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In the overweight or obese female, reproductive complications include poor oocyte quality, decreased fecundity, gestational diabetes, and higher risk of reproductive cancers. Using lean and hyperphagia-induced obese female mice aged 10 weeks, we determined that the ovary from obese female mice had elevated (P < 0.10) levels of ataxia telangiectasia mutated (ATM) protein in oocytes of both small and large follicles. Phosphorylated ATM at serine 1981 was greater (P < 0.05) in large relative to small follicles with no additional impact of obesity. Obesity increased (P < 0.05) γH2AX in small follicles in obese relative to lean ovaries, while large follicles of both lean and obese mice had detectable levels of γH2AX. Cleaved caspase 3 was reduced (P < 0.05) in the small follicles of obese relative to lean ovaries. In large follicles of lean mice, cleaved caspase 3 was increased in large compared to small follicles (P < 0.05) but this pattern was absent in obese mice. Breast cancer type 1 susceptibility protein (BRCA1) or the phosphorylated BRCA1 proteins were observably altered by obesity. These data demonstrate that markers of DNA damage and repair have a follicle-dependent stage location and that obesity alters ATM and cleaved caspase 3 in a follicular stage dependent manner.
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In brief
This review describes how heat stress causes systemic endocrine and metabolic alterations that contribute to intracellular ovarian perturbations, resulting in female infertility.
Abstract
Heat stress (HS) in mammals results from an imbalance in heat accumulation and dissipation. Fertility impairments consequential to HS have been recognized for decades in production animals, and more recently, observations have been extended to other species, including women. There are several systemic impacts of HS that can independently affect reproduction, including metabolic endotoxemia, reduced plane of nutrition, and endocrine disruption. At the level of the ovary, molecular pathways are altered by HS, such as inflammation, JAK–STAT, PI3K, oxidative stress, cell death, and heat shock response. Taken together, impaired ovarian function contributes to seasonal infertility that results from HS. This review paper describes the physiological and endocrine systemic impacts of HS that may independently and collaboratively impair fertility in the porcine model. The review then details ovarian intracellular events that are altered during HS and finally determines future needs in this area of research.