preserve beta cell function in animal models of diabetes. This study was undertaken to examine the effects of various free fatty acids and triglyceride on insulin secretion in isolated rat pancreatic islets. In addition, we examined the effects of antioxidants. METHODS: Pancreatic islets of normal Sprague-Dawley rats were isolated by intraductal injection of collagenase and Ficoll-gradient centrifugation. The islets were treated with palmitat0e (C16:0), oleate (C18:1), linoleate (C18:2), and triglyceride emulsions (intralipid) for 72hours. Basal and glucose-stimulated insulin secretions were measured. The effects of the antioxidants, vitamin E, alpha-lipoic acid, and N-acetyl cysteine, were examined on the fat-induced change of insulin secretion. RESULTS: All of the free fatty acids and the triglyceride increased the basal insulin secretion. In contrast, insulin secretion stimulated by 27 mM glucose was significantly decreased after the treatment with free fatty acids or triglycerides. The antioxidant could not prevent the fat-induced inhibition of insulin secretion. CONCLUSION: These results show that various free fatty acids and triglyceride commonly cause defects in insulin secretion. However, we could not confirm the the hypothesis that increased oxidative stress may be involved in the pathogenesis of insulin secretory defect associated with fat overload.
- Effects of Hydrogen Peroxide on Insulin Secretion in Rat Pancreatic Islets.
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Chul Hee Kim, Chan Hee Kim, Hyeong Kyu Park, Kyo Il Suh, Ki Up Lee
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Korean Diabetes J. 2002;26(4):265-273. Published online August 1, 2002
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It has been hypothesized that reactive oxygen species (ROS) are involved in the progression of beta cell dysfunction in both type 1 and type 2 diabetes mellitus. On the other hand, recent evidence suggests that ROS might be an integral component of intracellular signaling. This study was undertaken to examine effects of hydrogen peroxide (H2O2) on insulin secretion by various secretagogues in isolated rat pancreatic islets. METHODS: Pancreatic islets from normal Sprague-Dawley rats were isolated by intraductal injection of collagenase and Ficoll-gradient centrifugation. Isolated islets were treated with H2O2 directly added to the culture media or continuously generated by glucose-glucose oxidase system for 24 hours. Insulin secretion stimulated by glucose, arginine, and KCl was measured by radioimmunoassay. RESULTS: Basal insulin secretion was increased after treatment with H2O2. Treatment with low concentration of H2O2 stimulated insulin secretion in response to 27 mM glucose. In contrast, insulin secretion stimulated by 27 mM glucose was significantly decreased after treatment with high concentrations of H2O2. Arginine- stimulated insulin secretion was increased by both low- and high concentrations of H2O2. Insulin secretion stimulated by KCl was not affected by treatment with H2O2. CONCLUSION: These results suggest that the effect of H2O2 is diverse according to its concentration and different insulin secretagogues. In particular, H2O2 has a dual action on glucose-induced insulin secretion. At low concentration, H2O2 can stimulate insulin secretion probably by acting on signaling pathway of stimulus- secretion coupling. In contrast, high concentrations of H2O2 impairs glucose- induced insulin secretion, probably by acting as an oxidative stress.
- Effects of Antioxidants on Ethidium Bromide-induced Inhibition of Insulin Secretion in Rat Pancreatic Islets.
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Chul Hee Kim, Chan Hee Kim, Hyeong Kyu Park, Kyo Il Suh, Ki Up Lee
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Korean Diabetes J. 2002;26(3):179-187. Published online June 1, 2002
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It was recently shown that mitochondrial function in pancreatic beta-cells is essential in nutrient-stimulated insulin secretion. The inhibition of mitochondrial DNA (mtDNA) transcription by ethidium bromide (EtBr) has been reported to suppress glucose-induced insulin secretion in beta-cell lines. This study was undertaken to examine the effects of EtBr on insulin secretion in isolated normal rat pancreatic islets, and to see whether antioxidants could protect the beta-cell function against the EtBr-induced impairment. METHODS: Pancreatic islets of normal Sprague-Dawley rats were isolated by intraductal injection of collagenase followed by Ficoll-gradient centrifugation. Isolated islets were treated with 0.2 +/- 2.0 microgram/mL of EtBr for 2 to 6 days, and the glucose-stimulated insulin secretion measured. The effects of the antioxidant, vitamin E and alpha-lipoic acid, on the EtBr-induced inhibition of insulin secretion were also examined. RESULTS: EtBr inhibited the basal and glucose-stimulated insulin secretion in normal rat pancreatic islets in a dose- and time-dependent manner. Vitamin E and alpha-lipoic acid prevented the EtBr-induced inhibition of insulin secretion. CONCLUSION: Our results show that antioxidant can protect normal rat pancreatic islets from the EtBr-induced inhibition of insulin secretion. This suggests that oxidative stress is involved in the pathogenesis of the insulin secretory defect associated with mitochondrial dysfunction.
- Polymorphism of the Uncoupling Protein 1 (UCP-1) Gene and Fatty Acid Binding Protein 2 (FABP2) Gene in Korean Type 2 Diabetic Patients.
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Sun Gyu Kim, Chul Hee Kim, Seog Ki Yun, Yeo Il Yun, Yong Hyun Kim, Il Song Nam, Ju Young Lee, Ji O Mok, Hyeong Kyu Park, Young Sun Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo
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Korean Diabetes J. 2001;25(4):262-272. Published online August 1, 2001
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It is well known that genetic component plays an important role in developing obesity and type 2 diabetes mellitus. A number of candidate genes have been suggested, but the major gene determining the development of obesity and type 2 diabetes has not yet been uncovered. Previous studies suggest that polymorphisms of the intestinal fatty acid binding protein (FABP2) and uncoupling protein 1 (UCP-1) gene were related with obesity and/or insulin resistance in several populations. METHODS: We examined 76 type 2 diabetic patients (aged 44+/-6 years) and 96 healthy controls (aged 25+/-3 years). Ala54Thr polymorphism of the FABP2 gene and A to G polymorphism (-3826) of the UCP-1 gene were determined by polymerase chain reaction and restriction fragment length polymorphism method. RESULTS: The Thr54 allele of the FABP2 gene was found with a frequency of 0.33 in nondiabetic controls and 0.36 in type 2 diabetic patients. The genotype frequency of the Ala54Thr polymorphism was similar in nondiabetic and diabetic subjects ( 2=0.87, P=0.64). The -3826 G allele of UCP-1 gene was found with a frequency of 0.51 in nondiabetic controls, and 0.46 in type 2 diabetic patients. The genotype frequency of the -3826 A to G polymorphism was also similar in nondiabetic and diabetic subjects ( 2=1.46, p=0.46). When the subjects of each groups were subdivided into nonobese and obese group by BMI of 25 kg/m2, there was no significant difference in genotype frequencies of the UCP-1 and FABP2 gene polymorphisms. CONCLUSION: These results suggest that either the Ala54Thr polymorphism of the FABP2 gene or the A to G polymorphism (-3826) of UCP-1 gene do not play a major role in developing type 2 diabetes mellitus or obesity in Korean.
- Effects of High Fat Diet on Lipolysis in Skeletal Muscle and Adipose Tissue in Rats.
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Chul Hee Kim, Yun Ey Chung, Seong Jin Lee, Joong Yeol Park, Sung Kwan Hong, Hong Kyu Kim, Kyo Il Suh, Ki Up Lee
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Korean Diabetes J. 2000;24(6):641-651. Published online January 1, 2001
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It has been hypothesized that increased fat oxidation reduces glucose utilization in skeletal muscle, and is responsible for the insulin resistance associated with obesity or high-fat feeding. In contrast, there have been reports that fat oxidation capacity was decreased in skeletal muscles from insulin resistant subjects. This study was undertaken to examine whether insulin resistance in high- fat fed rats is associated with increased lipolysis in skeletal muscle and adipose tissue. METHODS: Two groups of Sprague-Dawley rats were fed either high-fat or low-fat diets for 4 weeks. Lipolysis in skeletal muscle and adipose tissue was determined by measurement of interstitial glycerol concentrations by a microdialysis method in basal and hyperinsulinemic-euglycemic clamp conditions. RESULTS: In basal state, plasma glycerol levels and interstitial glycerol concen trations of skeletal muscle, and adipose tissue were lower in high-fat fed than in low-fat fed rats. The degree of suppression of glycerol release by the hyperinsulinemia was smaller in the high-fat diet than in the low-fat diet group. However, plasma and interstitial glycerol concentrations during the hyperinsul inemic euglycemic clamps were also lower in the high-fat diet group. CONCLUSION: Lipolysis was decreased in skeletal muscle and adipose tissue of insulin resistant, high-fat fed rats. These results support the idea that limited fat oxidation capacity resulting in lipid accumulation in tissues, rather than increased fat oxida tion per se, is responsible for the insulin resistance associated with high-fat feeding.
- Association Between Uncoupling Protein-1 and 3-adrenergic Receptor Gene Polymorphisms and Energy Metabolism in normal Korean Adults.
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Jae Han Kim, Seog Ki Yun, Chul Hee Kim, Dong Won Byun, Young Sun Kim, Kyo Il Suh, Myung Hi Yoo
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Korean Diabetes J. 1999;23(6):803-813. Published online January 1, 2001
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The beta3-adrenergic receptor (beta3-AR) and uncoupling protein 1 (UCP-1), expressed mainly in brown adipose tissue, are involved in the regulation of thermogenesis and lipolysis. Recent studies have shown that polymorphisms of the 3-AR (Trp64Arg) and UCP-1 (-3826, A to G) genes are associated with low basal metabolic rate (BMR) and obesity. METHODS: We investigated the effects of the beta3- AR and UCP-1 gene polymorphisms on body fat and energy metabolism in 65 normal Korean men aged from 21 to 36 years. The Trp64Arg mutation of the beta3-AR gene and A to G polymorphism (-3826) of UCP-1 gene were detected by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) method. RESULT: In normal Koreans, Arg64 allele frequency of the beta3-AR was 0.15 and the allele frequency of the A to G substitution of the UCP-1 gene was 0.48. No significant difference was found in BMR, body fat and abdominal fat amount in relation to beta3-AR or UCP-1 genotypes. However, when the polymorphisms of the two genes were combined, the subjects with the polymorphisms of both UCP-1 and g-AR genes were found to have higher body mass index, higher total fat and abdominal fat amount, lower BMR, and lower fat oxidation rate when compared with the subjects without these polymorphisms. CONCLUSION: These results suggest that the polymorphisms of either beta3-AR or UCP-1 gene alone did not significantly affect BMR, fat oxidation and body fat amounts, but both UCP-1 and beta3-AR genes polymorphisms have synergistic effects on decreased basal metabolic rate, fat oxidation rate, and increased body fat in normal Korean adults.
- Association between FABP2 Gene Polymorphism and Energy Metabolism in Normal Korean.
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Seog Ki Yun, Chul Hee Kim, Young Sun Kim, Dong Won Byun, Kyo Il Suh, Myung Hi Yoo, Guk Bae Kim
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Korean Diabetes J. 1998;22(4):457-466. Published online January 1, 2001
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The human intestinal fatty acid binding protein (FABP2) locus has been proprosed to be a major candidate gene in determining insulin resistance. It has been hypothesized that alanine to threonine substitution at codon 54 (Ala54Thr) of the FABP2 gene may result in enhanced intestinal uptake of fatty acids, and thereby an impairment of insulin action. FABP2 polymorphism was recently shown to be associated with insulin resistance in several populations including Mexican-Americans, Pima Indians, and Japanese, but not associated in the English, Wales, and Finn. METHODS: We investigated the association ot the FABP2 gene polymorphism and insulin resistance, fat absorption, and body fuel metabolism in 96 normal Korean men aged between 21 and 36 years. RESULTS: In normal Koreans, the alanine-encoding allele frequency was 0.66 and threonine encoding allele frequency was 0.34. Subjects with threonine-encoding allele were found to have a higher mean fasting plasma insulin concentration, a higher insulin resistance index, and a higher basal fat oxidation rate compared with subjects who were homozygous for the alanine-encoding allele. CONCLUSION: These results show that the Ala54Thr substitution in the FABP2 gene is associated with increased fat oxidation and insulin resistance in normal Korean men.
- High Serum Lipoprotein ( a ) Levels in Korean Type 2 Diabetic Patients with Proliferative Diabetic retinopathy.
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Hyung Joo Park, Chul Hee Kim, Yun Ey Chung, Sang Wook Kim, Jin Yub Kim, Eun Sook Kim, Sung Kwan Hong, Ki Up Lee
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Korean Diabetes J. 1998;22(3):338-343. Published online January 1, 2001
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To examine the possible association between serum lipoprotein(a) (Lp(a)) concentration and proliferative diabetic retinopathy(PDR) in Korean patients with type 2 diabetes mellitus. METHODS: A total of 412 Korean outpatients with type 2 diabetes were examined. Diabetic retinopathy was determined by fundoscopic examination by an ophthalmologist and/or by fluorecein angiography. Semm Lp(a) levels were measured by one step sandwich ELISA method. RESULTS: The patient with PDR had higher serum Lp(a) levels than those with no retinopathy or non-proliferative diabetic retinopathy(NPDR). Multiple logistic regression analysis showed that serum Lp(a) level and the presence of diabetic nephropathy were independent variables having a statistically significant association with PDR. CONCLUSION: Korean type 2 diabetic patients with PDR had higher serum Lp(a) levels compared with those with no retinopathy or NPDR. Although these results suggested that Lp(a) might play a role in the occlusion of retinal capillaries leading to PDR, further prospective studies are required to prove causal relationship.
- The Frequency of ICA and anti-GAD Antibody in Korean IDDM and NIDDM Patients.
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Kyung Soo Ko, Sung Kwan Hong, Ki Up Lee, Nan Hee Kim, Dong Seop Choi, Sung Hee Ihm, Sung Woo Park, Chul Hee Kim, Dong Won Byun, Kyo Il Suh, Hak Chul Chang, Byoung Doo Rhee
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Korean Diabetes J. 1998;22(3):312-319. Published online January 1, 2001
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It has been suggested that the clinical and immunological characteristics of diabetes mellitus in Koreans are different from those of Caucasians. This study was undertaken to investigate the prevalence of autoimmune markers in Korean adults with IDDM and recent-onset NIDDM. METHODS: Seventy-seven Korean adults with IDDM and 245 recently(within 2 years) diagnosed NIDDM were included in the study. Islet cell cytoplasmic antibody was measured by immunohistochemical method, and anti-glutamic acid decarboxylase (anti-GAD) antibody was measured by radioimmunoassay. RESULTS: 1) The prevalence of ICA, anti-GAD antibody positivity was 27% and 40% in IDDM patients, and 5% and 4% in recent-onset NIDDM patients, respectively. 2) The prevalence of ICA positivity in IDDM patients decreased from 42% within one year to 21% over one year after clinical onset of disease. On the other hand, the positivity of anti-GAD antibody did not change according to the duration of diabetes. 3) The prevalence of ICA tends to be lower in IDDW patients with low serum C-peptide concentrations. In contrast, the prevalence of anti-GAD antibody was not different according to sernm C-peptide levels. CONCLUSION: These results suggested that the prevalence of ICA and antii-GAD antibody was lower in Korean adult IDDM and recent-onset NIDDM patients than that in Caucasians.
- Effects of Free Fatty Acids on Glutathione Redox Status in Cultured Endothelial Cells.
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Joong Yeol Park, Chul Hee Kim, Yun Ey Chung, Hong Kyu Kim, Young Il Kim, Sung Kwan Hong, Jae Dam Lee, Ki Up Lee
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Korean Diabetes J. 1998;22(3):262-270. Published online January 1, 2001
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Although plasma free fatty acids (FFA) are frequently elevated in diabetes mellitus, its role in the pathogenesis of diabetic vascular complications has not been well investigated. Recent stuclies reported that FFA may cause endothelial dysfunction through an enhancement of oxidative damage by decreasing glutathione redox cycle, an important anti-oxidant defense system in endothelial cells. In this study, we examined the effects of increased availability of FFA on intracellular glutathione redox cycle. METHODS: Bovine pulonary endothelial cells were exposed to 90 umol/L linoleic acid with or without 0.1 mM 2-bromopalmitate, an inhibitor of mitochondrial fatty acid oxidation, for 6hr. Components of the glutathione redox cycle such as total glutathione, reduced glutathione(GSH) and oxidized glutathione(GSSG) concentrations were measured by HPLC. RESULTS: Total glutathione concentration in cultured endothelial cells exposed to linoleic acid was significantly lower than that in control cells (10.8+ 0.5 vs 14.1+0.8 umol/g protein, P<0.05). Linoleic acid significantly decreased GSH concentrations (10.5+0.4 vs. 13.8+0.5 pmol/g protein, P<0.05) and the ratio of GSH/GSSG(26.3+1.3 vs. 47.0+2,1, P<0.05). Compared to cells exposed linoleic acid alone, total glutathione(13.5+0.5umol/g protein, P<0.05) and GSH concentration(13.2+0.4 pmol/g protein, P<0.05) significantly increased in cells treated with 2-bromopalmitate and linoleic acid. The ratio of GSH/GSSG in cells treated with 2-bromopalmitate and linoleic acid was higher th.an that in cells exposed to linoleic acid alone(44.1+1.3, P<0.05). CONCLUSION: Increased provision of FFA resulted in a derangement of glutathione redox cycle in cultured endothelial cells, which appears to be related to an increase in mitochondrial FFA oxidation. These results suggested that FFA can increase the risk of diabetic vascular complications.
- Effect of Exercise Training on Insulin Sensitivity and Intracellular Glucose Metabolism in Skeletal Muscle of High Fat-fed Rats.
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Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Kyong Soo Park, Hong Kyu Lee, Ki Up Lee
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Korean Diabetes J. 1998;22(2):231-242. Published online January 1, 2001
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Insulin resistance is a major characteristic of non-insulin-dependent diabetes mellitus and obesity. Many studies have indicated that increased intake of fat are associated with obesity and insulin resistance. On the other hand, chronic exercise is known to improve insulin sensitivity. However, the mechanisms by which high fat diet induces insulin resistance and exercise trainmg improves insulin sensitivity are not established. This study was undertaken to examine the mechanisms by which high fat diet and exercise training affect the insulin sensitivity in the whole body and in skeletal muscles. METHODS: Male Sprague-Dawley rats were divided into three groups: high fat sedentary group, high fat exercise group, and control(low fat sedentary) group. High fat diet consists of 66.5% fat and 12.5% carbohydrate, and control(low fat) diet consists of 12 5% fat and 66.5% carbohydrate. Exercise training was performed by swimming three hours per day. After 3 weeks, animals underwent hyperinsulinemic euglycemic clamp study to measure whole body glucose metabolic fluxes. Glycogen synthase activity and glucose-6-phosphate (G-6-P) levels were measured in skeletal muscle at the end of the clamp study. RESULTS: In the high fat diet group, whole body glycolysis and glycogen synthesis were decreased. Exercise training reversed the insulin resistance induced by high fat diet by increasing both glycolysis and glycogen synthesis. Glycogen synthase activity in skeletal muscle was reduced in high fat diet group, and it was partially reversed by exercise training. G-6-P level in skeletal muscle was increased in high fat diet group, and it was further increased by exercise training. CONCLUSION: These results suggested that the insulin resistance in high fat diet-fed rats is due to the impairment in glucose metabolism at sites distal to G-6-P, i.e. glycolysis and glycogen synthesis. In contrast, the improvement in insulin sensitivity by exercise training in high fat-fed rats is primarily due to the increased glucose metabolic flux proximal to G-6-P, i.e. glucose transport and phosphorylation.
- Changes in Serum True Insulin and C-peptide Levels during Oral Glucose Tolerance Test in Koreans with Glucose Intolerance.
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Young Il Kim, Chul Soo Choi, Sang Wook Kim, Hong Kyu Kim, Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
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Korean Diabetes J. 1998;22(2):192-198. Published online January 1, 2001
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Previous studies have shown that progression from normal glucose tolerance(NGT) to impaired glucose tolerance(IGT) is associated with the development of insulin resistance and hyper-insulinemia, while further progression from IGT to NIDDM results from an inability of the 8-cell to maintain high rate of insulin secretion. However, it is not established whether similar findings are also observed in Korean subjects with glucose intolerance. The aim of this study was to examine insulin secretory response after oral glucose stimulation in obese and non-obese Korean subjects according to varying degree of glucose intolerance. METHODS: Eighty eight Korean men underwent 75g oral glucose tolerance test. The subjects were classified into NGT(n=30), IGT(n=23), NIDDM(n= 35) according to National Diabetes Data Group criteria. Obesity was defined as body mass index (BMI) > 25 kg/m . Serum true insulin and C-peptide concentrations were measured by radioimmunoassay. RESULTS: Fasting serum true insulin and C-peptide levels were not different from each other among NGT, IGT and NIDDM groups, both in obese and non-obese subjects. Obese subjects with IGT had significantly higher serum true insulin and C-peptide levels at 120 min than those in NGT subjects, but the levels at 30 and 60 min were not different. On the other hand, non-obese subjects with IGT had lower serum true insulin level at 30 min and lower serum C-pepitde level at 60 min compared to those in NGT subjects. True insulin and C-pepitde levels at 30 and 60 min were significantly lower in patients with NIDDM than in those with NGT, both in obese and non-obese subjects. CONCLUSION: Hyperinsulinemia, especially at a later phase of oral glucose tolerance test, is apparent in obese subjects with IGT. On the other hand, early phase insulin secretory defect is prominent in non-obese subjects with IGT. These results suggest that impaired insulin secretion may play a primary role in the pathogenesis of non-obese NIDDM in Korea.
- Changes of Glomerular Filtration Rate and Urinary Albumin Excretion Rate in NIDDM patients with Microalbuminuria.
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Hyo Jung Kim, Jung Min Koh, Eun Sug Shin, Yun Ey Chung, Young Il Kim, Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
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Korean Diabetes J. 1997;21(4):414-424. Published online January 1, 2001
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We previously suggested that micro-albuminuria in the presence of retinopathy may represent a state of real incipient diabetic nephropathy with declining glomerular filtration rate(GFR), while the meaning of microalbuminuria in the absence of retinopathy may be more heterogeneous. This study was performed to further test this hypothesis. METHODS: We prospectively followed up the changes in GFR and urinary albumin excretinn rate (UAE) in microalbuminuric NIDDM patients with or without diabetic retinopathy for 3.1 years. RESULTS: 1) Among 45 patients who completed the followup, 27 had retinopathy from the baseline(group A), while 18 patients did not have retinopathy throughout the study(group B). 2) UAE at baseline was not statistically different between the group A and group B. During follow-up, VAE remained stable in the group B patients(40.0 [20.5 ~ 158.0) to 60.0[20.2 ~ 231.0] ug/min, NS). On the other hand, UAE significantly increased in the group A patients(47.9[20.0~186.0] to 140.0[24.5~2862.0] ug/min, P <0.001). 3) Thirty percent of the group A patients(8/27) progressed to overt proteinuria, while 11%(2/18) of the group B patients developed overt proteinuria(NS). 4) GFR significantly decreased both in the group A (113.0+21.2 to 89.1+24.0 mL/min/1.73 m, P < 0,001) and in the group B patients(134.1+27.2 to 121.5+27.3 mL/min/1.73 m, P<0.01). However, the magnitude of change in GFR was significantly higher in the group A than in the group B patients(7.7+7.6 vs 3.9+4.2 mL/min/1.73 m /year, P <0.05), 5) Multiple logistic regression analysis revealed that the presence of retinopathy was a independent risk factor for faster decline in GFR. CONCLUSION: It appears that clinical course is different in NIDDM patients with microalbuminuria, according to the presence or absence of diabetic retinopathy. Microalbuminuria in the presence of retinopathy predicts aggravation of albuminuria and decline in GFR. In contrast, the renal function in microalbuminuric NIDDM patients in the absence of retinopathy may remain stable for years.
- Effects of Free Fatty Acid on Insulin Secretion in Cultured Rat Pancreatic Islets.
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Hong Kyu Kim, Young Il Kim, Chul Hee Kim, Joong Yoel Park, Sung Kwan Hong, Jae Dam Lee, Ki Up Lee
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Korean Diabetes J. 1997;21(4):381-387. Published online January 1, 2001
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- BACKGROUND
It has been recently suggested that enhanced fat oxidation is responsible for the abnormal insulin secretory pattern in non-insulin-dependent diabetes mellitus. This study was undertaken to assess the effect of chronic exposure of pancreatic islets to free fatty acid on insulin secretion. METHODS: Rat pancreatic islets were cultured in various concentrations of glucose(5.5, 11, 27 mM) for 48 hrs with or without addition of free fatty acid(90 upM linoleic acid), and the basal and glucose-stimulated insulin secretion were measured. The effect of fatty acid oxidation inhibitor(2-bromopalmitate) was also tested. RESULTS: Islets cultured in high glucose concentrations showed a marked increase in basal insulin secretion. Free fatty acid stimulated the basal insulin secretion in islets cultured at 5.5 or 11 mM glucose, but no additional effect was seen in islets eultured at 27 mM glucose. In contrast, glucose-stimulated insulin secretion was decreased in islets cultured in high glucose media. Exposure to free fatty acid exerted an additive inhibitory effect on glucose-induced insulin secretion in islets cultured at 5.5 or 1 1 mM glucose, but not in islets cultured at 27M glucose, An inhibitor of fatty acid oxidation, 2-bromopalmitate, prevented the fatty acid-induced changes in both basal and glucosestimulated insulin secretion. CONCLUSION: These results showed that longterm exposure of pancreatic islets to free fatty acid altered the dynamics of insulin secretion, probably through a glucosefatty acid cycle.
- Plasminogen Activator Inhibitor ( PAI-1 ) Levels in Patients with non-insulin Dependent Diabetes Mellitus ( NIDDM ).
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Hong Kyu Kim, Chul Hee Kim, Eun Sug Shin, Hyo Jung Kim, Joong Yeol Park, Sung Kwan Hong, Hyun Sook Chi, Ki Up Lee
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Korean Diabetes J. 1997;21(1):29-38. Published online January 1, 2001
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Abstract
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- BACKGROUND
Conventional cardiovascular risk factors cannot fully explain high risk of cardiovascular disease in patients with non-insulin dependent diabetes mellitus(NIDDM). This study was undertaken to know whether plasma PAI-1 levels are increased in NIDDM patients, and to identify factors intluencing Pal-1 levels. METHODS: Forty three microalbuminuric, 41 normoalbuminuric NIDDM patients and 39 normal controls matched with age, sex and body mass index (BMI) participated in this study. Clinical characteristies and laboratory findings such as lipid profile, fasting serum C-peptide and PAI-1 levels were evaluated, RESULTS: NIDDM patients showed significantly higher PAI-1 levels than normal controls(44.3+17.4 ng/mL vs. 26.3+12.6ng/mL, p<0.05). However, we failed to show the differences in PAI-1 levels between NIDDM patients with microalbuminuria and normoalbuminuria. PAI-1 levels were significantly correlated to BMI, fasting plasma glucose, HbA1, triglyceride and serum C-peptide levels. Multiple regression analysis showed that serum triglyceride and fasting serum C-peptied levels were independently related to PAI-1 levels. Conclusion; These findings suggested that elevated PAI-1 levels may contribute to increased risk of cardiovascular disease in patients with NIDDM.
- Transplantation of microencapsulated canine pancreatic islets to streptozotocin-induced diabetic rats.
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Chul Hee Kim, Joo Jun Koh, Joong Yeol Park, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min, Seung Eun Yang, Seng Jin Lee
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Korean Diabetes J. 1992;16(2):129-135. Published online January 1, 2001
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- No abstract available.
- A clinical study on the complications of non-insulin-dependent diabetes mellitus in Korea.
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Kyung Soo Ko, Tae Gun Oh, Chul Hee Kim, Kyong Soo Park, Moon Kyu Lee, Seong Yeon Kim, Bo Yeon Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min
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Korean Diabetes J. 1991;15(2):257-262. Published online January 1, 2001
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- No abstract available.
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KDA
