<b><i>Background:</i></b> Prenatal malnutrition can affect the phenotype of offspring by altering epigenetic regulation. Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. <b><i>Aims:</i></b> We hypothesized that a Ca-deficient diet during pregnancy would alter insulin resistance and secretion in more than 1 generation of offspring. <b><i>Methods:</i></b> Female Wistar rats consumed either a Ca-deficient or a control diet ad libitum from 3 weeks before conception to 21 days after parturition and were mated with control males. Randomly selected F1 and F2 females were mated with males of each generation on postnatal day 70. The F1 and F2 dams were fed a control diet ad libitum during pregnancy and lactation. All offspring were fed a control diet starting at the time of weaning and were sacrificed on day 180. <b><i>Results:</i></b> HOMA-β% decreased in F1 through F3, and levels in F2 and F3 males and females were significantly lower than in controls. The mean levels of insulin and HOMA-IR were higher in F1 males but lower in F3 males than in control males. The HOMA-IR did not differ between any of the female offspring and controls. <b><i>Conclusions:</i></b> Maternal Ca restriction during pregnancy and/or lactation influences insulin secretion in 3 generations of offspring.
Background Prenatal 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. Methodology We 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 Findings In 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. Conclusions These findings indicated that maternal Ca restriction during pregnancy and/or lactation alters postnatal growth, Hsd11b1 expression, and insulin resistance in a sex-specific manner.
Schools in Japan were closed nationwide from March to May 2020 because of the coronavirus disease 2019 (COVID-19) pandemic. Many suspect that this school closure affected children's mental and physical health. We investigated changes in school-age children's physiques to determine the effects of the COVID-19 lockdown and restrictions on their health.Data were extracted from a database of school physical examinations in Osaka elementary and junior high schools for 4 consecutive years from 2018 to 2021. The following characteristics were analyzed: short stature, tall stature, underweight, mild obesity, middle grade obesity, and severe obesity. The paired Student t-test was used to compare school examination data in the prepandemic period (2018-2019), pandemic lockdown (2019-2020), and post-lockdown period (2020-2021).Obesity rates in elementary school students aged 6-12 years, particularly in boys, were significantly higher during the lockdown than they were in 2019. After the pandemic, the tall stature rate continued to rise, while rates of short stature and underweight decreased in both sexes in 2020. In junior high school students aged 12-15 years, rates of obesity and underweight tended to decrease in 2020. However, these rates rebounded and rose in 2021 when the lockdown was lifted.During the COVID-19 pandemic lockdown, elementary school students gained weight, while junior high school students lost weight. The lockdown that was implemented during the COVID-19 pandemic had an unfavorable effect on weight gain, particularly in young school-age children.
Magnesium deficiency during pregnancy as a result of insufficient or low intake of magnesium is common in developing and developed countries. Previous reports have shown that intracellular magnesium of cord blood platelets is lower among small for gestational age (SGA) groups than that of appropriate for gestational age (AGA) groups, suggesting that intrauterine magnesium deficiency may result in SGA. Additionally, the risk of adult-onset diseases such as insulin resistance syndrome is greater among children whose mothers were malnourished during pregnancy, and who consequently had a low birth weight. In a number of animal models, poor nutrition during pregnancy leads to offspring that exhibit pathophysiological changes similar to human diseases. The offspring of pregnant rats fed a magensium restricted diet have developed hypermethylation in the hepatic 11β-hydroxysteroid dehydrogenase-2 promoter. These findings indicate that maternal magnesium deficiencies during pregnancy influence regulation of non-imprinted genes by altering the epigenetic regulation of gene expression, thereby inducing different metabolic phenotypes. Magnesium deficiency during pregnancy may be responsible for not only maternal and fetal nutritional problems, but also lifelong consequences that affect the offspring throughout their life. Epidemiological, clinical, and basic research on the effects of magnesium deficiency now indicates underlying mechanisms, especially epigenetic processes.