Calcium-Deficiency during Pregnancy Affects Insulin Resistance in Offspring

被引:13
|
作者
Takaya, Junji [1 ]
机构
[1] Kawachi Gen Hosp, Dept Pediat, 1-31 Yokomakura, Higashiosaka, Osaka 5780954, Japan
关键词
calcium; glucocorticoid receptor; homeostasis model assessment of insulin resistance; homeostasis model assessment of beta-cell function; insulin resistance; pregnancy; 11 beta-hydroxysteroid dehydrogenase-1; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1; HIGH-FAT DIET; DOSE-RESPONSE METAANALYSIS; VITAMIN-D SUPPLEMENTATION; HEPATIC GENE-EXPRESSION; METABOLIC SYNDROME; MATERNAL CALCIUM; ADIPOSE-TISSUE; BETA-CELL; RESTRICTED DIET;
D O I
10.3390/ijms22137008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Prenatal malnutrition is known to affect the phenotype of the offspring through changes in epigenetic regulation. Growing evidence suggests that epigenetics is one of the mechanisms by which nutrients and minerals affect metabolic traits. Although the perinatal period is the time of highest phenotypic plasticity, which contributes largely to developmental programming, there is evidence of nutritional influence on epigenetic regulation during adulthood. Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Cortisol, the most important glucocorticoid, is considered to lead to insulin resistance and metabolic syndrome. 11 beta-hydroxysteroid dehydrogenase-1 is a key enzyme that catalyzes the intracellular conversion of cortisone to physiologically active cortisol. This brief review aims to identify the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in the offspring. Those findings demonstrate that maternal Ca deficiency during pregnancy may affect the epigenetic regulation of gene expression and thereby induce different metabolic phenotypes. We aim to address the need for Ca during pregnancy and propose the scaling-up of clinical and public health approaches that improved pregnancy outcomes.
引用
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页数:15
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