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High-fat diet promotion of endometriosis in an immunocompetent mouse model is associated with altered peripheral and ectopic lesion redox and inflammatory status

ABSTRACT: Endometriosis is a benign gynecological condition that causes significant morbidity due to reduced fertility, pelvic pain and inflammatory dysfunctions. High-fat dietary intake has been linked to higher systemic inflammation and oxidative stress, which are both features of women with endometriosis. We evaluated the effects of high-fat diet (HFD) on endometriosis progression using immunocompetent mouse model wherein ectopic lesion was induced in wildtype and kruppel-like factor 9 (KLF9)- null donor mice. Results showed that HFD leads to increased ectopic lesion numbers and higher body weight gain. The HFD-promotion of lesion establishment was associated with decreased stromal estrogen receptor 1 and progesterone receptor expression, increased macrophage infiltration, and enhanced expression of pro-inflammarory and pro-oxidative stress pathway genes. Further, lesion-bearing mice had higher peritoneal fluid TNF-α and elevated local/systemic redox status than control-fed mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE80603 | GEO | 2017/04/23

SECONDARY ACCESSION(S): PRJNA319477

REPOSITORIES: GEO

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High-fat diet promotion of endometriosis in an immunocompetent mouse model is associated with altered peripheral and ectopic lesion redox and inflammatory status

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