title: Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance.
abstract: OBJECTIVE
  Epicatechin (EC) intake has been suggested to be beneficial for the prevention of cardiovascular disorders, and it is well known that adipose tissue inflammation is one of the major risk factors for coronary heart diseases. The purpose of the present study was to determine the in vitro and in vivo effects of EC on adipose tissue inflammation and obesity.
  
  
  RESULTS
  DNA microarray analysis was performed to evaluate the effects of EC on gene expression in adipocytes co-cultured with bacterial endotoxin-stimulated macrophages. To determine the in vivo effects of the catechin, C57BL/6 mice were fed either a high-fat diet (HFD) or HFD combined with EC, and metabolic changes were observed EC suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (CC motif) ligand 19 (CCL19) expression. The target cell of EC appeared to macrophages. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. Accordingly, the expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice.
  
  
  CONCLUSIONS
  EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since we previously reported that mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, it can be concluded that the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression.
authors.affiliation: Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sano
authors.affiliation: Department of Dental Science for Health Promotion, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Nagayasu
authors.affiliation: Department of Dental Science for Health Promotion, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.affiliation: Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Iwashita
authors.affiliation: Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Yamashita
authors.affiliation: Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Shinjo
authors.affiliation: Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sanui
authors.affiliation: Division of Metabolic Diseases, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Kushiyama
authors.affiliation: Department of Cellular and Molecular Pharmacology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kanematsu
authors.affiliation: Department of Biological Chemistry, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Asano
authors.affiliation: Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan. Electronic address: fusanori@dent.kyushu-u.ac.jp.
authors.forename: F
authors.initials: F
authors.lastname: Nishimura
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002392:Catechin / Q000494:pharmacology*; D054415:Chemokine CCL19 / Q000235:genetics / Q000378:metabolism*; D018920:Coculture Techniques; D059305:Diet, High-Fat / Q000009:adverse effects*; D004195:Disease Models, Animal; D015536:Down-Regulation; D007333:Insulin Resistance; D008262:Macrophage Activation / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D015434:Panniculitis / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D000067996:RAW 264.7 Cells; D013997:Time Factors
chemical_list: D000893:Anti-Inflammatory Agents; C515461:Ccl19 protein, mouse; D054415:Chemokine CCL19; D002392:Catechin
keywords: Adipocyte–macrophage interaction; Adipokine; CCL19; Epicatechin; Inflammation