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Antihistamine treatments increased body weight gain, gonadal fat deposition, liver weight, and hepatic steatosis in wild-type mice but not in ApoE\u2212\/\u2212 mice. Lobular inflammation, acute inflammation, and necrosis were not affected by H1-antihistamines in either genotype. Serum biomarkers of liver injury tended to increase in antihistamine-treated wild-type mice. Serum level of glucose was increased by fexofenadine, whereas lipase was increased by cetirizine. H1-antihistamines reduced the mRNA expression of ApoE and carbohydrate response element-binding protein in wild-type mice, without altering the mRNA expression of sterol regulatory element-binding protein 1c, fatty acid synthase, or ApoB100, in either genotype. Fexofenadine increased both triglycerides and cholesterol ester, whereas cetirizine increased only cholesterol ester in liver, with a concomitant decrease in serum triglycerides by both antihistamines in wild-type mice. Antihistamines increased hepatic levels of conjugated bile acids in wild-type mice, with the effect being significant in fexofenadine-treated animals. The increase was associated with changes in the expression of organic anion transport polypeptide 1b2 and bile salt export pump. These results suggest that H1-antihistamines increase the progression of fatty liver disease in wild-type mice, and there seems to be an association between the severity of disease, presence of ApoE, and increase in hepatic bile acid levels.<\/jats:p>","DOI":"10.1152\/ajpgi.00027.2014","type":"journal-article","created":{"date-parts":[[2014,5,23]],"date-time":"2014-05-23T08:05:45Z","timestamp":1400832345000},"page":"G219-G228","source":"Crossref","is-referenced-by-count":21,"title":["H1-antihistamines exacerbate high-fat diet-induced hepatic steatosis in wild-type but not in apolipoprotein E knockout mice"],"prefix":"10.1152","volume":"307","author":[{"given":"Vineesh V.","family":"Raveendran","sequence":"first","affiliation":[{"name":"Division of Allergy, Clinical Immunology, and Rheumatology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karen M.","family":"Kassel","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Toxicology, and 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