{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T14:35:44Z","timestamp":1786631744351,"version":"build-2736575974"},"reference-count":56,"publisher":"American Chemical Society (ACS)","issue":"3","license":[{"start":{"date-parts":[[2017,12,29]],"date-time":"2017-12-29T00:00:00Z","timestamp":1514505600000},"content-version":"vor","delay-in-days":1452,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Background: Hexabromocyclododecane (HBCD) is an additive flame retardant used in the textile industry and in polystyrene foam manufacturing. Because of its lipophilicity and persistency, HBCD accumulates in adipose tissue and thus has the potential of causing metabolic disorders through disruption of lipid and glucose homeostasis. However, the association between HBCD and obesity remains unclear.<\/jats:p>\n                  <jats:p>Objectives: We investigated whether exposure to HBCD contributes to initiation and progression of obesity and related metabolic dysfunction in mice fed a normal diet (ND) or a high-fat diet (HFD).<\/jats:p>\n                  <jats:p>Methods: Male C57BL\/6J mice were fed a HFD (62.2 kcal% fat) or a ND and treated orally with HBCD (0, 1.75, 35, or 700 \u03bcg\/kg body weight) weekly from 6 to 20 weeks of age. We examined body weight, liver weight, blood biochemistry, histopathological changes, and gene expression profiles in the liver and adipose tissue.<\/jats:p>\n                  <jats:p>Results: In HFD-fed mice, body and liver weight were markedly increased in mice treated with the high (700 \u03bcg\/kg) and medium (35 \u03bcg\/kg) doses of HBCD compared with vehicle. This effect was more prominent in the high-dose group. These increases were paralleled by increases in random blood glucose and insulin levels and enhancement of microvesicular steatosis and macrophage accumulation in adipose tissue. HBCD-treated HFD-fed mice also had increased mRNA levels of Pparg (peroxisome proliferator-activated receptor-\u03b3) in the liver and decreased mRNA levels of Glut4 (glucose transporter 4) in adipose tissue compared with vehicle-treated HFD-fed mice.<\/jats:p>\n                  <jats:p>Conclusions: Our findings suggest that HBCD may contribute to enhancement of diet-induced body weight gain and metabolic dysfunction through disruption of lipid and glucose homeostasis, resulting in accelerated progression of obesity.<\/jats:p>\n                  <jats:p>Citation: Yanagisawa R, Koike E, Win-Shwe TT, Yamamoto M, Takano H. 2014. Impaired lipid and glucose homeostasis in hexabromocyclododecane-exposed mice fed a high-fat diet. Environ Health Perspect 122:277\u2013283;\u2002http:\/\/dx.doi.org\/10.1289\/ehp.1307421<\/jats:p>","DOI":"10.1289\/ehp.1307421","type":"journal-article","created":{"date-parts":[[2014,1,7]],"date-time":"2014-01-07T14:54:00Z","timestamp":1389106440000},"page":"277-283","source":"Crossref","is-referenced-by-count":76,"title":["Impaired Lipid and Glucose Homeostasis in Hexabromocyclododecane-Exposed Mice Fed a High-Fat Diet"],"prefix":"10.1021","volume":"122","author":[{"given":"Rie","family":"Yanagisawa","sequence":"first","affiliation":[{"name":"Center for Environmental Health Sciences, National Institute for Environmental Studies, Tsukuba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eiko","family":"Koike","sequence":"additional","affiliation":[{"name":"Center for Environmental Health Sciences, National Institute for Environmental Studies, Tsukuba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tin-Tin","family":"Win-Shwe","sequence":"additional","affiliation":[{"name":"Center for Environmental Health Sciences, National Institute for Environmental Studies, Tsukuba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megumi","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Department of Basic Medical Sciences, National Institute for Minamata Disease, Minamata, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hirohisa","family":"Takano","sequence":"additional","affiliation":[{"name":"Graduate School of Engineering, Kyoto University, Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"316","published-online":{"date-parts":[[2014,1,7]]},"reference":[{"issue":"9","key":"2026080602020387500_micit1","doi-asserted-by":"crossref","first-page":"1972","DOI":"10.2337\/dc10-2303","article-title":"Association between type 2 diabetes and exposure to persistent organic pollutants.","volume":"34","author":"Airaksinen","year":"2011","journal-title":"Diabetes Care"},{"key":"2026080602020387500_micit2","doi-asserted-by":"publisher","first-page":"761","DOI":"10.1289\/ehp.10554","article-title":"Polychlorinated biphenyl-77 induces adipocyte differentiation and proinflammatory adipokines and promotes obesity and atherosclerosis.","volume":"116","author":"Arsenescu","year":"2008","journal-title":"Environ Health Perspect"},{"issue":"2","key":"2026080602020387500_micit3","doi-asserted-by":"crossref","first-page":"185","DOI":"10.1089\/107555302317371479","article-title":"Chemical toxins: a hypothesis to explain the global obesity epidemic.","volume":"8","author":"Baillie-Hamilton","year":"2002","journal-title":"J Altern Complement Med"},{"issue":"2","key":"2026080602020387500_micit4","doi-asserted-by":"crossref","first-page":"G194","DOI":"10.1152\/ajpgi.00413.2005","article-title":"Lipid metabolism and liver inflammation. 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