Abstract
A maternal Western-style diet (WSD) is associated with poor reproductive outcomes, but whether this is from the diet itself or underlying metabolic dysfunction is unknown. Here, we performed a longitudinal study using regularly cycling female rhesus macaques (n = 10) that underwent 2 consecutive in vitro fertilization (IVF) cycles, one while consuming a low-fat diet and another 6–8 months after consuming a high-fat WSD. Metabolic data were collected from the females prior to each IVF cycle. Follicular fluid (FF) and oocytes were assessed for cytokine/steroid levels and IVF potential, respectively. Although transition to a WSD led to weight gain and increased body fat, no difference in insulin levels was observed. A significant decrease in IL-1RA concentration and the ratio of cortisol/cortisone was detected in FF after WSD intake. Despite an increased probability of isolating mature oocytes, a 44% reduction in blastocyst number was observed with WSD consumption, and time-lapse imaging revealed delayed mitotic timing and multipolar divisions. RNA sequencing of blastocysts demonstrated dysregulation of genes involved in RNA binding, protein channel activity, mitochondrial function and pluripotency versus cell differentiation after WSD consumption. Thus, short-term WSD consumption promotes a proinflammatory intrafollicular microenvironment that is associated with impaired preimplantation development in the absence of large-scale metabolic changes.
Highlights
Obesity is often associated with various physiological, metabolic, and psychological diseases and disorders, including hypertension, diabetes, arthritis, and depression, in both men and women [1,2,3,4,5,6]
There was a significant difference in glucose levels 4 months after Western-style diet (WSD), no significant differences in metabolic parameter measurements were observed after controlled ovarian stimulation (COS) #1 and after COS #2, which included HOMA-IR (Figure 2B), glucose (Figure 2C), and insulin (Figure 2D) levels
Maternal obesity and its negative impact on in vitro fertilization (IVF) treatments has been reported in both humans and rodents [7, 35, 36], but it was unclear if these effects were due to the diet itself or the subsequent development of metabolic dysfunction
Summary
Obesity is often associated with various physiological, metabolic, and psychological diseases and disorders, including hypertension, diabetes, arthritis, and depression, in both men and women [1,2,3,4,5,6]. In obese women undergoing infertility treatment, findings of unresponsiveness or a delayed response to controlled ovarian stimulation (COS) by administration of exogenous gonadotropins [8, 14,15,16], as well as poor in vitro fertilization (IVF) outcomes [17,18,19], suggests that the ovarian follicular microenvironment can be altered with obesity. This conclusion is consistent with other IVF studies, whereby increased pregnancy failure rates in obese women returned to normal if donor oocytes were used [20]. The identity of these factors and at which stage of preimplantation development the defects occurred, remains to be defined
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