Abstract
Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Osteocalcin (OC), a bone formation biomarker, acts directly on β-cells and increases insulin secretion. We determined the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in offspring. Female Wistar rats consumed either a Ca-deficient or control diet ad libitum from three weeks preconception to 21 days postparturition. Pups were allowed to nurse their original mothers until weaning. The offspring were fed a control diet beginning at weaning and were killed on day 180. Serum carboxylated OC (Gla-OC) and undercarboxylated OC (Glu-OC), insulin and adipokines in offspring were measured. In males, mean levels of insulin, glucose, and HOMA-IR were higher in the Ca-deficient group than in the control group. In addition, ionized Ca (iCa) was inversely associated with serum Glu-OC and adiponectin in males. In females, mean levels of Glu-OC and Gla-OC in the Ca-deficient group were higher than in the control group. In all offspring, serum leptin levels were correlated with serum insulin levels, and inversely correlated with iCa. In conclusion, maternal Ca restriction during pregnancy and/or lactation influences postnatal offspring Ca metabolism and insulin resistance in a sex-specific manner.
Highlights
Prenatal environmental factors clearly affect physiological cues related to developmental plasticity and can affect offspring phenotype at birth [1,2]
Differences in serum Gla-OC, Glu-OC, adiponectin, ionized Ca (iCa), and iMg concentrations were compared between Ca-deficient and control offspring
Due to the well-known antagonism between Mg and Ca [21], we anticipated that an imbalance within the Ca/Mg ratio might play a role for glucose metabolism
Summary
Prenatal environmental factors clearly affect physiological cues related to developmental plasticity and can affect offspring phenotype at birth [1,2]. Maternal insults during intrauterine development impact offspring risk for various health conditions, including adult-onset insulin resistance syndrome [3,4,5]. A number of studies have investigated the role of calcium (Ca) on the pathogenesis of insulin resistance syndrome, showing that Ca deficiency is a risk factor for developing these diseases [6,7]. We previously reported that maternal Ca deficiency during pregnancy can influence the regulation of non-imprinted genes by altering epigenetic regulation, thereby inducing different metabolic phenotypes [8]. It was previously reported that sex-specific differences in DNA methylation are associated with altered expression and secretion of insulin in human pancreatic islets [10]. The early life environment influence on metabolic disease risk in a sex specific manner remains unclear
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