Abstract
BackgroundWe have shown recently that maternal undernutrition (UN) advanced female pubertal onset in a manner that is dependent upon the timing of UN. The long-term consequence of this accelerated puberty on ovarian function is unknown. Recent findings suggest that oxidative stress may be one mechanism whereby early life events impact on later physiological functioning. Therefore, using an established rodent model of maternal UN at critical windows of development, we examined maternal UN-induced changes in offspring ovarian function and determined whether these changes were underpinned by ovarian oxidative stress.Methodology/Principal FindingsOur study is the first to show that maternal UN significantly reduced primordial and secondary follicle number in offspring in a manner that was dependent upon the timing of maternal UN. Specifically, a reduction in these early stage follicles was observed in offspring born to mothers undernourished throughout both pregnancy and lactation. Additionally, antral follicle number was reduced in offspring born to all mothers that were UN regardless of whether the period of UN was restricted to pregnancy or lactation or both. These reductions were associated with decreased mRNA levels of genes critical for follicle maturation and ovulation. Increased ovarian protein carbonyls were observed in offspring born to mothers UN during pregnancy and/or lactation and this was associated with peroxiredoxin 3 hyperoxidation and reduced mRNA levels; suggesting compromised antioxidant defence. This was not observed in offspring of mothers UN during lactation alone.ConclusionsWe propose that maternal UN, particularly at a time-point that includes pregnancy, results in reduced offspring ovarian follicle numbers and mRNA levels of regulatory genes and may be mediated by increased ovarian oxidative stress coupled with a decreased ability to repair the resultant oxidative damage. Together these data are suggestive of maternal UN potentially contributing to premature ovarian ageing in offspring.
Highlights
There is considerable epidemiological and experimental evidence indicating that early life environmental signals, including nutrition, affect subsequent development leading to pathophysiologies including obesity and insulin resistance [1]
We propose that maternal UN, at a time-point that includes pregnancy, results in reduced offspring ovarian follicle numbers and mRNA levels of regulatory genes and may be mediated by increased ovarian oxidative stress coupled with a decreased ability to repair the resultant oxidative damage
We have previously shown that nutritional deficits and excesses during intrauterine, lactational and post-weaning periods resulted in the acceleration of pubertal onset and subsequent changes in ovarian function [5]
Summary
There is considerable epidemiological and experimental evidence indicating that early life environmental signals, including nutrition, affect subsequent development leading to pathophysiologies including obesity and insulin resistance [1]. These signals induce highly integrated responses in endocrine-related homeostasis, resulting in persistent changes to the developmental trajectory producing an altered adult phenotype. This phenomenon has been termed developmental programming, whereby early life events trigger processes that prepare the individual for particular circumstances that are anticipated in the postnatal environment [1,2,3]. Using an established rodent model of maternal UN at critical windows of development, we examined maternal UN-induced changes in offspring ovarian function and determined whether these changes were underpinned by ovarian oxidative stress
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