Abstract
BackgroundPrenatal malnutrition can affect the phenotype of offspring by changing epigenetic regulation of specific genes. Several lines of evidence demonstrate that calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. We hypothesized that pregnant female rats fed a Ca-deficient diet would have offspring with altered hepatic glucocorticoid-related gene expression and that lactation would modify these alterations.MethodologyWe determined the effects of Ca deficiency during pregnancy and/or lactation on hepatic 11β-hydroxysteroid dehydrogenase-1 (Hsd11b1) expression in offspring. Female Wistar rats consumed either a Ca-deficient (D: 0.008% Ca) or control (C: 0.90% Ca) diet ad libitum from 3 weeks preconception to 21 days postparturition. On postnatal day 1, pups were cross-fostered to the same or opposite dams and divided into the following four groups: CC, DD, CD, and DC (first letter: original mother's diet; second letter: nursing mother's diet). All offspring were fed a control diet beginning at weaning (day 21) and were killed on day 200±7. Serum insulin and adipokines in offspring were measured using ELISA kits.Principal FindingsIn males, mean levels of insulin, glucose, and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) were higher in the DD and DC groups than in the CC group. We found no difference in HOMA-IR between the CC and CD groups in either males or females. Expression of Hsd11b1 was lower in male DD rats than in CC rats. Hsd11b1 expression in male offspring nursed by cross-fostered dams was higher than that in those nursed by dams fed the same diet; CC vs. CD and DD vs. DC. In females, Hsd11b1 expression in DC rats was higher than that in CC rats.ConclusionsThese findings indicated that maternal Ca restriction during pregnancy and/or lactation alters postnatal growth, Hsd11b1 expression, and insulin resistance in a sex-specific manner.
Highlights
Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome and obesity, suggesting that hypocalcemia is a risk factor for developing these conditions [1,2]
We previously reported that a low Ca diet alters glucocorticoid metabolism, leading to hepatic up-regulation of Hsd11b1 in rats [23]
These findings show that maternal Ca deficiency during pregnancy can affect regulation of non-imprinted genes by altering epigenetic regulation of gene expression, thereby inducing different metabolic phenotypes
Summary
Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome and obesity, suggesting that hypocalcemia is a risk factor for developing these conditions [1,2]. The Coronary Artery Risk Development in Young Adults Study suggests an intriguing and exciting negative relationship between Ca intake or dairy consumption and obesity and insulin resistance syndrome in young adults [6]. Maternal malnutrition and the resulting low birth weight predispose offspring to various diseases, including adult-onset insulin resistance syndrome [7,8,9,10]. Several lines of evidence demonstrate that calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. We hypothesized that pregnant female rats fed a Ca-deficient diet would have offspring with altered hepatic glucocorticoid-related gene expression and that lactation would modify these alterations
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