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We began analyzing https://link.springer.com/article/10.1177/1933719109349536, but it redirected us to https://link.springer.com/article/10.1177/1933719109349536. The analysis below is for the second page.

Title[redir]:
Maternal Vitamin D Deficiency Leads to Cardiac Hypertrophy in Rat Offspring | Reproductive Sciences
Description:
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.

Matching Content Categories {📚}

  • Education
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Content Management System {📝}

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Keywords {🔍}

article, google, scholar, vitamin, cas, deficiency, cardiac, phd, offspring, heart, rat, hypertrophy, tare, parkington, morley, black, pregnancy, cardiomyocytes, med, privacy, cookies, content, research, maternal, development, cardiomyocyte, access, holick, biochem, function, publish, search, bsc, bubb, weeks, age, lactation, number, failure, cell, health, clin, pubmed, simpson, res, department, university, victoria, australia, data,

Topics {✒️}

month download article/chapter underappreciated d-lightful hormone dark-skinned pregnant women holick mf vitamin d-replete diet related subjects intrauterine growth restriction cardiac failure full article pdf privacy choices/manage cookies article gezmish hl-1 cardiac myocyte altered cardiac function marianne tare phd subsequent enhanced growth cardiac myocyte proliferation brain development postnatal development nutrition examination survey efficient stereological methods quantifying follicular numbers alters vascular compliance negative endocrine regulator renin-angiotension system renin-angiotensin system ruth morley mb conditions privacy policy jr soc med cardiac hypertrophy european economic area physical freshly excised hearts dilated cardiomyopathy due heart parkington phd & kristen altern med rev accepting optional cookies mol cell cardiol salt-sensitive hypertension rat offspring published main content log early life leads lactation stimulates nephrogenesis 25-dihydroxyvitamin d3 regulation development check access pathological research instant access journal finder publish article log

Questions {❓}

  • Does a nephron deficit in rats predispose to salt-sensitive hypertension?
  • Vitamin D deficiency an important, common, and easily treatable cardiovascular risk factor?

Schema {🗺️}

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         headline:Maternal Vitamin D Deficiency Leads to Cardiac Hypertrophy in Rat Offspring
         description: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.
         datePublished:2010-12-30T00:00:00Z
         dateModified:2010-12-30T00:00:00Z
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      headline:Maternal Vitamin D Deficiency Leads to Cardiac Hypertrophy in Rat Offspring
      description: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.
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