PPAR Research · 2007 · 89 citations · 101 references
PharmacyEndocrinologyToxicologyEnvironmental ToxicologyReproductive EndocrinologyReproductive ToxicologyEndocrine ToxicityEnvironmental EndocrinologyFemale Reproductive ToxicologyGonadal ToxicologyMale Reproductive ToxicologyReproductive ToxicityFemale Reproductive EndocrinologyFemale Reproductive PhysiologyPeroxisome Proliferator-activated Receptor SignalingPeroxisome Proliferator-activated ReceptorsPhthalate ExposurePhthalatesReproductive Endocrine ToxicityReproductive Tract Health
There is growing evidence that male as well as female reproductive function has been declining in human and wildlife populations over the last 40 years. Several factors such as lifestyle or environmental xenobiotics other than genetic factors may play a role in determining adverse effects on reproductive health. Among the environmental xenobiotics phthalates, a family of man-made pollutants are suspected to interfere with the function of the endocrine system and therefore to be endocrine disruptors. The definition of endocrine disruption is today extended to broader endocrine regulations, and includes activation of metabolic sensors, such as the peroxisome proliferator-activated receptors (PPARs). Toxicological studies have shown that phthalates can activate a subset of PPARs. Here, we analyze the epidemiological and experimental evidence linking phthalate exposure to both PPAR activation and adverse effects on male and female reproductive health.
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mPPAR gamma 2: tissue-specific regulator of an adipocyte enhancer.
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Steven A. Kliewer, Scott S. Sundseth, Stacey A. Jones et al. · Proceedings of the National Academy of Sciences · 1997 · 2.2K citations · Full text
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PPARγ Is Required for Placental, Cardiac, and Adipose Tissue Development
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Life Sciences, Developmental Biology, Molecular Genetics +12