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Min Seon Kim  (Kim MS) 14 Articles
Frequency of Silent Myocardial Ischemia Detected by Thallium-201 SPECT in Patients with Type 2 Diabetes.
Dong Woo Kim, Eun Hee Jung, Eun Hee Koh, Min Seon Kim, Joong Yeol Park, Seung Whan Lee, Seong Wook Park, Jin Sook Ryu, Ki Up Lee
Korean Diabetes J. 2009;33(3):225-231.   Published online June 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.3.225
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BACKGROUND
Silent myocardial ischemia (SMI) is more common in diabetic patients than among the general population. It is not yet established whether a routine screening test for SMI is necessary, and which screening test would be most useful. The purpose of this study was to estimate the prevalence of SMI detected by Thallium-201 perfusion single photon emission computed tomography (SPECT) in type 2 diabetic patients. METHODS: A total of 173 asymptomatic type 2 diabetic patients were included in the study. Thallium-201 perfusion SPECT was performed to screen for SMI. RESULTS: Among the 173 patients, abnormal perfusion patterns were found in 11 patients. Coronary angiography was carried out for these patients, and significant coronary artery stenosis was found in ten of them (positive predictive value; 90.9%). There was a significant association between SMI and overt albuminuria (OR = 7.33, 95% CI, 1.825-29.437). CONCLUSION: Thallium-201 perfusion SPECT is not sensitive enough to identify SMI, but is accurate in detecting decreased myocardial perfusion. This may be a useful screening tool for detecting SMI in type 2 diabetic patients with impaired renal function.
Anti-GAD Antibody in Patients with Adult-Onset Diabetes in Korea.
Sang Ah Lee, Eui Young Kim, Eun Hee Kim, Ji Yun Jeong, Eun Heui Jeong, Dong Woo Kim, Eun Hee Cho, Eun Hee Koh, Min Seon Kim, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2009;33(1):16-23.   Published online February 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.1.16
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  • 10 Crossref
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BACKGROUND
It is well known that the clinical characteristics of diabetes mellitus in Korean people are different from those of Western people. The purpose of this study was to investigate the prevalence of the anti-GAD antibody (GADA) in a large number of Korean patients with adult-onset diabetes. METHODS: The GADA was measured by radioimmunoassay for 11,472 adult-onset diabetic patients who visited the Asan Medical Center from 1998 to 2007. According to the fasting C-peptide levels, we classified the patients into an insulin dependent diabetes mellitus group (IDDM; C-peptide < 0.6 ng/mL) and non-insulin dependent diabetes mellitus group (NIDDM; C-peptide > or = 1.0 ng/mL). Other clinical and laboratory data were obtained from medical records. RESULTS: Among the 11,147 diabetic patients, 9,250 patients were classified as NIDDM, 922 patients were classified as IDDM and 975 patients excluded. Within the latter group 472 patients were to absolute insulin deficient (C-peptide < 0.1 ng/mL). The prevalence of GADA was 22.0% in the IDDM group and 4.7% in the NIDDM group. GADA was more prevalent in younger-onset NIDDM patients (25~40 years of age; 12.4%) than in older-onset NIDDM patients (> or = 40 years of age; 3.8%). The GADA-positive NIDDM patients had lower C-peptide and BMI levels, and higher rates of typical diabetic symptoms and insulin treatment. CONCLUSION: The prevalence of GADA in Korean patients with IDDM and NIDDM was lower than that reported in Western populations. It is thus suggested that autoimmunity is a rarer cause of diabetes in Korean people. However, since over 10% of younger-onset NIDDM patients were positive for GADA, routine GADA measurement in such patients is recommended.

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  • Distinct changes to pancreatic volume rather than pancreatic autoantibody positivity: insights into immune checkpoint inhibitors induced diabetes mellitus
    Hung-Hui Wei, Ying-Chieh Lai, Gigin Lin, Cheng-Wei Lin, Ya-Chu Chang, John Wen-Cheng Chang, Miaw-Jene Liou, I-Wen Chen
    Diabetology & Metabolic Syndrome.2024;[Epub]     CrossRef
  • Recent information on test utilization and intraindividual change in anti-glutamic acid decarboxylase antibody in Korea: a retrospective study
    Rihwa Choi, Wonseo Park, Gayoung Chun, Jiwon Lee, Sang Gon Lee, Eun Hee Lee
    BMJ Open Diabetes Research & Care.2022; 10(3): e002739.     CrossRef
  • The effect of glargine versus glimepiride on pancreatic β-cell function in patients with type 2 diabetes uncontrolled on metformin monotherapy: open-label, randomized, controlled study
    Jun Sung Moon, Kyoung Soo Ha, Ji Sung Yoon, Hyoung Woo Lee, Hyun Chul Lee, Kyu Chang Won
    Acta Diabetologica.2014; 51(2): 277.     CrossRef
  • Successful treatment of latent autoimmune diabetes in adults with Traditional Chinese Medicine: a case report
    Jiaxing Tian, Wenke Liu, Zhong Zhen, Xiaolin Tong
    Journal of Traditional Chinese Medicine.2013; 33(6): 766.     CrossRef
  • The prevalence and characteristics of latent autoimmune diabetes in adults (LADA) and its relation with chronic complications in a clinical department of a university hospital in Korea
    Mi-Oh Roh, Chan-Hee Jung, Bo-Yeon Kim, Ji-Oh Mok, Chul-Hee Kim
    Acta Diabetologica.2013; 50(2): 129.     CrossRef
  • Prevalence and Clinical Characteristics of Recently Diagnosed Type 2 Diabetes Patients with Positive Anti-Glutamic Acid Decarboxylase Antibody
    Yul Hwangbo, Jin Taek Kim, Eun Ky Kim, Ah Reum Khang, Tae Jung Oh, Hak Chul Jang, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Young Min Cho
    Diabetes & Metabolism Journal.2012; 36(2): 136.     CrossRef
  • Body Composition Analysis in Newly Diagnosed Diabetic Adolescent Girls
    Yong Hyuk Kim, Min Kyoung Song, Sochung Chung
    Journal of Korean Society of Pediatric Endocrinology.2011; 16(3): 172.     CrossRef
  • Increasing Trend in the Number of Severe Hypoglycemia Patients in Korea
    Jin Taek Kim, Tae Jung Oh, Ye An Lee, Jun Ho Bae, Hyo Jeong Kim, Hye Seung Jung, Young Min Cho, Kyong Soo Park, Soo Lim, Hak Chul Jang, Hong Kyu Lee
    Diabetes & Metabolism Journal.2011; 35(2): 166.     CrossRef
  • Progression to insulin deficiency in Korean patients with Type 2 diabetes mellitus positive for anti‐GAD antibody
    S. A. Lee, W. J. Lee, E. H. Kim, J. H. Yu, C. H. Jung, E. H. Koh, M.‐S. Kim, J.‐Y. Park, K.‐U. Lee
    Diabetic Medicine.2011; 28(3): 319.     CrossRef
  • Anti-GAD Antibody in Patients with Adult-Onset Diabetes in Korea
    Eun-Gyoung Hong
    Korean Diabetes Journal.2009; 33(1): 13.     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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No absrtact available.
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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  • 3 Crossref
AbstractAbstract 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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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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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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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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No abstract available.
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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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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No Abstract available.
Fetal Protein Deficiency Causes Long Term Changes in Mitochondrial DNA Content of Liver and Muscle in Female Sprague-Dawley Rats.
Suk Kyeong Kim, Min Seon Kim, Youn Young Kim, Do Joon Park, Kyong Soo Park, Ki Up Lee, Hong Kyu Lee
Korean Diabetes J. 2003;27(2):115-122.   Published online April 1, 2003
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BACKGROUND
Epidemiological data suggest a strong association between low birth weight and the increased risk of metabolic syndrome, including type 2 diabetes, hypertension and cardiovascular disease, in adult life. However, the underlying mechanisms are largely unknown. In our previous study, the mitochondrial DNA (mtDNA) copy number in peripheral blood leukocytes was decreased in patients with type 2 diabetes and insulin resistance. To test the hypothesis that mitochondrial changes may serve as a link between fetal under nutrition and insulin resistance in later life, the effects of fetal protein malnutrition on the mitochondria of the liver and skeletal muscle, the main sites of insulin action in adulthood, were investigated. METHODS: Eight-week old female rats were divided into 2 groups and fed on either a control diet (casein 180 g/kg diet) (n=5) or a low protein diet (casein 80 g/kg diet) (n=7) for 15 days prior to mating. They were mated with 10 week-old male Sprague Dawley rats that had been fed on the control diet. The female offspring, born to the mothers fed the low protein diet, were randomly divided into 2 groups 4 weeks after birth, and weaned on either the low protein (low protein group, n=48) or control diet (resuscitated group, n=48). As a control group, the offspring born to the mothers fed the control diet were weaned on the control diet (n=48). The animals in each group were again randomly divided into 4 groups, and sacrificed at 5, 10, 15 and 20 weeks of age, respectively (n=12 per group). The body weight, liver and muscle mtDNA content were measured at weeks 5, 10, 15 and 20. RESULTS: The mtDNA contents of the liver and skeletal muscle were reduced in fetal malnourished adult rats, and were not restored to normal levels even when proper nutrition was supplied after weaning. CONCLUSION: Our findings indicate that under nutrition in early life causes long lasting changes in the mitochondria DNA content of the liver and muscles, which may contribute to the development of insulin resistance in later life.
Anti-obesity Effects of alpha-lipoic Acid in OLETF Rats.
Kee Ho Song, Ji Young Youn, Chul Nam Koong, Min Jeong Shin, Jae Won Ryu, Hye Sun Park, Min Seon Kim, Joong Youl Park, Ki Up Lee
Korean Diabetes J. 2002;26(6):460-468.   Published online December 1, 2002
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AbstractAbstract PDF
BACKGROUND
Obesity is closely related to the development of type 2 diabetes mellitus, hypertension and cardiovascular disease. While the prevalence of obesity is rapidly increasing in most parts of the world, its effective treatment is not available due to the limited efficacy, and the side effects, of anti-obesity drugs. We unexpectedly found that administration of alpha-lipoic acid (ALA) resulted in a significant reduction in the body weight of rodents. This study aimed to investigate the mechanisms of the anti-obesity effect of ALA in the obese diabetic models of Otsuka Long Evans Tokushima (OLETF) rats. MATERIALS AND METHODS: Ten weeks old male OLETF rats were randomly assigned into one of three groups (n=6 per group): 1) the control group, fed with normal rat chow 2) the ALA group, fed with rat chow containing ALA (0.5% of food weight) and 3) the pair-fed group, fed with normal rat chow, but given the same amount of food as consumed by the ALA group. The body weight and food intakes were monitored for 3 weeks. At the end of the study, abdominal CT scans were performed to measure the visceral fat content. The energy expenditure and respiratory quotient were measured on days 3, 9 and 21 using an indirect calorimeter. The expression of the uncoupling protein-1 mRNA in the white and brown adipose tissues were determined by Northern blot analyses. The oxidation of fatty acids in the skeletal muscle, liver and adipose tissue was also measured. RESULTS: The administration of ALA induced a significant weight loss and reduction in food intake throughout the study period. The weight loss in the ALA group was greater than in the pair-fed group (p<0.05), suggesting an enhanced energy metabolism in the ALA group. In the ALA treated animals, the energy expenditure was significantly increased together with an elevated expression of UCP-1 mRNA in the brown, and an ectopic expression of UCP-1 mRNA in the white adipose tissues. The oxidation of fat in the brown adipose tissue and skeletal muscle was also increased after the ALA treatment, which was in line with the reduced respiratory quotient in the ALA group. The abdominal CT scan revealed a reduction in the visceral fat content in the ALA group compared to the control group. CONCLUSION: The present study demonstrated, for the first time, a novel anti-obesity action of ALA in obese OLETF rats, which proceeds through at least three different mechanisms: 1) reduction in food intake, 2) increase in energy expenditure and 3) enhancement of fat oxidation.
Expression of ghrelin and its receptor according to feeding state in rats.
Min Seon Kim, Cho Ya Yoon, Young Joo Park, Hyung Kyu Park, Chen Ji Jin, Kyong Han Park, Chan Soo Shin, Kyong Soo Park, Seong Youn Kim, Bo Youn Cho, Hong Kyu Lee
Korean Diabetes J. 2002;26(3):169-178.   Published online June 1, 2002
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BACKGROUND
Ghrelin is a newly discovered gut peptide, produced mainly in the stomach, which is secreted into the circulating blood and acts on the hypothalamus and the pituitary gland. Although ghrelin was originally identified as an endogenous growth hormone secretagogue, recent studies have suggested its role is in the regulation of food intake and energy homeostasis. The aim of this study was to investigate changes in the expression of ghrelin in the stomach, and of its receptors in the hypothalamus and the pituitary gland in relation to the feeding state. METHODS: Sprague Dawley male rats, divided into 3 groups, freely fed, fasted for 48 hrs and fasted for 48 hrs followed by feeding for 24 hrs, were investigated. The stomach fundus, the hypothalamus and the pituitary glands were collected. The gastric ghrelin mRNA expression was determined by Northern blot analysis and the ghrelin protein by immunohistochemistry. The ghrelin receptor mRNA levels in the hypothalamus and anterior pituitary gland were determined by real time PCR. RESULTS: The ghrelin mRNA levels in the stomach were increased by fasting but reduced again by allowing feeding. The number of ghrelin-immunoreactive gastric epithelial cells tended to increase with fasting. Moreover, the ghrelin receptor mRNA levels increased fold in the hypothalamus, and about 3 fold in the anterior pituitary gland harvested from the rats that had fasted for 48 hrs compared to those that were freely fed. CONCLUSION: Our data demonstrate that expression of both ghrelin in stomach and its receptor in target organs increased in the fasted state, which would be helpful for magnifying the orexigenic effect of ghrelin in the negative energy balance state. Dynamic changes in ghrelin and ghrelin receptor according to altered metabolic state may suggest a physiologic role of ghrelin in the regulation of energy homeostasis.
Effect of cisapride on diabetic gastroparesis.
Min Seon Kim, Jae Hoon Chung, Yong Soo Park, Kyong Soo Park, Seong Yeun Kim, Myung Chul Lee, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min
Korean Diabetes J. 1993;17(4):395-402.   Published online January 1, 2001
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No abstract available.

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