Knockout of the l-pgds gene aggravates obesity and atherosclerosis in mice
| Autor: | Kin Mou, Norio Wake, Naomi Eguchi, Fumi Takahashi-Yanaga, Yoshihiro Urade, Yoshikazu Miwa, Reiko Tanaka, Sachio Morimoto, Toshiyuki Sasaguri, Morimasa Tomikawa |
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| Rok vydání: | 2009 |
| Předmět: |
Apolipoprotein E
medicine.medical_specialty Interleukin-1beta Biophysics Inflammation Lipocalin Biology Weight Gain Biochemistry Apolipoproteins E Fats Gene Knockout Techniques Mice Internal medicine medicine Animals Obesity Molecular Biology Aorta Chemokine CCL2 Gene knockout Mice Knockout Wild type Cell Biology Atherosclerosis Lipocalins Intramolecular Oxidoreductases Endocrinology Immunology Knockout mouse medicine.symptom |
| Zdroj: | Biochemical and Biophysical Research Communications. 378:851-856 |
| ISSN: | 0006-291X |
| Popis: | 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-1beta 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. |
| Databáze: | OpenAIRE |
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