Prenatal calcium deficiency induce an altered phenotype in offspring via changes in the epigenetic regulation

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591614
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Embryonic/Neonatal medicine
• Research Institution: Kansai Medical University
• Principal Investigator: TAKAYA JUNJI 関西医科大学, 医学部, その他 (80247923)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: エピジェネティクス / カルシウム / マグネシウム / インスリン抵抗性

Outline of Final Research Achievements

Prenatal under-nutrition can induce an altered phenotype in offspring via changes in the epigenetic regulation of specific genes. Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. We investigated the methylation of individual CpG in glucocorticoid-related genes in liver tissue of offspring from Ca-deficient mothers. The methylation levels of Hsd11b1 was lower in the Ca-deficient group.
In addition, 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 and were killed on day 200. In males, mean levels of insulin, glucose, and HOMA-IR were higher in the DD and DC groups than in the CC group.
A Ca-deficient diet in a mother during gestation and early nursing alter glucocorticoid metabolism and insulin resistance in a sex-specific manner.

Free Research Field

代謝内分泌