Maternal vitamin D deficiency leads to cardiac hypertrophy in rat offspring

Oksan Gezmish1, Marianne Tare, Helena C Parkington

  • 1Department of Anatomy & Developmental Biology, Monash University, Clayton, Victoria, Australia.

Insights

Vitamin D deficiency from conception impacts offspring heart development. Early deficiency delayed cardiomyocyte maturation, leading to increased left ventricle growth and cell size by 4 weeks of age.

Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Nutritional Science

Background:

  • Vitamin D is crucial for numerous physiological processes, including cardiovascular health.
  • Maternal nutrition during pregnancy significantly influences fetal development.
  • The impact of early-life vitamin D deficiency on cardiac development requires further elucidation.

Purpose of the Study:

  • To investigate the effects of maternal vitamin D deficiency from conception to 4 weeks postpartum on rat offspring cardiac development.
  • To assess the impact on cardiomyocyte number, size, and differentiation.

Main Methods:

  • Sprague-Dawley rats were assigned to vitamin D-deplete or replete diets pre-pregnancy, during gestation, and lactation.
  • Stereological techniques (optical disector/fractionator) were used to quantify cardiomyocyte number and size in offspring hearts at postnatal day 3 and 4 weeks.
  • Cardiomyocytes were isolated to determine the proportion of mononucleated and binucleated cells.

Main Results:

  • No significant differences in cardiomyocyte number, size, or proportion of mononucleated/binucleated cells were observed at postnatal day 3.
  • By 4 weeks of age, vitamin D deficiency resulted in increased left ventricle volume.
  • This increase was associated with a higher cardiomyocyte number, larger cardiomyocyte size, and a greater proportion of mononucleated cardiomyocytes.

Conclusions:

  • Maternal vitamin D deficiency during gestation and early life leads to delayed cardiomyocyte maturation in rat offspring.
  • This delay is followed by compensatory enhanced growth (proliferation and hypertrophy) of left ventricle cardiomyocytes.
  • These developmental alterations may predispose offspring to altered cardiac function later in life.

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