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Yanggu, South Korea

Hwang S.Y.,Korea University | Lee K.W.,Ajou University | Nam M.S.,Inha University | Park Y.S.,Hanyang University | And 3 more authors.
Diabetes | Year: 2012

Recent studies have suggested that a novel adipokine, C1q/tumor necrosis factor-related protein-3 (CTRP-3), a paralog of adiponectin, may play an important role in the regulation of glucose metabolism and innate immunity. Pigment epithelium-derived factor (PEDF), a multifunctional protein with antioxidant and anti-inflammatory properties, is associated with insulin resistance and metabolic syndrome. We examined circulating CTRP-3 and PEDF concentrations in 345 subjects with diverse glucose tolerance statuses. Furthermore, we evaluated the involvement of CTRP-3 and PEDF with cardiometabolic risk factors including insulin resistance, high-sensitivity C-reactive protein (hsCRP), estimated glomerular filtration rate (eGFR), and brachial-ankle pulse wave velocity (baPWV). CTRP-3 concentrations were significantly higher in patients with type 2 diabetes or prediabetes than the normal glucose tolerance group, whereas PEDF levels were not different. Subjects with metabolic syndrome showed significantly higher levels of both CTRP-3 and PEDF compared with subjects without metabolic syndrome. Both CTRP-3 and PEDF were significantly associated with cardiometabolic parameters, including waist-to-hip ratio, triglycerides, HDL-cholesterol, alanine aminotransferase, eGFR, hsCRP, and baPWV. In conclusion, circulating CTRP-3 concentrations were elevated in patients with glucose metabolism dysregulation. Both CTRP-3 and PEDF concentrations were increased in subjects with metabolic syndrome and associated with various cardiometabolic risk factors. © 2012 by the American Diabetes Association. Source


Kim H.-K.,University of Ulsan | Youn B.-S.,AdipoGen Inc. | Shin M.-S.,Asan Medical Center | Namkoong C.,University of Ulsan | And 7 more authors.
Diabetes | Year: 2010

OBJECTIVE - The angiopoietin-like protein 4 (Angptl4)/fasting-induced adipose factor (Fiaf) is known as a regulator of peripheral lipid and glucose metabolism. In the present study, we investigated the physiological role of Angptl4 in central regulation of body weight homeostasis. RESEARCH DESIGN AND METHODS - Hypothalamic Angptl4 expression levels were measured using immunoblot assay during feeding manipulation or after administration of leptin, insulin, and nutrients. The effects of Angptl4 on food intake, body weight, and energy expenditure were determined following intracerebroventricular (ICV) administration of Angptl4 in C57BL/6 mice. Food intake, energy metabolism, and feeding responses to leptin, insulin, and nutrients were compared between Angptl4-null mice and their wild littermates. Finally, the relationship of hypothalamic AMP-activated protein kinase (AMPK) and Angptl4 was studied. RESULTS - Hypothalamic Angptl4 expression levels were increased upon food intake or administration of leptin, insulin, and nutrients. Furthermore, central administration of Angptl4 suppressed food intake and body weight gain but enhanced energy expenditure. These effects were mediated via suppression of hypothalamic AMPK activities. Consistently, Angptl4-null mice displayed increased body weight and hypothalamic AMPK activity but reduced energy expenditure. Food intake following a fast was significantly greater in Angptl4-null mice, which was normalized by centrally administered Angptl4. Moreover, anorectic responses to leptin, insulin, and glucose were diminished in Angptl4-null mice. In contrast, Angptl4-null mice were resistant to diet-induced obesity, indicating obesity-promoting effects of Angptl4 under the condition of fat-enriched diet. CONCLUSIONS - We have demonstrated that hypothalamic Angptl4 is regulated by physiological appetite regulators and mediates their anorexigenic effects via inhibition of hypothalamic AMPK activity. Therefore, Angptl4 appears to have an important role in central regulation of energy metabolism. © 2010 by the American Diabetes Association. Source


Choi K.M.,Korea University | Hwang S.Y.,Korea University | Hong H.C.,Korea University | Choi H.Y.,Korea University | And 4 more authors.
Cardiovascular Diabetology | Year: 2014

Background: C1q/TNF-related protein-3 (CTRP-3), an adiponectin paralog, and progranulin were recently identified as novel adipokines which may link obesity with glucose dysregulation and subclinical inflammation. We analyzed the relationship between CTRP-3, progranulin and coronary artery disease (CAD) in Korean men and women. Methods: Circulating CTRP-3 and progranulin levels were examined in 362 Korean adults with acute coronary syndrome (ACS, n = 69), stable angina pectoris (SAP, n = 85), and control subjects (n = 208) along with various kinds of cardiometabolic risk factors. Results: CTRP-3 concentrations were significantly decreased in patients with ACS or SAP compared to control subjects (P <0.001, respectively), whereas progranulin and adiponectin levels were similar. Correlation analysis adjusted for age and gender exhibited that CTRP-3 levels showed significant negative relationship with glucose (r = -0.110, P = 0.041) and high sensitive C-reactive protein (hsCRP) levels (r = -0.159, P = 0.005), and positive relationship with HDL-cholesterol (r = 0.122, P = 0.025) and adiponectin levels (r = 0.194, P <0.001). In a multivariate logistic regression analysis, the odds ratio for CAD risk was 5.14 (95% CI, 1.83-14.42) in the second, and 9.04 (95% CI, 2.81-29.14) in the first tertile of CTRP-3 levels compared to third tertile after adjusting for other cardiometabolic risk variables. Conclusions: Patients with ACS or SAP had significantly lower circulating CTRP-3 concentrations compared to control subjects, although progranulin levels were not different. These results suggest the possibility that CTRP-3 might be useful for assessing the risk of CAD.Trial registration: (Clinical trials No.: NCT01594710). © 2014 Choi et al.; licensee BioMed Central Ltd. Source


Park J.-W.,Korea University | Saravan Kallempudi S.,Sabanci University | Niazi J.H.,Sabanci University | Gurbuz Y.,Sabanci University | And 2 more authors.
Biosensors and Bioelectronics | Year: 2012

A single-stranded DNA (ssDNA) aptamer was successfully developed to specifically bind to nicotinamide phosphoribosyl transferase (Nampt) through systematic evolution of ligands by exponential enrichment (SELEX) and successfully implemented in a gold-interdigitated (GID) capacitor-based biosensor. Surface plasmon resonance (SPR) analysis of the aptamer revealed high specificity and affinity (Kd=72.52nM). Changes in surface capacitance/charge distribution or dielectric properties in the response of the GID capacitor surface covalently coupled to the aptamers in response to changes in applied AC frequency were measured as a sensing signal based on a specific interaction between the aptamers and Nampt. The limit of detection for Nampt was 1ng/ml with a dynamic serum detection range of up to 50ng/ml; this range includes the clinical requirement for both normal Nampt level, which is 15.8ng/ml, and Nampt level in type 2 diabetes mellitus (T2DM) patients, which is 31.9ng/ml. Additionally, the binding kinetics of aptamer-Nampt interactions on the capacitor surface showed that strong binding occurred with increasing frequency (range, 700MHz-1GHz) and that the dissociation constant of the aptamer under the applied frequency was improved 120-240 times (Kd=0.3-0.6nM) independent on frequency. This assay system is an alternative approach for clinical detection of Nampt with improved specificity and affinity. © 2012 Elsevier B.V. Source


Park M.,York University | Park M.,Institute Pasteur Korea | Youn B.,AdipoGen Inc. | Zheng X.-L.,University of Calgary | And 4 more authors.
PLoS ONE | Year: 2011

Cardiomyocyte apoptosis is an important remodeling event contributing to heart failure and adiponectin may mediate cardioprotective effects at least in part via attenuating apoptosis. Here we used hypoxia-reoxygenation (H/R) induced apoptosis in H9c2 cells to examine the effect of adiponectin and cellular mechanisms of action. We first used TUNEL labeling in combination with laser scanning cytometry to demonstrate that adiponectin prevented H/R-induced DNA fragmentation. The anti-apoptotic effect of adiponectin was also verified via attenuation of H/R-induced phosphatidylserine exposure using annexin V binding. H/R-induced apoptosis via the mitochondrial-mediated intrinsic pathway of apoptosis as assessed by cytochrome c release into cytosol and caspase-3 activation, both of which were attenuated by adiponectin. Mechanistically, we demonstrated that adiponectin enhanced anti-oxidative potential in these cells which led to attenuation of the increase in intracellular reactive oxygen species (ROS) caused by H/R. To further address the mechanism of adiponctins anti-apoptotic effects we used siRNA to efficiently knockdown adiponectin receptor (AdipoR1) expression and found that this attenuated the protective effects of adiponectin on ROS production and caspase 3 activity. Knockdown of APPL1, an important intracellular binding partner for AdipoR, also significantly reduced the ability of adiponectin to prevent H/R-induced ROS generation and caspase 3 activity. In summary, H/R-induced ROS generation and activation of the intrinsic apoptotic pathway was prevented by adiponectin via AdipoR1/APPL1 signaling and increased anti-oxidant potential. © 2011 Park et al. Source

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