title: In utero and postnatal exposure to a phytoestrogen-enriched diet increases parameters of acute inflammation in a rat model of TNBS-induced colitis.
abstract: Inflammatory bowel disease (IBD) is very common in Europe and USA. Its incidence in East Asia has been traditionally low, albeit the risk of IBD increases in Asian immigrants adopting western lifestyles, suggesting a strong role of environmental/dietary factors in IBD. A lifelong exposure to phytoestrogen-rich diets has been associated with a decreased risk of developing breast cancer and might also be protective against IBD. We studied the influence of in utero and postnatal exposure to a phytoestrogen (PE)-rich diet on acute inflammation in an animal model of TNBS-induced colitis. Wistar rats were exposed in utero and postnatally to high (genistein: 240 microg/g feed; daidzein: 232 microg/g feed) or very low levels (genistein and daidzein <10 microg/g feed) of phytoestrogen isoflavones fed to pregnant dams with the diet and throughout nursing. After weaning, the offspring had free access to these diets. At the age of 11 weeks, colitis was induced with an enema of TNBS. After 3 days, animals were sacrificed and tissues were collected for histological evaluation and analysis of molecular markers of inflammation. Animals kept on a PE-rich diet (PRD) had higher colon weights than animals on low PE-levels (PDD), suggesting enhanced acute inflammation by phytoestrogens. This result was supported by histological findings and by analysis of myeloperoxidase activity. Interestingly, relative mRNA and protein expression of cyclooxygenase-2 (COX-2) were modulated in rats on PRD, providing evidence that COX-2, the inducible isoform of the enzyme, is involved in the management of colonic inflammation. Our results suggest that early-in-life exposure to PE might not protect against the development of IBD but enhances the extent of acute inflammation.
authors.affiliation: Department of Molecular and Cellular Sports Medicine, DSHS Cologne, Am Sportpark Müngersdorf, 50933 Cologne, Germany. seibel.jan@googlemail.com
authors.forename: Jan
authors.initials: J
authors.lastname: Seibel
authors.forename: Almut F
authors.initials: AF
authors.lastname: Molzberger
authors.forename: Torsten
authors.initials: T
authors.lastname: Hertrampf
authors.forename: Ute
authors.initials: U
authors.lastname: Laudenbach-Leschowski
authors.forename: Gisela H
authors.initials: GH
authors.lastname: Degen
authors.forename: Patrick
authors.initials: P
authors.lastname: Diel
mesh_terms: D000208:Acute Disease; D000821:Animal Feed / Q000032:analysis; D000818:Animals; D003092:Colitis / Q000139:chemically induced* / Q000201:enzymology / Q000473:pathology; D003106:Colon / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004032:Diet; D004195:Disease Models, Animal; D005260:Female; D009929:Organ Size; D009195:Peroxidase / Q000378:metabolism; D048789:Phytoestrogens / Q000008:administration & dosage / Q000009:adverse effects*; D011247:Pregnancy; D011270:Pregnancy, Animal; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity; D014599:Uterus / Q000378:metabolism
chemical_list: D048789:Phytoestrogens; D012333:RNA, Messenger; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase; D051546:Cyclooxygenase 2