ReviewInternational journal of molecular sciences2021
Calcium-Deficiency during Pregnancy Affects Insulin Resistance in Offspring.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- The effect of the social and interpersonal-based intervention on calcium consumption among pregnant women.Frontiers in public health · 2025Trial
- BMI modifies the effect of pregnancy complications on risk of small- or large-for-gestational-age newborns.Pediatric research · 2025Article
- Micro-nutrient sufficiency in mothers and babies: management of deficiencies while avoiding overload during pregnancy.Frontiers in nutrition · 2025Review
- Evaluating the Reliability of Health Portals' Nutrition and Supplementation Advice for Pregnant Women: A Comprehensive Review.Nutrients · 2024Review
- Review
- Maternal Western diet programs cardiometabolic dysfunction and hypothalamic inflammation via epigenetic mechanisms predominantly in the male offspring.Molecular metabolism · 2024Article
- Maternal Mineral Nutrition Regulates Fetal Genomic Programming in Cattle: A Review.Metabolites · 2023Review
- Association of Gut Microbiota Enterotypes with Blood Trace Elements in Women with Infertility.Nutrients · 2022Article
- Maternal Exposure to D-galactose Reduces Ovarian Reserve in Female Rat Offspring Later in Life.International journal of endocrinology and metabolism · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
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. 11β-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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.