Diabetes & Metabolism Journal

Woo Je Lee (Lee WJ)

11 Articles

Nitric Oxide Increases Insulin Sensitivity in Skeletal Muscle by Improving Mitochondrial Function and Insulin Signaling.: Woo Je Lee, Hyoun Sik Kim, Hye Sun Park, Mi Ok Kim, Mina Kim, Ji Young Yun, Eun Hee Kim, Sang Ah Lee, Seung Hun Lee, Eun Hee Koh, Joong Yeol Park, Ki Up Lee; Korean Diabetes J. 2009;33(3):198-205. Published online June 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.3.198

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BACKGROUND
Accumulating evidence has suggested that nitric oxide (NO) is involved in the regulation of insulin sensitivity in skeletal muscle. Recent studies also suggested NO as an important molecule regulating mitochondrial biogenesis. This study examined the effect of the NO donor, 3-morpholinosydnonimine (SIN-1), on glucose metabolism in skeletal muscle and tested the hypothesis that NO's effect on glucose metabolism is mediated by its effect on mitochondrial function. METHODS: In Sprague-Dawley (SD) rats treated with SIN-1 for 4 weeks, insulin sensitivity was measured by a glucose clamp study. Triglyceride content and fatty acid oxidation were measured in the skeletal muscle. In addition, mitochondrial DNA content and mRNA expression of mitochondrial biogenesis markers were assessed by real-time polymerase chain reaction and expression of insulin receptor substrate (IRS)-1 and Akt were examined by Western blot analysis in skeletal muscle. In C2C12 cells, insulin sensitivity was measured by 2-deoxyglucose uptake and Western blot analysis was used to examine the expression of IRS-1 and Akt. RESULTS: SIN-1 improved insulin sensitivity in C2C12 cells and skeletal muscles of SD rats. In addition, SIN-1 decreased triglyceride content and increased fatty acid oxidation in skeletal muscle. Mitochondrial DNA contents and biogenesis in the skeletal muscle were increased by SIN-1 treatment. Moreover, SIN-1 increased the expression of phosphor-IRS-1 and phosphor-Akt in the skeletal muscle and muscle cells. CONCLUSION: Our results suggest that NO mediates glucose uptake in skeletal muscle both in vitro and in vivo by improving mitochondrial function and stimulating insulin signaling pathways.

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NO-Rich Diet for Lifestyle-Related Diseases
Jun Kobayashi, Kazuo Ohtake, Hiroyuki Uchida
Nutrients.2015; 7(6): 4911. CrossRef
Metformin Activates AMP Kinase through Inhibition of AMP Deaminase
Jiangyong Ouyang, Rahulkumar A. Parakhia, Raymond S. Ochs
Journal of Biological Chemistry.2011; 286(1): 1. CrossRef

Retraction: Protective Effect of PGC-1 on Lipid Overload-induced Apoptosis in Vascular Endothelial Cell.: Eun Hee Koh, Youn Mi Kim, Ha Jung Kim, Woo Je Lee, Jong Chul Won, Min Seon Kim, Ki Up Lee, Joong Yeol Park; Korean Diabetes J. 2008;32(3):293-293. Published online June 1, 2008; DOI: https://doi.org/10.4093/kdj.2008.32.3.293

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Abstract PDF: No absrtact available.

Cytoprotective Effect by Antioxidant Activity of Quercetin in INS-1 Cell Line.: Min Jeong Kwon, Hye Sook Jung, Mi Kyung Kim, Seong Hoon Kang, Gwang Wook Seo, Jae Kwang Song, Tae Yeon Yoon, Min Kyeong Jeon, Tae Hwan Ha, Chang Shin Yoon, Mi Kyung Kim, Woo Je Lee, Jeong Hyun Noh, Soo Kyung Kwon, Dong Joon Kim, Kyung Soo Koh, Byung Doo Rhee, Kyung Ho Lim, Soon Hee Lee, Jeong Hyun Park; Korean Diabetes J. 2007;31(5):383-390. Published online September 1, 2007; DOI: https://doi.org/10.4093/jkda.2007.31.5.383

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Abstract PDF

BACKGROUND
Oxidative stress is induced under diabetic conditions and causes various forms of tissue damages in the patients with diabetes. Recently, pancreatic beta cells are regarded as a putative target of oxidative stress-induced tissue damage, and this seems to explain in part the progressive deterioration of beta cell function in type 2 diabetes. The aim of this study was to examine the potential of Quercetin (QE) to protect INS-1 cells from the H2O2-induced oxidative stress and the effects of QE on the glucose-stimulated insulin secretion in INS-1 cells. METHODS: To study the cell viability, cells were incubated with H2O2 and/or QE at the various concentrations. To confirm the protective effect by QE in response to H2O2, the levels of antioxidant enzymes were assessed by RT-PCR and Western blot, and glutathione peroxidase activities were quantified by spectrophotometrical method. Glucose-stimulated insulin secretion (GSIS) was measured by ELISA. RESULTS: Cell incubations were performed with 80 microM of H2O2 for 5 hours to induce 40 - 50% of cell death. QE gradually showed protective effect (IC50 = 50 microM) in dose-dependent manner. Superoxide dismutase (SOD) mRNA level in H2O2 + QE group was increased as compared to H2O2 group, but catalase did not changed. And the QE recruited glutathione peroxidase activity against H2O2-induced oxidative injuries in INS-1 cells. CONCLUSION: In conclusion, these findings suggest that QE might have protective effect on beta cells by ameliorating oxidative stress and preserving insulin secretory function.

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Anti-diabetic effects of Allium tuberosum rottler extracts and lactic acid bacteria fermented extracts in type 2 diabetic mice model
Bae Jin Kim, Seung Kyeung Jo, Yoo Seok Jeong, Hee Kyoung Jung
Korean Journal of Food Preservation.2015; 22(1): 134. CrossRef
Protective Effects of Sasa Borealis Leaves Extract on High Glucose-Induced Oxidative Stress in Human Umbilical Vein Endothelial Cells
Ji-Young Hwang, Ji-Sook Han
Journal of the Korean Society of Food Science and Nutrition.2010; 39(12): 1753. CrossRef

Changes in the Prevalence of Metabolic Syndrome in a Rural Area of Korea Defined by Two Criteria, Revised National Cholesterol Education Program and International Diabetes Federation.: Jong Chul Won, Joong Yeol Park, Kee Ho Song, Woo Je Lee, Eun Hee Koh, Il Sung Nam-Goong, Sung Min Han, Moo Song Lee, Min Seon Kim, Ki Up Lee; Korean Diabetes J. 2007;31(3):284-292. Published online May 1, 2007; DOI: https://doi.org/10.4093/jkda.2007.31.3.284

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Abstract PDF

BACKGROUND
The prevalence of obesity is increasing in Korea, including rural areas. We examined the changes in the prevalence of metabolic syndrome (MetS), defined by revised National Cholesterol Education Program (NCEP) or International Diabetes Federation (IDF) criteria, in a rural area of Korea during the past 6 years. METHODS: A total of 1,119 subjects (424 men and 695 women) aged > or = 30 years were initially recruited in 1997. Baseline clinical data and various laboratory values were obtained. Six years later, we performed a follow-up study in 814 subjects (316 men and 498 women) of which 558 were original participants and 256 subjects were new. The prevalence of MetS was assessed by the criteria of NCEP or IDF. RESULTS: The prevalence of central obesity and impaired fasting glucose increased in both sexes during the period between 1997 and 2003. The prevalence of MetS according to the IDF criteria also increased. In men, the age-adjusted prevalence of MetS was 10.9% in 1997 and 23.3% in 2003. In women, it was 42.2% in 1997 and 43.4% in 2003. However, the prevalence of MetS according to the NCEP criteria increased only in men. CONCLUSION: There have been increases in the prevalence of central obesity and MetS according to the IDF criteria during the recent 6 years in a rural area of Korea.

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The Association between Midnight Salivary Cortisol and Metabolic Syndrome in Korean Adults
Yun-Mi Jang, Eun Jung Lee, Dong Lim Kim, Suk Kyeong Kim, Kee-Ho Song
Diabetes & Metabolism Journal.2012; 36(3): 245. CrossRef
The Diagnostic Criteria of Metabolic Syndrome and the Risk of Coronary Heart Disease according to Definitions in Men
Hyouk-Soo Seo, Sung-Hi Kim, Soon-Woo Park, Jong-Yeon Kim, Geon-Ho Lee, Hye-Mi Lee
Korean Journal of Family Medicine.2010; 31(3): 198. CrossRef
Metabolic syndrome is associated with erosive esophagitis
Jung Ho Park, Dong IL Park, Hong Joo Kim, Yong Kyun Cho, Chong IL Sohn, Woo Kyu Jeon, Byung Ik Kim
World Journal of Gastroenterology.2008; 14(35): 5442. CrossRef

Protective Effect of PGC-1 on Lipid Overload-induced Apoptosis in Vascular Endothelial Cell.: Eun Hee Koh, Youn Mi Kim, Ha Jung Kim, Woo Je Lee, Jong Chul Won, Min Seon Kim, Ki Up Lee, Joong Yeol Park; Korean Diabetes J. 2006;30(3):151-160. Published online May 1, 2006; DOI: https://doi.org/10.4093/jkda.2006.30.3.151

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Abstract PDF: BACKGROUND
Fatty acids contribute to endothelial cell dysfunction and apoptosis by inducing accumulation of long chain fatty acyl CoA (LCAC), which increases oxidative stress in vascular endothelial cells. Forced expression of PGC-1 was shown to induce mitochondrial biogenesis and to control expression of mitochondrial enzymes involved in fatty acid oxidation. This study was undertaken to test the hypothesis that PGC-1 overexpression could prevent endothelial cell apoptosis by enhancing fatty acid oxidation and relieving oxidative stress in vascular endothelium. METHODS: Adenoviruses containing human PGC-1 (Ad-PGC-1) and beta-galactosidase (Ad-beta-gal) were transfected to confluent human aortic endothelial cells (HAECs). To investigate the effect of adenoviral PGC-1 gene transfer on apoptosis, combined treatment of linoleic acid (LA), an unsaturated fatty acid, was performed. RESULTS: PGC-1 overexpression inhibited the increase in ROS production and apoptosis of HAECs induced by LA. Also, PGC-1 led to a significant increase in fatty acid oxidation and decrease in triglyceride content in HAECs. LA caused the decrease of adenine nucleotide translocase (ANT) activity and transient mitochondrial hyperpolarization, which was followed by depolarization. PGC-1 overexpression prevented these processes. CONCLUSION: In summary, PGC-1 overexpression inhibited mitochondrial dysfunction and apoptosis by facilitating fatty acid oxidation and protecting against the damage from oxidative stress in HAECs. The data collectively suggest that the regulation of intracellular PGC-1 expression might play a critical role in preventing atherosclerosis.

Increase in Fatty Acid Oxidation by AICAR: the Role of p38 MAPK.: Woo Je Lee, Jin Yob Kim, Sung Jin Bae, Eun Hee Koh, Sung Min Han, Hye Sun Park, Hyun Sik Kim, Min Seon Kim, Joong Yeol Park, Ki Up Lee; Korean Diabetes J. 2005;29(1):15-21. Published online January 1, 2005

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Abstract PDF: BACKGROUND
AMPK is an enzyme that increases glucose transport and fatty acid oxidation in skeletal muscle. The activation of AMPK stimulates fatty acid oxidation by decreasing the acetyl CoA carboxylase (ACC) activity and the concentration of malonyl-CoA. However, a recent study has reported a dissociation of AMPK activity and ACC phosphorylation in skeletal muscle during periods of prolonged exercise. This suggested that there is an additional mechanism for AMPK-induced fatty acid oxidation in skeletal muscle. METHODS: Plamitate oxidation was measured via the generation of [3H]-water generation from 9,10[3H]-palmitate after treating various concentrations of AICAR on the C2C12 mouse skeletal muscle cell line. Western analysis was used to test for the possible activation of p38 MAPK by AICAR. Involvement of p38 MAPK in the AICAR-induced increase in fatty acid oxidation was tested for by using SB203580, a p38 MAPK inhibitor. RESULTS: C2C12 cell treated with AICAR exhibited a dose-dependent increase in fatty acid oxidation compared to the cells that were not treated with AICAR. Western blot analysis revealed that phosphorylation of p38 MAPK was increased 2.5 folds after AICAR treatment. The increase of fatty acid oxidation with AICAR treatment was significantly inhibited by a treatment of SB203580; this indicated the involvement of p38 MAPK on the AICAR-induced increase in fatty acid oxidation. CONCLUSION: AICAR stimulated the fatty acid oxidation by activating p38 MAPK. This is a novel pathway by which AMPK activation in skeletal muscle increases the fatty acid oxidation

AMPK Activator AICAR Inhibits Hepatic Gluconeogenesis and Fatty Acid Oxidation.: Jin Yob Kim, Eun Hee Koh, Woo Je Lee, Seong Min Han, Ji Young Youn, Hye Sun Park, Hyun Sik Kim, Min Seon Kim, Joong Yeol Park, Ki Up Lee; Korean Diabetes J. 2005;29(1):6-14. Published online January 1, 2005

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Abstract PDF: BACKGROUND
Recent studies have demonstrated that adiponectin and metformin activate AMPK in the liver, and adiponectin and metformin stimulate fatty acid oxidation while inhibiting glucose production in liver. These results are in contrast to previous studies that have demonstrated that increased fatty acid oxidation in the liver is associated with increased gluconeogenesis. The present study was undertaken to reinvestigate the effects of AMPK activation by AICAR on hepatic fatty acid oxidation and gluconeogenesis. METHODS: HePG2 cells were treated with various concentrations of AICAR, and then the fatty acid oxidation and gluconeogenesis of the cells were determined. To investigate the in vivo effect of AICAR, Sprague-Dawely rats were infused with AICAR (bolus, 40 mg/g; constant, 7.5 mg/g/min-1) for 90min. RESULTS: Incubation of the HePG2 cells with higher concentrations (=1 mM) of AICAR increased fatty acid oxidation and gluconeogenesis. On the other hand, incubation of HePG2 cells with lower concentrations (0.05 and 0.1 mM) of AICAR decreased fatty acid oxidation and gluconeogenesis. Consistent with this in vitro data, the intravenous administration of AICAR to rats lowered their plasma glucose concentration and inhibited hepatic gluconeogenesis. Fatty acid oxidation in the liver tissue was significantly decreased by the administration of AICAR. CONCLUSION: The present study has demonstrated that AICAR decreased gluconeo-genesis in the liver. In contrast to previous studies, AICAR profoundly decreased hepatic fatty acid oxidation in rats and also in cultured hepatocytes

The Role of AMPK in Vascular Endothelium.: Woo Je Lee, Jin Yob Kim, Eun Hee Koh, Sung Min Han, Min Seon Kim, Ki Up Lee, Joong Yeol Park; Korean Diabetes J. 2005;29(1):1-5. Published online January 1, 2005

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Hypothalamic AMPK Activity in Diabetic Rats.: Churl Namkoong, Min Seon Kim, Woo Je Lee, Pil Geum Jang, Seong Min Han, Eun Hee Koh, Joong Yeol Park, Ki Up Lee; Korean Diabetes J. 2004;28(6):468-477. Published online December 1, 2004

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Abstract PDF: BACKGROUND
AMP-activated protein kinase (AMPK) acts as a cellular energy sensor that is activated during states of low energy charge and it regulates the various metabolic pathways to reestablish the normal cellular energy balance. It has recently been demonstrated that AMPK activity is altered by the state of energy metabolism in the hypothalamic neurons and this mediates the feeding response. METHODS: Diabetes was induced by an intra-peritoneal injection of streptozotocin (STZ) in Sprague-Dawley rats. The diabetic rats were maintained for 3 weeks with or without insulin treatment. 3 weeks later, we collected hypothalamus and we then assayed the phosphorylation of AMPK and the activity of acetyl CoA carboxylase (ACC) and isoform-specfic AMPK. To determine the effect of hypothalamic AMPK inhibition on diabetic hyperphagia, we administered an AMPK inhibitor, compound C, into the third ventricle in the STZ-induced diabetic rats. RESULTS: Phosphorylation of AMPK, which is a marker of AMPK activation, increased in the hypothalamus of the STZ-induced diabetic rats (DR). Moreover, 2-AMPK activity, but not 1-AMPK activity, increased by 2-fold in hypothalamus of the DRs. Phosphorylation of hypothalamic acetyl CoA carboxylase (ACC), a key downstream enzyme of AMPK, also increased in the DRs and this caused a reduction in ACC activity. Insulin treatment completely reversed the diabetesinduced changes in the hypothalamic AMPK and ACC, suggesting that insulin deficiency was associated with the changes in hypothalamic AMPK and ACC. Inhibition of AMPK by an intracerebroventricular administration of AMPK inhibitor, compound C, attenuated the development of diabetic hyperphagia and reduced the blood glucose levels in DRs. CONCLUSION: We have demonstrated that hypothalamic AMPK activity increased in the DRs, and inhibition of hypothalamic AMPK activity attenuated the development of diabetic hyperphagia. These data indicate that the enhanced hypothalamic AMPK activity may contribute to the development of diabetic hyperphagia

Recent Advances in the Treatment of Obesity.: Woo Je Lee, Eun Hee Koh, Min Seon Kim, Joong Yeol Park, Ki Up Lee; Korean Diabetes J. 2004;28(5):347-355. Published online October 1, 2004

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Prevalence of Islet Cell Autoantibodies and Mitochondrial DNA Mutation among Typical and Atypical Type 1 Diabetic Patients in Korea.: Hong kyu Lee, Kee Up Lee, Sung Kwan Hong, Byuong Doo Rhee, Dong Seop Choi, Hyoung Woo Lee, Sang Wook Kim, Hee Jin Kim, Nan Hee Kim, Kyong Soo Park, Woo Je Lee, Kyung Soo Ko; Korean Diabetes J. 1999;23(4):541-551. Published online January 1, 2001

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Abstract PDF: BACKGROUND
American Diabetes Association (ADA) proposed new criteria for the classification of diabetic patients, which were mainly based on the presence of autoimmune markers. But it is questionable if we can apply the new ADA criteria to Korean type 1 diabetic patients directly. In this study, we measured several autoantibodies to islet cell in Korean subjects with typical and atypical clinical manifestations of type 1 diabetes mellitus. And mutation of mitochondrial DNA was analyzed in the same patients. METHODS: We measured fasting serum C-peptide in 1870 diabetic patients attending the diabetes clinic of Asan Medical Center. Among the 117 patients with fasting serum C-peptide less than 0.6 ng/mL, glucagon-stimulated C-peptide was measured, and 57 Patients showed the level less than 1 ng/mL and they were diagnosed as type 1 diabetic patients. They were subgrouped into typical (n=26, needed insulin injection within 1 year after diagnosis) and atypical (n=30, did not need insulin for more than l year after diagnosis) type 1 diabetic patients. ICA was measured by indirect immunofluorescence method. Anti-GAD antibody was measured by radioimmunoassay. Anti-ICA512 antibody was measured by western blotting. Mitochondrial DNA 3243 mutation was detected using restriction enzyme Apa-I digestion of the amplified genomic DNA from the subjects. RESULTS: 1) Median age of onset was 40 years for atypical type 1 diabetes patients, while it was 27.5 years for typical type 1 diabetes patients. Average duration of insulin requirement was 0.18 years for typical group and 5.73 years for atypical group. In this series, only typical type 1 diabetic patients experienced diabetic ketoacidosis. 2) Only 50 % of typical type 1 diabetic patients and 47 % of atypical type 1 diabetic patients had at least one autoantibody among ICA, anti-GAD antibody and anti-ICA512 antibody. 3) Mitochondrial DNA 3243 point mutation was detected in 3 patients with atypical type 1 diabetes (10 %), but it was not found in patients with typical type 1 diabetes. CONCLUSION: These results suggest that the prevalence of autoantibodies in Korean type 1 diabetic patients was lower than that reported in Caucasians irrespective of clinical features. Therefore, it may not be easy to apply this new diabetes classification of ADA to Korean type 1 diabetic patients. In addition, mitochondrial DNA mutation may be responsible for some of the Korean atypical type 1 diabetic patients.

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