Food intake, tumor growth, and weight loss in EP2 receptor subtype knockout mice bearing PGE2-producing tumors
2015 (English)In: Physiological Reports, E-ISSN 2051-817X, ISSN 2051-817X, Vol. 3, no 7, 1-7 p., e12441Article in journal (Refereed) Published
Previous studies in our laboratory have demonstrated that prostaglandin (PG) E2 is involved in anorexia/cachexia development in MCG 101 tumor‐bearing mice. In the present study, we investigate the role of PGE receptor subtype EP2 in the development of anorexia after MCG 101 implantation in wild‐type (EP2+/+) or EP2‐receptor knockout (EP2−/−) mice. Our results showed that host absence of EP2 receptors attenuated tumor growth and development of anorexia in tumor‐bearing EP2 knockout mice compared to tumor‐bearing wild‐type animals. Microarray profiling of the hypothalamus revealed a relative twofold change in expression of around 35 genes including mRNA transcripts coding for Phospholipase A2 and Prostaglandin D2 synthase (Ptgds) in EP2 receptor knockout mice compared to wild‐type mice. Prostaglandin D2 synthase levels were increased significantly in EP2 receptor knockouts, suggesting that improved food intake may depend on altered balance of prostaglandin production in hypothalamus since PGE2 and PGD2 display opposing effects in feeding control.
Place, publisher, year, edition, pages
2015. Vol. 3, no 7, 1-7 p., e12441
Anorexia, cachexia, EP receptor, hypothalamus, microarray analysis, Prostaglandin D synthase
Cell and Molecular Biology
IdentifiersURN: urn:nbn:se:liu:diva-125249DOI: 10.14814/phy2.12441PubMedID: 26197930OAI: oai:DiVA.org:liu-125249DiVA: diva2:903987