Un Ju Jung
Columbia University
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Featured researches published by Un Ju Jung.
Molecular Nutrition & Food Research | 2008
Kwon-Il Seo; Myung-Sook Choi; Un Ju Jung; Hye-Jin Kim; Jiyoung Yeo; Seon-Min Jeon; Mi-Kyung Lee
We investigated the effect of curcumin on insulin resistance and glucose homeostasis in male C57BL/KsJ-db/db mice and their age-matched lean non-diabetic db/+ mice. Both db/+ and db/db mice were fed with or without curcumin (0.02%, wt/wt) for 6 wks. Curcumin significantly lowered blood glucose and HbA 1c levels, and it suppressed body weight loss in db/db mice. Curcumin improved homeostasis model assessment of insulin resistance and glucose tolerance, and elevated the plasma insulin level in db/db mice. Hepatic glucokinase activity was significantly higher in the curcumin-supplemented db/db group than in the db/db group, whereas glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities were significantly lower. In db/db mice, curcumin significantly lowered the hepatic activities of fatty acid synthase, beta-oxidation, 3-hydroxy-3-methylglutaryl coenzyme reductase, and acyl-CoA: cholesterol acyltransferase. Curcumin significantly lowered plasma free fatty acid, cholesterol, and triglyceride concentrations and increased the hepatic glycogen and skeletal muscle lipoprotein lipase in db/db mice. Curcumin normalized erythrocyte and hepatic antioxidant enzyme activities (superoxide dismutase, catalase, gluthathione peroxidase) in db/db mice that resulted in a significant reduction in lipid peroxidation. However, curcumin showed no effect on the blood glucose, plasma insulin, and glucose regulating enzyme activities in db/+ mice. These results suggest that curcumin seemed to be a potential glucose-lowering agent and antioxidant in type 2 diabetic db/db mice, but had no affect in non-diabetic db/+ mice.
Metabolism-clinical and Experimental | 2008
Eun-Mi Jang; Myung-Sook Choi; Un Ju Jung; Myung-Joo Kim; Hye-Jin Kim; Seon-Min Jeon; Su-Kyung Shin; Chi-Nam Seong; Mi-Kyung Lee
This study investigated the effect of curcumin (0.05-g/100-g diet) supplementation on a high-fat diet (10% coconut oil, 0.2% cholesterol, wt/wt) fed to hamsters, one of the rodent species that are most closely related to humans in lipid metabolism. Curcumin significantly lowered the levels of free fatty acid, total cholesterol, triglyceride, and leptin and the homeostasis model assessment of insulin resistance index, whereas it elevated the levels of high-density lipoprotein cholesterol and apolipoprotein (apo) A-I and paraoxonase activity in plasma, compared with the control group. The levels of hepatic cholesterol and triglyceride were also lower in the curcumin group than in the control group. In the liver, fatty acid beta-oxidation activity was significantly higher in the curcumin group than in the control group, whereas fatty acid synthase, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and acyl coenzyme A:cholesterol acyltransferase activities were significantly lower. Curcumin significantly lowered the lipid peroxide levels in the erythrocyte and liver compared with the control group. These results indicate that curcumin exhibits an obvious hypolipidemic effect by increasing plasma paraoxonase activity, ratios of high-density lipoprotein cholesterol to total cholesterol and of apo A-I to apo B, and hepatic fatty acid oxidation activity with simultaneous inhibition of hepatic fatty acid and cholesterol biosynthesis in high-fat-fed hamsters.
Diabetes-metabolism Research and Reviews | 2008
Myung-Sook Choi; Un Ju Jung; Jiyoung Yeo; Myung-Joo Kim; Mi-Kyung Lee
Non‐obese diabetic (NOD) mice are regarded as being excellent animal models of human type 1 diabetes or insulin dependent diabetes (IDDM). This study investigated the beneficial effects of genistein and daidzein on IDDM, an autoimmune disease.
Arteriosclerosis, Thrombosis, and Vascular Biology | 2012
Un Ju Jung; Claudia Torrejon; Chuchun L. Chang; Hiroko Hamai; Tilla S. Worgall; Richard J. Deckelbaum
Objective—Macrophage endothelial lipase (EL) is associated with increased atherosclerosis and inflammation. Because of their anti-inflammatory properties we hypothesized that n-3 fatty acids, in contrast to saturated fatty acids, would lower macrophages and arterial EL and inflammatory markers. Methods and Results—Murine J774 and peritoneal macrophages were incubated with eicosapentaenoic acid or palmitic acid in the presence or absence of lipopolysaccaride (LPS). LPS increased EL mRNA and protein. Palmitic acid alone or with LPS dose-dependently increased EL mRNA and protein. In contrast, eicosapentaenoic acid dose-dependently abrogated effects of LPS or palmitic acid on increasing EL expression. EL expression closely linked to peroxisome proliferator activated receptor (PPAR)&ggr; expression. Eicosapentaenoic acid blocked rosiglitazone (a PPAR&ggr; agonist)-mediated EL activation and GW9662 (a PPAR&ggr; antagonist)-blocked palmitic acid-mediated EL stimulation. Eicosapentaenoic acid alone or with LPS blunted LPS-mediated stimulation of macrophage proinflammatory interleukin-6, interleukin-12p40, and toll-like receptor-4 mRNA and increased anti-inflammatory interleukin-10 and mannose receptor mRNA. In vivo studies in low density lipoprotein receptor knockout mice showed that high saturated fat rich diets, but not n-3 diets, increased arterial EL, PPAR&ggr;, and proinflammatory cytokine mRNA. Conclusion—n-3 fatty acids, in contrast to saturated fatty acids, decrease EL in parallel with modulating pro- and anti-inflammatory markers, and these effects on EL link to PPAR&ggr;.
Phytotherapy Research | 2009
Hye-Jin Kim; Seon-Min Jeon; Mi-Kyung Lee; Un Ju Jung; Su-Kyung Shin; Myung-Sook Choi
The objective of this study was to determine the effects of green tea extract (GTE) on lipid metabolism in obese animal models. Male C57BL/6J‐Lepob/ob mice were divided into control and GTE (0.05 g/100 g diet) groups, which were fed a high‐fat (20 g/100 g diet) diet for 12 weeks. Supplementation of GTE significantly reduced (p < 0.01) perirenal and total white adipose tissue weights compared with the control group. Also, the plasma HDL‐cholesterol level was significantly higher in the GTE group than in the control group, therefore the GTE group showed a higher HDL‐cholesterol/total‐cholesterol ratio (HTR) and lower atherogenic index (AI) level than the control group. A reduction of hepatic triglyceride content and adipose tissue weight in the GTE group was related to the suppression of enzyme activities for fatty acid synthesis (glucose‐6‐phosphate dehydrogenase and malic enzyme) without affecting fatty acid oxidation enzyme (β‐oxidation and carnitine palmitoyl transferase) activities in hepatic and adipose tissue. The current results showed that supplementation of green tea extract is beneficial for antiobesity by the suppression of lipogenesis via regulation of related enzyme activities in hepatic and adipose tissue. Copyright
Atherosclerosis | 2014
Chuchun L. Chang; Claudia Torrejon; Un Ju Jung; Kristin Graf; Richard J. Deckelbaum
OBJECTIVE Effects of progressive substitution of dietary n-3 fatty acids (FA) for saturated FA (SAT) on modulating risk factors for atherosclerosis have not been fully defined. Our previous reports demonstrate that SAT increased, but n-3 FA decreased, arterial lipoprotein lipase (LpL) levels and arterial LDL-cholesterol deposition early in atherogenesis. We now questioned whether incremental increases in dietary n-3 FA can counteract SAT-induced pro-atherogenic effects in atherosclerosis-prone LDL-receptor knockout (LDLR-/-) mice and have identified contributing mechanisms. METHODS AND RESULTS Mice were fed chow or high-fat diets enriched in SAT, n-3, or a combination of both SAT and n-3 in ratios of 3:1 (S:n-3 3:1) or 1:1 (S:n-3 1:1). Each diet resulted in the expected changes in fatty acid composition in blood and aorta for each feeding group. SAT-fed mice became hyperlipidemic. By contrast, n-3 inclusion decreased plasma lipid levels, especially cholesterol. Arterial LpL and macrophage levels were increased over 2-fold in SAT-fed mice but these were decreased with incremental replacement with n-3 FA. n-3 FA partial inclusion markedly decreased expression of pro-inflammatory markers (CD68, IL-6, and VCAM-1) in aorta. SAT diets accelerated advanced atherosclerotic lesion development, whereas all n-3 FA-containing diets markedly slowed atherosclerotic progression. CONCLUSION Mechanisms whereby dietary n-3 FA may improve adverse cardiovascular effects of high-SAT, high-fat diets include improving plasma lipid profiles, increasing amounts of n-3 FA in plasma and the arterial wall. Even low levels of replacement of SAT by n-3 FA effectively reduce arterial lipid deposition by decreasing aortic LpL, macrophages and pro-inflammatory markers.
The American Journal of Clinical Nutrition | 2008
Un Ju Jung; Claudia Torrejon; Ann P. Tighe; Richard J. Deckelbaum
Food and Chemical Toxicology | 2007
Un Ju Jung; Nam-In Baek; Hae-Gon Chung; Myun-Ho Bang; J.-S. Yoo; Tae-Sook Jeong; Kyung-Tae Lee; Young-Jin Kang; Mi-Kyung Lee; Hyo Jung Kim; Jiyoung Yeo; Myung-Sook Choi
Prostaglandins Leukotrienes and Essential Fatty Acids | 2007
Claudia Torrejon; Un Ju Jung; Richard J. Deckelbaum
Clinical Nutrition | 2008
Un Ju Jung; Nam-In Baek; Hae-Gon Chung; Myun-Ho Bang; Tae-Sook Jeong; Kyung Tae Lee; Young-Jin Kang; Mi-Kyung Lee; Hye-Jin Kim; Jiyoung Yeo; Myung-Sook Choi