Knockout of the l-pgds gene aggravates obesity and atherosclerosis in mice

Reiko Tanaka, Yoshikazu Miwa, Kin Mou, Morimasa Tomikawa, Naomi Eguchi, Yoshihiro Urade, Fumi Takahashi-Yanaga, Sachio Morimoto, Norio Wake, Toshiyuki Sasaguri

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51 Citations (Scopus)


This study was designed to determine whether lipocalin type-prostaglandin D synthase (l-pgds) deficiency contributes to atherogenesis using gene knockout (KO) mice. A high-fat diet was given to 8-week-old C57BL/6 (wild type; WT), l-pgds KO (LKO), apolipoprotein E (apo E) KO (AKO) and l-pgds/apo E double KO (DKO) mice. The l-pgds deficient mice showed significantly increased body weight, which was accompanied by increased size of subcutaneous and visceral fat tissues. Fat deposition in the aortic wall induced by the high-fat diet was significantly increased in LKO mice compared with WT mice, although there was no significant difference between AKO and DKO mice. In LKO mice, atherosclerotic plaque in the aortic root was also increased and, furthermore, macrophage cellularity and the expression of pro-inflammatory cytokines such as interleukin-1β and monocyte chemoattractant protein-1 were significant increased. In conclusion, l-pgds deficiency induces obesity and facilitates atherosclerosis, probably through the regulation of inflammatory responses.

Original languageEnglish
Pages (from-to)851-856
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - Jan 23 2009

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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