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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.
Abstract:
The aim of this study was to determine the effect of vitamin D deficiency from conception until 4 weeks of age on the development of the heart in rat offspring. Sprague-Dawley (SD) rats were fed either a vitamin D deplete or vitamin D-replete diet for 6 weeks prior to pregnancy, during pregnancy and throughout lactation. Cardiomyocyte number was determined in fixed hearts of offspring at postnatal day 3 and 4 weeks of age using an optical disector/fractionator stereological technique. In other litters, cardiomyocytes were isolated from freshly excised hearts to determine the proportion of mononucleated and binucleated cardiomyocytes. Maternal vitamin D deficiency had no effect on cardiomyocyte number, cardiomyocyte area, or the proportion of mononucleated/binucleated cardiomyocytes in 3-day-old male and female offspring. Importantly, however, vitamin D deficiency led to an increase in left ventricle (LV) volume that was accompanied by an increase in cardiomyocyte number and size, and in the proportion of mononucleated cardiomyocytes at 4 weeks of age. Our findings suggest that exposure to vitamin D deficiency in utero and early life leads to delayed maturation and subsequent enhanced growth (proliferation and hypertrophy) of cardiomyocytes in the LV. This may lead to altered cardiac function later in life.
