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Metabolic Risk/Epidemiology
Insulin Resistance Increases Serum Immunoglobulin E Sensitization in Premenopausal Women
Seung Eun Lee, Ji Yeon Baek, Kyungdo Han, Eun Hee Koh
Diabetes Metab J. 2021;45(2):175-182.   Published online April 14, 2020
DOI: https://doi.org/10.4093/dmj.2019.0150
  • 6,328 View
  • 123 Download
  • 2 Web of Science
  • 2 Crossref
Graphical AbstractGraphical Abstract AbstractAbstract PDFPubReader   ePub   
Background

Although studies have shown that obesity is associated with aeroallergen sensitization (atopy), controversy still exists. We aimed to investigate the association between metabolic status, obesity, and atopy stratified by sex and menopausal status.

Methods

A total of 1,700 adults from the 2010 Korean National Health and Nutrition Examination Survey were classified into metabolically healthy nonobese (MHNO), metabolically unhealthy nonobese (MUNO), metabolically healthy obese (MHO), and metabolically unhealthy obese (MUO) by body mass index and insulin resistance. Atopy was defined as a positive response to at least one aeroallergen. Multiple regression analysis was used to evaluate the risk of immunoglobulin E (IgE) elevation or atopy in relation to the degree of metabolic abnormality and obesity.

Results

In premenopausal women, total IgE was positively correlated with obesity and insulin resistance. MUNO participants had a higher risk of having elevated total IgE compared to MHNO participants (odds ratio [OR], 2.271; 95% confidence interval [CI], 1.201 to 4.294), while MHO participants did not show a significant difference (OR, 1.435; 95% CI, 0.656 to 3.137) in premenopausal women. MUNO, but not MHO was also associated with atopy (OR, 2.157; 95% CI, 1.284 to 3.625). In men and postmenopausal women, there was no significant difference between metabolic status, obesity, and atopy among groups.

Conclusion

Increased insulin resistance is associated with total IgE and atopy in premenopausal women but not in postmenopausal women or men.

Citations

Citations to this article as recorded by  
  • Association of serum total IgE and allergen-specific IgE with insulin resistance in adolescents: an analysis of the NHANES database
    Yaping Liu, Xiaoxia Wang, Yong Liu
    BMC Pediatrics.2024;[Epub]     CrossRef
  • Is There a Relationship between Insulin Resistance and Eosinophil, Inflammatory Parameters Neutrophil to lymphocyte ratio, C-Reactive Protein Values?
    Meltem YİĞİT, Özgür OLUKMAN
    Medical Records.2024; 6(1): 32.     CrossRef
Cardiovascular Risk/Epidemiology
Impact of Diabetes Control on Subclinical Atherosclerosis: Analysis from Coronary Computed Tomographic Angiography Registry
Gyung-Min Park, Chang Hoon Lee, Seung-Whan Lee, Sung-Cheol Yun, Young-Hak Kim, Yong-Giun Kim, Ki-Bum Won, Soe Hee Ann, Shin-Jae Kim, Dong Hyun Yang, Joon-Won Kang, Tae-Hwan Lim, Eun Hee Koh, Woo Je Lee, Min-Seon Kim, Joong-Yeol Park, Hong-Kyu Kim, Jaewon Choe, Sang-Gon Lee
Diabetes Metab J. 2020;44(3):470-479.   Published online November 22, 2019
DOI: https://doi.org/10.4093/dmj.2019.0073
  • 8,802 View
  • 70 Download
  • 8 Web of Science
  • 8 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   
Background

There are limited data on the impact of diabetes control on the risk of subclinical coronary atherosclerosis.

Methods

We analyzed 6,434 consecutive asymptomatic individuals without previous history of coronary artery disease who underwent coronary computed tomographic angiography (CCTA) (mean age, 53.7±7.6 years and 4,694 men [73.0%]). The degree and extent of subclinical coronary atherosclerosis were assessed by CCTA, and ≥50% diameter stenosis was defined as significant. A cardiac event was defined as a composite of all-cause death, myocardial infarction, unstable angina, or coronary revascularization. Study participants were categorized as normal (n=5,319), controlled diabetes (glycosylated hemoglobin [HbA1c] <7%, n=747), or uncontrolled diabetes (HbA1c ≥7%, n=368), respectively.

Results

Compared with normal individuals, there were no statistically significant differences in the risk of for any atherosclerotic plaque (odds ratio [OR], 1.16; 95% confidence interval [CI], 0.98 to 1.38; P=0.086) and significant coronary artery stenosis (OR, 1.08; 95% CI, 0.82 to 1.42; P=0.583) in controlled diabetic individuals. In contrast, uncontrolled diabetic individuals had consistently higher risks of any atherosclerotic plaque (OR, 2.16; 95% CI, 1.70 to 2.75; P<0.001) and significant coronary artery stenosis (OR, 3.34; 95% CI, 2.52 to 4.43; P<0.001) than normal individuals. During a follow-up of median 5.4 years, there was no significant difference in cardiac events between normal and controlled diabetic individuals (P=0.365). However, uncontrolled diabetes was associated with an increased risk of cardiac events compared with normal individuals (P<0.001) and controlled diabetic individuals (P=0.023).

Conclusion

Asymptomatic uncontrolled diabetes was associated with significant subclinical coronary atherosclerosis with subsequent high risk for cardiac events.

Citations

Citations to this article as recorded by  
  • Carotid Ultrasound Abnormalities of People Living With HIV in Kunming, China: Multiple Correspondence Analysis Approach to Identify Influencing Factors
    Shuishui Pan, Haiyan Fu, Zhiqiong Ai, Chongxi Li, Jinsong Bai
    International Journal of STD & AIDS.2023; 34(10): 710.     CrossRef
  • Differential Impact of Degree of Hypertension on Subclinical Coronary Atherosclerosis in Asymptomatic Subjects With and Without Diabetes Mellitus
    Hyun Woo Park, Sangyong Jo, Kyung Sun Park, Hyeji Lee, Young-Jee Jeon, Sangwoo Park, Soe Hee Ann, Yong-Giun Kim, Seong Hoon Choi, Woon Jung Kwon, Young-Rak Cho, Jon Suh, Gyung-Min Park
    The American Journal of Cardiology.2023; 203: 343.     CrossRef
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    Kou-Gi Shyu, Bao-Wei Wang, Wei-Jen Fang, Chun-Ming Pan, Chiu-Mei Lin
    International Journal of Molecular Sciences.2022; 23(3): 1095.     CrossRef
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    Su Bin Kim, Hae Won Jung
    Medicine.2022; 101(47): e31816.     CrossRef
  • Time to Reach Target Glycosylated Hemoglobin Is Associated with Long-Term Durable Glycemic Control and Risk of Diabetic Complications in Patients with Newly Diagnosed Type 2 Diabetes Mellitus: A 6-Year Observational Study
    Kyoung Jin Kim, Jimi Choi, Jae Hyun Bae, Kyeong Jin Kim, Hye Jin Yoo, Ji A Seo, Nan Hee Kim, Kyung Mook Choi, Sei Hyun Baik, Sin Gon Kim, Nam Hoon Kim
    Diabetes & Metabolism Journal.2021; 45(3): 368.     CrossRef
  • Frequency and Significance of Right Bundle Branch Block and Subclinical Coronary Atherosclerosis in Asymptomatic Individuals
    Hyeji Lee, Young-Jee Jeon, Byung Ju Kang, Tae Young Lee, Eun Ji Park, Sangwoo Park, Soe Hee Ann, Yong-Giun Kim, Yongjik Lee, Seong Hoon Choi, Gyung-Min Park
    The American Journal of Cardiology.2021; 158: 30.     CrossRef
  • The association between glucose-related variables and plaque morphology in patients with ST-segment elevated myocardial infarction
    Jinxin Liu, Shanjie Wang, Can Cui, Hengxuan Cai, Rong Sun, Weili Pan, Shaohong Fang, Bo Yu
    Cardiovascular Diabetology.2020;[Epub]     CrossRef
  • Choosing Antithrombotic Therapy in Patients with Coronary Heart Disease and Type 2 Diabetes Mellitus: How to Reduce the Risk of Death
    N. A. Koziolova, P. G. Karavaev, A. S. Veklich
    Kardiologiia.2020; 60(4): 109.     CrossRef
Basic Research
Inhibition of Ceramide Accumulation in Podocytes by Myriocin Prevents Diabetic Nephropathy
Chang-Yun Woo, Ji Yeon Baek, Ah-Ram Kim, Chung Hwan Hong, Ji Eun Yoon, Hyoun Sik Kim, Hyun Ju Yoo, Tae-Sik Park, Ranjan Kc, Ki-Up Lee, Eun Hee Koh
Diabetes Metab J. 2020;44(4):581-591.   Published online November 4, 2019
DOI: https://doi.org/10.4093/dmj.2019.0063
  • 6,320 View
  • 165 Download
  • 27 Web of Science
  • 30 Crossref
AbstractAbstract PDFPubReader   ePub   
Background

Ceramides are associated with metabolic complications including diabetic nephropathy in patients with diabetes. Recent studies have reported that podocytes play a pivotal role in the progression of diabetic nephropathy. Also, mitochondrial dysfunction is known to be an early event in podocyte injury. Thus, we tested the hypothesis that ceramide accumulation in podocytes induces mitochondrial damage through reactive oxygen species (ROS) production in patients with diabetic nephropathy.

Methods

We used Otsuka Long Evans Tokushima Fatty (OLETF) rats and high-fat diet (HFD)-fed mice. We fed the animals either a control- or a myriocin-containing diet to evaluate the effects of the ceramide. Also, we assessed the effects of ceramide on intracellular ROS generation and on podocyte autophagy in cultured podocytes.

Results

OLETF rats and HFD-fed mice showed albuminuria, histologic features of diabetic nephropathy, and podocyte injury, whereas myriocin treatment effectively treated these abnormalities. Cultured podocytes exposed to agents predicted to be risk factors (high glucose, high free fatty acid, and angiotensin II in combination [GFA]) showed an increase in ceramide accumulation and ROS generation in podocyte mitochondria. Pretreatment with myriocin reversed GFA-induced mitochondrial ROS generation and prevented cell death. Myriocin-pretreated cells were protected from GFA-induced disruption of mitochondrial integrity.

Conclusion

We showed that mitochondrial ceramide accumulation may result in podocyte damage through ROS production. Therefore, this signaling pathway could become a pharmacological target to abate the development of diabetic kidney disease.

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    Amit Talukdar, Mandira Basumatary
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Sulwon Lecture 2018
Pathophysiology
Mitochondrial Dysfunction in Adipocytes as a Primary Cause of Adipose Tissue Inflammation
Chang-Yun Woo, Jung Eun Jang, Seung Eun Lee, Eun Hee Koh, Ki-Up Lee
Diabetes Metab J. 2019;43(3):247-256.   Published online March 27, 2019
DOI: https://doi.org/10.4093/dmj.2018.0221
  • 8,733 View
  • 260 Download
  • 70 Web of Science
  • 71 Crossref
AbstractAbstract PDFPubReader   

Adipose tissue inflammation is considered a major contributing factor in the development of obesity-associated insulin resistance and cardiovascular diseases. However, the cause of adipose tissue inflammation is presently unclear. The role of mitochondria in white adipocytes has long been neglected because of their low abundance. However, recent evidence suggests that mitochondria are essential for maintaining metabolic homeostasis in white adipocytes. In a series of recent studies, we found that mitochondrial function in white adipocytes is essential to the synthesis of adiponectin, which is the most abundant adipokine synthesized from adipocytes, with many favorable effects on metabolism, including improvement of insulin sensitivity and reduction of atherosclerotic processes and systemic inflammation. From these results, we propose a new hypothesis that mitochondrial dysfunction in adipocytes is a primary cause of adipose tissue inflammation and compared this hypothesis with a prevailing concept that “adipose tissue hypoxia” may underlie adipose tissue dysfunction in obesity. Recent studies have emphasized the role of the mitochondrial quality control mechanism in maintaining mitochondrial function. Future studies are warranted to test whether an inadequate mitochondrial quality control mechanism is responsible for mitochondrial dysfunction in adipocytes and adipose tissue inflammation.

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Original Articles
Obesity and Metabolic Syndrome
Statins Increase Mitochondrial and Peroxisomal Fatty Acid Oxidation in the Liver and Prevent Non-Alcoholic Steatohepatitis in Mice
Han-Sol Park, Jung Eun Jang, Myoung Seok Ko, Sung Hoon Woo, Bum Joong Kim, Hyun Sik Kim, Hye Sun Park, In-Sun Park, Eun Hee Koh, Ki-Up Lee
Diabetes Metab J. 2016;40(5):376-385.   Published online April 5, 2016
DOI: https://doi.org/10.4093/dmj.2016.40.5.376
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AbstractAbstract PDFPubReader   
Background

Non-alcoholic fatty liver disease is the most common form of chronic liver disease in industrialized countries. Recent studies have highlighted the association between peroxisomal dysfunction and hepatic steatosis. Peroxisomes are intracellular organelles that contribute to several crucial metabolic processes, such as facilitation of mitochondrial fatty acid oxidation (FAO) and removal of reactive oxygen species through catalase or plasmalogen synthesis. Statins are known to prevent hepatic steatosis and non-alcoholic steatohepatitis (NASH), but underlying mechanisms of this prevention are largely unknown.

Methods

Seven-week-old C57BL/6J mice were given normal chow or a methionine- and choline-deficient diet (MCDD) with or without various statins, fluvastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin (15 mg/kg/day), for 6 weeks. Histological lesions were analyzed by grading and staging systems of NASH. We also measured mitochondrial and peroxisomal FAO in the liver.

Results

Statin treatment prevented the development of MCDD-induced NASH. Both steatosis and inflammation or fibrosis grades were significantly improved by statins compared with MCDD-fed mice. Gene expression levels of peroxisomal proliferator-activated receptor α (PPARα) were decreased by MCDD and recovered by statin treatment. MCDD-induced suppression of mitochondrial and peroxisomal FAO was restored by statins. Each statin's effect on increasing FAO and improving NASH was independent on its effect of decreasing cholesterol levels.

Conclusion

Statins prevented NASH and increased mitochondrial and peroxisomal FAO via induction of PPARα. The ability to increase hepatic FAO is likely the major determinant of NASH prevention by statins. Improvement of peroxisomal function by statins may contribute to the prevention of NASH.

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Complications
Serum Total Bilirubin Levels Provide Additive Risk Information over the Framingham Risk Score for Identifying Asymptomatic Diabetic Patients at Higher Risk for Coronary Artery Stenosis
Jaechan Leem, Eun Hee Koh, Jung Eun Jang, Chang-Yun Woo, Jin Sun Oh, Min Jung Lee, Joon-Won Kang, Tae-Hwan Lim, Chang Hee Jung, Woo Je Lee, Joong-Yeol Park, Ki-Up Lee
Diabetes Metab J. 2015;39(5):414-423.   Published online October 22, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.5.414
  • 4,341 View
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AbstractAbstract PDFPubReader   
Background

The diagnosis of coronary artery disease (CAD) is often delayed in patients with type 2 diabetes. Serum total bilirubin levels are inversely associated with CAD. However, no studies have examined whether this can be used as a biochemical marker for identifying asymptomatic diabetic patients at higher risk for having obstructive CAD.

Methods

We performed a cross-sectional study of 460 consecutive asymptomatic patients with type 2 diabetes. All patients underwent coronary computed tomographic angiography, and their serum total bilirubin levels were measured. Obstructive CAD was defined as ≥50% diameter stenosis in at least one coronary artery.

Results

Serum total bilirubin tertiles showed an inverse association with the prevalence of obstructive CAD. In multivariate logistic regression analysis, the odds ratio for the highest versus the lowest tertile of total bilirubin was 0.227 (95% confidence interval [CI], 0.130 to 0.398), and an increment of 1 µmol/L in serum total bilirubin level was associated with a 14.6% decrease in obstructive CAD after adjustment for confounding variables. Receiver operating characteristic curve analysis showed that the area under the curve for the Framingham Risk Score (FRS) plus serum total bilirubin level was 0.712 (95% CI, 0.668 to 0.753), which is significantly greater than that of the FRS alone (P=0.0028).

Conclusion

Serum total bilirubin level is inversely associated with obstructive CAD and provides additive risk information over the FRS. Serum total bilirubin may be helpful for identifying asymptomatic patients with type 2 diabetes who are at higher risk for obstructive CAD.

Citations

Citations to this article as recorded by  
  • DECREASE IN SERUM BILIRUBIN AS AN UNFAVORABLE MARKER OF CARDIOVASCULAR DISORDERS
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Clinical Features and Causes of Endogenous Hyperinsulinemic Hypoglycemia in Korea
Chang-Yun Woo, Ji Yun Jeong, Jung Eun Jang, Jaechan Leem, Chang Hee Jung, Eun Hee Koh, Woo Je Lee, Min-Seon Kim, Joong-Yeol Park, Jung Bok Lee, Ki-Up Lee
Diabetes Metab J. 2015;39(2):126-131.   Published online March 9, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.2.126
  • 5,346 View
  • 85 Download
  • 22 Web of Science
  • 20 Crossref
AbstractAbstract PDFPubReader   
Background

Endogenous hyperinsulinemic hypoglycemia (EHH) is characterized by an inappropriately high plasma insulin level, despite a low plasma glucose level. Most of the EHH cases are caused by insulinoma, whereas nesidioblastosis and insulin autoimmune syndrome (IAS) are relatively rare.

Methods

To evaluate the relative frequencies of various causes of EHH in Korea, we retrospectively analyzed 84 patients who were diagnosed with EHH from 1998 to 2012 in a university hospital.

Results

Among the 84 EHH patients, 74 patients (88%), five (6%), and five (6%) were diagnosed with insulinoma, nesidioblastosis or IAS, respectively. The most common clinical manifestation of EHH was neuroglycopenic symptoms. Symptom duration before diagnosis was 14.5 months (range, 1 to 120 months) for insulinoma, 1.0 months (range, 6 days to 7 months) for nesidioblastosis, and 2.0 months (range, 1 to 12 months) for IAS. One patient, who was diagnosed with nesidioblastosis in 2006, underwent distal pancreatectomy but was later determined to be positive for insulin autoantibodies. Except for one patient who was diagnosed in 2007, the remaining three patients with nesidioblastosis demonstrated severe hyperinsulinemia (157 to 2,719 µIU/mL), which suggests that these patients might have had IAS, rather than nesidioblastosis.

Conclusion

The results of this study suggest that the prevalence of IAS may be higher in Korea than previously thought. Therefore, measurement of insulin autoantibody levels is warranted for EHH patients, especially in patients with very high plasma insulin levels.

Citations

Citations to this article as recorded by  
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Various Oscillation Patterns of Serum Fibroblast Growth Factor 21 Concentrations in Healthy Volunteers
Sang Ah Lee, Eunheiu Jeong, Eun Hee Kim, Mi-Seon Shin, Jenie Yoonoo Hwang, Eun Hee Koh, Woo Je Lee, Joong-Yeol Park, Min-Seon Kim
Diabetes Metab J. 2012;36(1):29-36.   Published online February 17, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.1.29
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AbstractAbstract PDFPubReader   
Background

Fibroblast growth factor 21 (FGF21) was originally identified as a paroxysm proliferator activated receptor-α target gene product and is a hormone involved in metabolic regulation. The purpose of this study was to investigate the diurnal variation of serum FGF21 concentration in obese and non-obese healthy volunteers.

Methods

Blood samples were collected from five non-obese (body mass index [BMI] ≤23 kg/m2) and five obese (BMI ≥25 kg/m2) healthy young men every 30 to 60 minutes over 24 hours. Serum FGF21 concentrations were determined by radioimmunoassay. Anthropometric parameters, glucose, free fatty acid, insulin, leptin, and cortisol concentrations were also measured.

Results

The serum FGF21 concentrations displayed various individual oscillation patterns. The oscillation frequency ranged between 6 and 12 times per day. The average duration of oscillation was 2.52 hours (range, 1.9 to 3.0 hours). The peaks and troughs of FGF21 oscillation showed no circadian rhythm. However, the oscillation frequency had a diurnal variation and was lower during the light-off period than during the light-on period (2.4 vs. 7.3 times, P<0.001). There was no difference in the total frequency or duration of oscillations between non-obese and obese subjects, but obese individuals had increased numbers of larger oscillations (amplitude ≥0.19 ng/mL).

Conclusion

Various oscillation patterns in serum FGF21 concentration were observed, and reduced oscillation frequencies were seen during sleep. The oscillation patterns of serum FGF21 concentration suggest that FGF21 may be secreted into systemic circulation in a pulsatile manner. Obesity appeared to affect the amplitude of oscillations of serum FGF21.

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The Prevalence of Peripheral Arterial Disease in Korean Patients with Type 2 Diabetes Mellitus Attending a University Hospital
Ji Hee Yu, Jenie Yoonoo Hwang, Mi-Seon Shin, Chang Hee Jung, Eun Hee Kim, Sang Ah Lee, Eun Hee Koh, Woo Je Lee, Min-Seon Kim, Joong-Yeol Park, Ki-Up Lee
Diabetes Metab J. 2011;35(5):543-550.   Published online October 31, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.5.543
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AbstractAbstract PDFPubReader   
Background

Peripheral arterial disease (PAD) is a common manifestation of systemic atherosclerosis and is associated with significant morbidity and mortality. Diabetes is known to increase the risk of PAD two- to four-fold. The prevalence of PAD in Korean diabetic patients has not been established. In this study, we investigated the prevalence of PAD in Korean patients with type 2 diabetes attending a large university hospital and analyzed the factors associated with PAD.

Methods

A total of 2,002 patients with type 2 diabetes who underwent ankle-brachial index (ABI) measurement in an outpatient clinic were enrolled. PAD was defined as an ABI ≤0.9. Clinical characteristics of 64 patients with PAD were compared with those of 192 age- and sex-matched control patients without PAD.

Results

Of the 2,002 type 2 diabetic patients, 64 (3.2%) were diagnosed as having PAD. PAD was associated with higher prevalences of retinopathy, nephropathy, neuropathy, cerebrovascular and coronary artery disease. Patients with PAD had higher systolic blood pressure and serum triglyceride level and reported higher pack-years of smoking. Multivariate analysis showed that the presence of micro- and macrovascular complications and high systolic blood pressure are factors independently associated with PAD.

Conclusion

The prevalence of PAD in diabetic patients was 3.2%, suggesting that the prevalence in Korean diabetic patients is lower than that of patients in Western countries.

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Homocysteine as a Risk Factor for Development of Microalbuminuria in Type 2 Diabetes
Eun-Hee Cho, Eun Hee Kim, Won Gu Kim, Eun Hui Jeong, Eun Hee Koh, Woo-Je Lee, Min-Seon Kim, Joong-Yeol Park, Ki-Up Lee
Korean Diabetes J. 2010;34(3):200-206.   Published online June 30, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.3.200
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AbstractAbstract PDFPubReader   
Background

Kidney function is critical in homocysteine clearance, and plasma homocysteine level is frequently increased in patients with renal failure. On the other hand, recent studies in animals have shown that hyperhomocysteinemia induces renal injury. In this study, we determined whether hyperhomocysteinemia can be a risk factor for the development of microalbuminuria in patients with type 2 diabetes.

Methods

A nested case-control study. Of 887 patients with type 2 diabetes who did not have microalbuminuria at baseline, 76 developed microalbuminuria during follow-up (mean, 36.0 ± 11.7 months; range, 18 to 76 months). The control group consisted of 152 age- and sex-matched subjects who did not develop microalbuminuria. Baseline plasma homocysteine concentrations were measured in stored samples.

Results

Baseline plasma homocysteine concentrations and mean HbA1C levels during follow-up were significantly higher in patients who developed microalbuminuria than in those who remained normoalbuminuric. Multivariate logistic regression analysis showed that baseline plasma homocysteine level and mean HbA1C were independent predictors of microalbuminuria in type 2 diabetes.

Conclusion

Hyperhomocysteinemia was associated with increased risk of microalbuminuria in patients with type 2 diabetes supporting the concept that hyperhomocysteinemia has an etiologic role in the pathogenesis of diabetic nephropathy.

Citations

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    Emir Muzurović, Ivana Kraljević, Mirsala Solak, Siniša Dragnić, Dimitri P. Mikhailidis
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Review
Adenine Nucleotide Translocator as a Regulator of Mitochondrial Function: Implication in the Pathogenesis of Metabolic Syndrome
Eun Hee Kim, Eun Hee Koh, Joong-Yeol Park, Ki-Up Lee
Korean Diabetes J. 2010;34(3):146-153.   Published online June 30, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.3.146
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AbstractAbstract PDFPubReader   

Mitochondria play key roles in energy production and intracellular reactive oxygen species (ROS) generation. Lines of evidence have shown that mitochondrial dysfunction contributes to the development of metabolic syndrome. The causes of mitochondrial dysfunction are complex, but overnutrition and sedentary living are among the best known causes of mitochondrial dysfunction. ATP synthesized in the mitochondria is exchanged for cytosolic ADP by adenine nucleotide translocator (ANT) to provide a continuous supply of ADP to mitochondria. We recently found that ANT function is essential for peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC-1α)'s action on endothelial cells. PGC-1α is a transcriptional coactivator of nuclear receptors, playing an important role in fatty acid oxidation and mitochondrial biogenesis. Recent studies have shown that PGC-1α decreases intracellular ROS generation by increasing the expression of antioxidant genes. In our study, PGC-1α reduced cell apoptosis and ROS generation in endothelial cells by increasing ATP/ADP translocase activity of ANT and ANT1 expression. Here we review the role of ANT in maintaining proper mitochondrial function, and possible role of ANT dysfunction in the pathogenesis of metabolic syndrome.

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Original Articles
Lack of Association between Serum Cystatin C Levels and Coronary Artery Disease in Diabetic Patients
Eun Hee Kim, Ji Hee Yu, Sang Ah Lee, Eui Young Kim, Won Gu Kim, Seung Hun Lee, Eun Hee Cho, Eun Hee Koh, Woo Je Lee, Min-Seon Kim, Joong-Yeol Park, Ki-Up Lee
Korean Diabetes J. 2010;34(2):95-100.   Published online April 30, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.2.95
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AbstractAbstract PDFPubReader   
Background

Serum cystatin C level is a more sensitive marker of renal dysfunction than serum creatinine level. Serum cystatin C level was recently reported to predict the development of cardiovascular disease. This study was performed to evaluate whether the cystatin C level is associated with coronary artery disease (CAD), independent of diabetic nephropathy.

Methods

We conducted a case-control study to assess the relationship between serum cystatin C level and coronary artery disease in diabetic patients. Among 460 diabetic patients, 38 diabetic patients had CAD. The control group consisted of 38 diabetic patients who were matched to cases by age, sex, and presence/absence of diabetic nephropathy. Serum cystatin C level was measured in stored samples.

Results

Serum cystatin C level was significantly higher in patients with diabetic nephropathy, both in CAD and non-CAD patients. However, serum cystatin C level did not differ between CAD and non-CAD patients, regardless of diabetic nephropathy.

Conclusion

Serum cystatin C level is a marker of renal dysfunction, but not coronary artery disease, in diabetic patients.

Citations

Citations to this article as recorded by  
  • Higher Levels of Cystatin C in HIV/AIDS Patients with Metabolic Syndrome
    Gordana Dragović, Danica Srdić, Khawla Al Musalhi, Ivan Soldatović, Jovana Kušić, Djordje Jevtović, Devaki Nair
    Basic & Clinical Pharmacology & Toxicology.2018; 122(4): 396.     CrossRef
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    Aditya Batra, Aditya Kapoor, R.K. Sharma, Nitin Agrawal, Archana Sinha, Sudeep Kumar, Naveen Garg, Satyendra Tewari, Pravin K. Goel
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    Xie Qing, Wang Furong, Liu Yunxia, Zhang Jian, Wang Xuping, Gao Ling
    Cardiovascular Diabetology.2012;[Epub]     CrossRef
  • Response: Lack of Association between Serum Cystatin C Levels and Coronary Artery Disease in Diabetic Patients (Korean Diabetes J 2010;34:95-100)
    Eun Hee Kim, Ki-Up Lee
    Korean Diabetes Journal.2010; 34(3): 209.     CrossRef
  • Serum Cystatin C as a Biomarker for Predicting Coronary Artery Disease in Diabetes
    Jee-Young Oh
    Korean Diabetes Journal.2010; 34(2): 84.     CrossRef
  • Letter: Lack of Association between Serum Cystatin C Levels and Coronary Artery Disease in Diabetic Patients (Korean Diabetes J 2010;34:95-100)
    Kyu-Chang Won
    Korean Diabetes Journal.2010; 34(3): 207.     CrossRef
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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AbstractAbstract PDF
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.
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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AbstractAbstract PDF
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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    Jun Kobayashi, Kazuo Ohtake, Hiroyuki Uchida
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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
AbstractAbstract PDF
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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Diabetes Metab J : Diabetes & Metabolism Journal