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Updated: Jul 7, 2026
Mouse Oocyte Microinjection, Maturation and Ploidy Assessment
Published on: July 23, 2011
Low protein diet fed exclusively during mouse oocyte maturation leads to behavioural and cardiovascular abnormalities
Adam J Watkins1, Adrian Wilkins, Colm Cunningham
1School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK. ajw7@soton.ac.uk
Insights
Maternal protein restriction during oocyte development in mice caused anxiety and high blood pressure in offspring. This highlights the impact of early nutrition on long-term health and disease risk.
Area of Science:
- Reproductive biology and developmental programming
- Maternal nutrition and offspring health
- Epigenetics and disease etiology
Background:
- Maternal undernutrition during early embryonic development is linked to postnatal disease.
- The impact of maternal nutrition on oocyte development and subsequent offspring health is less understood.
- Investigating the effects of short-term dietary changes on gamete quality and developmental outcomes.
Purpose of the Study:
- To determine if maternal protein restriction during oocyte maturation affects offspring phenotype.
- To investigate the long-term behavioral and cardiovascular consequences in offspring.
- To analyze kidney development and its relationship with blood pressure in offspring.
Main Methods:
- Mice were fed either a normal protein diet (NPD) or a low protein diet (LPD) for 3.5 days before mating.
- Offspring were assessed for anxiety-related behavior, systolic blood pressure (SBP), and arterial responsiveness.
- Kidney and heart size, along with nephron number, were analyzed in adult offspring.
Main Results:
- Maternal LPD induced abnormal anxiety-related behavior in offspring.
- Offspring exhibited elevated SBP, with males showing hypertension earlier.
- Male offspring displayed reduced arterial responsiveness, and females had altered kidney development (smaller size, increased nephron number).
Conclusions:
- Maternal protein restriction during oocyte development sensitizes offspring to behavioral and cardiovascular abnormalities.
- These findings suggest a direct effect of nutrient restriction on gamete quality, impacting offspring health.
- The study identifies critical windows of developmental vulnerability to maternal diet, with implications for disease prevention.
Abstract:
Early embryonic development is known to be susceptible to maternal undernutrition, leading to a disease-related postnatal phenotype. To determine whether this sensitivity extended into oocyte development, we examined the effect of maternal normal protein diet (18% casein; NPD) or isocaloric low protein diet (9% casein; LPD) restricted to one ovulatory cycle (3.5 days) prior to natural mating in female MF-1 mice. After mating, all females received NPD for the remainder of gestation and all offspring were litter size adjusted and fed standard chow. No difference in gestation length, litter size, sex ratio or postnatal growth was observed between treatments. Maternal LPD did, however, induce abnormal anxiety-related behaviour in open field activities in male and female offspring (P < 0.05). Maternal LPD offspring also exhibited elevated systolic blood pressure (SBP) in males at 9 and 15 weeks and in both sexes at 21 weeks (P < 0.05). Male LPD offspring hypertension was accompanied by attenuated arterial responsiveness in vitro to vasodilators acetylcholine and isoprenaline (P < 0.05). LPD female offspring adult kidneys were also smaller, but had increased nephron numbers (P < 0.05). Moreover, the relationship between SBP and kidney or heart size or nephron number was altered by diet treatment (P < 0.05). These data demonstrate the sensitivity of mouse maturing oocytes in vivo to maternal protein undernutrition and identify both behavioural and cardiovascular postnatal outcomes, indicative of adult disease. These outcomes probably derive from a direct effect of protein restriction, although indirect stress mechanisms may also be contributory. Similar and distinct postnatal outcomes were observed here compared with maternal LPD treatment during post-fertilization preimplantation development which may reflect the relative contribution of the paternal genome.
