Department of Nutritional Sciences . Major in Nutrition, University of Nebraska- Lincoln M. S. 1. 99. 8 Major in Nutritional Science and Dietetics, University of Nebraska- Lincoln. M. S. 1. 99. 4 Major in Food Chemistry, Kyung Hee University, Seoul, South Korea. B. S. 1. 99. 1 Major in Foods and Nutrition, Kyung Hee University, Seoul, South Korea. PROFESSIONAL EXPERIENCEAssociate Professor (July 2. Present),Department of Nutritional Sciences, University of Connecticut Assistant Professor (July 2. June 2. 01. 0),Department of Nutrition and Health Sciences, University of Nebraska- Lincoln Postdoctoral Fellow (June 2. June 2. 00. 5),Department of Pathology, Wake Forest University School of Medicine HONORS/AWARDSFellow, American Heart Association, Arteriosclerosis, Thrombosis, and Vascular Biology Council, May 2. American Society for Nutrition, 1st Korean Nutrition Society Award, 2. Recognition of Junior Faculty for Excellence in Research, Agriculture Research Division, University of Nebraska- Lincoln, 2. Luella Selover Memorial Scholarship, 2. Widaman Trust Distinguished Graduate Assistant Award, 2. Undergraduate Scholarship, Kyung Hee University, Seoul, South Korea, 1. ![]() This article focuses on providing cavalier King Charles spaniels the dietary nutrition they need to best prepare them for fighting the genetic disorders they may be. It is widely accepted that obesity and associated metabolic diseases, including type 2 diabetes, are intimately linked to diet. However, the gut microbiota has also. Tangeretin stimulates glucose uptake via regulation of AMPK signaling pathways in C2C12 myotubes and improves glucose tolerance in high-fat diet-induced obese mice. NOTABLE PROFESSIONAL ACTIVITIES Grant reviewer, NIH ZRG1 EMNR- V, July 2. Grant reviewer, American Heart Association Lipid Bsc 2, April 2. Grant reviewer, NIH Integrative Nutrition and Metabolic Processes (INMP) Study Section, February 2. Grant reviewer, American Heart Association Lipid Bsc 2, October 2. Grant reviewer, NIH Integrative Nutrition and Metabolic Processes (INMP) Study Section, October 2. Grant reviewer, American Heart Association Lipid Bsc 2, April 2. Grant reviewer, American Heart Association Lipid Bsc 2, October 2. ![]() A recent study reported that among people who carried a single copy of the high-risk allele for the FTO gene, which is associated with fat mass and obesity, the risk. Obesity is associated with an increased risk of developing insulin resistance and type 2 diabetes. In obese individuals, adipose tissue releases. ![]() Grant reviewer, American Heart Association Strategically Focused Research Networks (SFRN) grant, May 2. Grant reviewer, American Heart Association Lipid Bsc 2, April 2. Grant reviewer, NIH NCCAM Special Emphasis Panel ZAT1 SM2. March 2. 01. 2. Editorial board member, Journal of Nutritional Biochemistry, July 2. Editorial board member, Journal of Human Nutrition and Food Science, July 2. Review editor, Journal of Medicinal Food, January 2. Editorial board member, Nutrition Research and Practice, January 2. Editorial board member, Journal of Physiobiochemical Metabolism, May 2. Editorial board member, Journal of Nutrition and Intermediary Metabolism, July 2. Editorial board member, Korean Journal of Nutrition, May 2. ![]() Editorial board member, Journal of Nutrition and Health, May 2. Editorial board member, Endocrinology & Diabetes Research, May 2. Editorial board member, Food and Nutrition Sciences, August 2. March 2. 01. 4. SOCIETY MEMBERSHIPSPremium member, American Heart Association (Since 2. Member, Korean Society for Food Science and Nutrition (Since 2. Member, American Association for the Advancement of Science (Since 2. Regular Member, American Society for Nutrition (Since 2. Early Career Member, American Heart Association, Council of Atherosclerosis, Thrombosis and Vascular Biology (2. Associate Member, American Society for Nutritional Science (2. Student Member, American Society for Nutritional Sciences (1. Registered Dietitian, Korean Society for Registered Dietitian (Since 1. RESEARCH INTERESTDysregulation of energy metabolism, chronic inflammation and dyslipidemia are major contributors to the development of obesity- associated disease such as insulin resistance, non- alcoholic fatty liver disease, type 2 diabetes and cardiovascular disease. My research focuses on the identification of molecular mediators that are involved in lipid metabolism and inflammatory signaling pathways, and on the elucidation of molecular mechanisms by which dietary factors, such as blue- green algae, berries, phospholipids and astaxanthin, play regulatory roles in the integration of lipid metabolism and inflammation. The primary foci of my research program elegantly address a new concept of “immunometabolism” to link inflammatory signaling pathways to energy metabolism using state of the art molecular techniques and cell bioenergetics tools in various cells and animal models. In addition, another research focus lies on the identification of molecular targets that critically impact on the process of liver fibrosis with attempts to develop preventive and therapeutic strategies for liver fibrosis. In particular, how dietary factors regulate histone deacetylases as an epigenetic mode of action for the regulation of gene transcription in metabolic, inflammatory, and fibrogenic pathways are actively underway in my laboratory. PUBLICATIONSPeer- Reviewed Articles. L. Bioavailability of anthocyanins and colonic polyphenol metabolites following consumption of aronia berry extract. Food Chem 2. 01. 6; (In press). Anti- inflammatory effect of Spirulina platensis in macrophages is beneficial for adipocyte differentiation and maturation by inhibiting Nuclear factor- k. B pathway in 3. T3- L1 adipocytes. J Med Food 2. 01. In press). Epub ahead of print on May 2. S. Vitamin A or E and a catechin synergize as vaccine adjuvant to enhance immune responses in mice through induction of early IL- 1. IL- 1b. Immunology 2. In press). Epub ahead of print on May 2, 2. Selenium reduces enterohemorrhagic Escherichia coli O1. H7 verotoxin production and globotriaosylceramide receptor expression on host cells. Future Microbiol 2. In press). Epub ahead of print on May 1. B. Astaxanthin, a xanthophyll carotenoid, inhibited inflammation and fibrosis in the adipose and the liver of diet- induced obesity and liver fibrosis mice. J Nutr Biochem 2. In press). Epub ahead of print on March 2, 2. Astaxanthin prevents and reverses the activation of mouse primary hepatic stellate cells. J Nutr Biochem 2. Epub ahead of print on Nov 2. Dietary consumption lowers systemic inflammation and liver enzymes in typically low- dairy consumers with clinical characteristics of metabolic syndrome. J Am Coll Nutr 2. Epub ahead of print on Nov 2. Eliciting the mitochondrial unfolded protein response via NAD+ repletion prevents fatty liver disease. Hepatology 2. 01. Epub ahead of print on Sept 2. Relationship between oxidative stress and bone mass in obesity and effects of berry supplementation on bone remodeling in obese male mice: an exploratory study. Epub ahead of print on Sept 8, 2. Hypolipidemic effect of a blue- green alga (Nostoc commune) is attributed to its nonlipid fraction by decreasing intestinal cholesterol absorption in C5. BL/6. J mice. J Med Food 2. Epub ahead of print on July 1. Blue- green algae inhibit the development of atherosclerotic lesions in apolipoprotein E knockout mice. J Med Food 2. 01. Epub ahead of print on Nov 1. Green tea lowers hepatic COX- 2 and prostaglandin E2 in rats with dietary fat- induced nonalcoholic steatohepatitis. J Med Food 2. 01. Epub ahead of print on Dec 2, 2. Polyphenol- rich blackcurrant extract exerts hypolipidemic and hypoglyceridemic effects in mice fed a diet containing high fat and cholesterol. Br J Nutr 2. 01. 5: 1. Astaxanthin prevents transforming growth factor b. Smad. 3 activation in hepatic stellate cells. Biochimica Biophysica Acta 2. Astaxanthin lowered plasma triglyceride and increased hepatic antioxidant gene expression in diet- induced obesity mice. Br J Nutr 2. 01. 4; 1. Polyphenol- rich blackcurrant extract prevents inflammation in diet- induced obesity mice. J Nutr Biochem 2. Development of cyclobutene- and cyclobutane- functionalized fatty acids with inhibitory activity against Mycobacterium tuberoculosis. Chem. Med. Chem 2. Egg intake during carbohydrate restriction alters peripheral blood mononuclear cell inflammation and cholesterol homeostasis in metabolic syndrome. Nutrients 2. 01. 4; 6: 2. Long- term effect of blue- green algae on lipid metabolism in C5. BL/6. J mice. J Nutr Health and Food Sci 2. Berry anthocyanins suppress the expression and secretin of pro- inflammatory mediators in macrophages by inhibiting nuclear translocation of NF- k. B independent of NRF2- mediated mechanism. J Nutr Biochem 2. Dietary fructose feeding increases adipose methylglyoxal accumulation in association with low expression and activity of glyoxalase- 2. Nutrients 2. 01. 3; 5: 3. Astaxanthin: structure, metabolism, and health benefits. J Hum Nutr Food Sci 2. Acute glutathione depletion induces hepatic methylglyoxal accumulation by impairing its detoxification to D- lactate. Expt Biol Med 2. 01. Egg consumption during carbohydrate restriction modulates HDL lipid composition and increases the cholesterol- accepting capacity of serum in metabolic syndrome. Lipids 2. 01. 3; 4. Polyphenol- rich chokeberry extract regulates the expression of genes for lipogenesis and cholesterol transport in Caco- 2 cells. J Nutr Biochem 2. Aronia melanocarpa (chokeberry) polyphenol rich extract improves antioxidant function and reduces total plasma cholesterol in apolipoprotein E knockout mice. Nutr Res 2. 01. 3; 3. Health Benefits of blue- green algae: Prevention of cardiovascular disease and nonalcoholic fatty liver disease. J Med Food 2. 01. Edible blue- green algae reduce the production of pro- inflammatory cytokines by inhibiting NF- k. B pathway in macrophages and splenocytes. Biochimica Biophysica Acta 2. Trust your gut: Galvanizing nutritional interest in intestinal cholesterol metabolism for protection against cardiovascular diseases. Nutrients 2. 01. 3; 5: 2. Dietary regulation of histone acetylase and deacetylase for the prevention of metabolic diseases. Nutrients 2. 01. 2; 4: 1. Grape consumption increases anti- inflammatory markers and upregulates peripheral nitric oxide synthase in the absence of dyslipidemias in men with metabolic syndrome. Nutrients 2. 01. 2; 4: 1. Lipopolysaccharide represses the expression of ATP- binding cassette transporter G1 and scavenger receptor class B, type I in murine macrophages. Inflamm Res 2. 01. Unsaturated fatty acids repress expression of ATP binding cassette transporter A1 and G1 in RAW 2. J Nutr Biochem 2. ATP binding cassette transporter A- I and HDL metabolism: Effects of fatty acids. J Nutr Biochem 2. Pathogenesis of type 2 diabetes mellitus. INTRODUCTIONType 2 diabetes mellitus is characterized by hyperglycemia, insulin resistance, and relative impairment in insulin secretion. It is a common disorder with a prevalence that rises markedly with increasing degrees of obesity (figure 1) . The prevalence of type 2 diabetes has risen alarmingly in the past decade . Patients present with a combination of varying degrees of insulin resistance and relative insulin deficiency, and it is likely that both contribute to type 2 diabetes . Furthermore, each of the clinical features can arise through genetic or environmental influences, making it difficult to determine the exact cause in an individual patient. Moreover, hyperglycemia itself can impair pancreatic beta- cell function and exacerbate insulin resistance, leading to a vicious cycle of hyperglycemia causing a worsening metabolic state . This constellation of clinical conditions is referred to as the metabolic syndrome . Hyperinsulinemia occurring in response to insulin resistance may play an important role in the genesis of these abnormalities. Increased free fatty acid levels, inflammatory cytokines from fat, and oxidative factors have all been implicated in the pathogenesis of metabolic syndrome, type 2 diabetes, and their cardiovascular complications. As an example, in a prospective study of over 6. British civil servants without diabetes at baseline, 5. In those who developed diabetes compared with those who did not, there was a marked decrease in insulin sensitivity during the five years prior to diagnosis. Beta- cell function (insulin secretion) increased three to four years prior to diagnosis and then decreased until diagnosis. In addition, a seven- year prospective study of 7. Mexican- Americans suggested that decreased insulin secretion and insulin resistance were independent risk factors for type 2 diabetes . Among Pima Indians, in whom the frequency of diabetes is very high, the transition from normal glucose tolerance to impaired glucose tolerance to diabetes is characterized by concomitant decreases in insulin- stimulated glucose disposal and glucose- stimulated insulin secretion . A mouse model with a genetic alteration affecting GLUT- 2 expression produced mice with glucose intolerance; similar changes in GLUT- 2 could be induced in normal mice fed a high- fat diet .
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