Obesity and related disorders are thought to have their roots in metabolic "thriftiness" that evolved to combat periodic starvation. The association of low birth weight with obesity in later life caused a shift in the concept from thrifty gene to thrifty phenotype or anticipatory fetal programming. The assumption of thriftiness is implicit in obesity research. We examine here, with the help of a mathematical model, the conditions for evolution of thrifty genes or fetal programming for thriftiness. The model suggests that a thrifty gene cannot exist in a stable polymorphic state in a population. The conditions for evolution of thrifty fetal programming are restricted if the correlation between intrauterine and lifetime conditions is poor. Such a correlation is not observed in natural courses of famine. If there is fetal programming for thriftiness, it could have evolved in anticipation of social factors affecting nutrition that can result in a positive correlation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136239 | PMC |
| http://dx.doi.org/10.1155/2011/861049 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Enhanced myocardial perfusion in late gestation fetal lambs with impaired left ventricular inflow.
J Physiol
January 2025
Center for Developmental Health, Oregon Health & Science University, Portland, OR, USA.
Robust preclinical models of asymmetric ventricular loading in late gestation reflecting conditions such as hypoplastic left heart syndrome are lacking. We characterized the morphometry and microvascular function of the hypoplastic left ventricle (LV) and remaining right ventricle (RV) in a sham-controlled late gestation fetal lamb model of impaired left ventricular inflow (ILVI). Singleton fetuses were instrumented at ∼120 days gestational age (dGA; term is ∼147 days) with vascular catheters, an aortic flow probe and a deflated left atrial balloon.
View Article and Find Full Text PDFImpact of high maternal body mass index on fetal cerebral cortical and cerebellar volumes.
J Perinat Med
January 2025
Tufts Medical Center, Mother Infant Research Institute, Boston, MA, USA.
Objectives: Maternal obesity increases a child's risk of neurodevelopmental impairment. However, little is known about the impact of maternal obesity on fetal brain development.
Methods: We prospectively recruited 20 healthy pregnant women across the range of pre-pregnancy or first-trimester body mass index (BMI) and performed fetal brain magnetic resonance imaging (MRI) of their healthy singleton fetuses.
Building a growing genomic repository for maternal and fetal health through the PING Consortium.
Pediatr Res
January 2025
Center for Genetic Medicine, Children's National Research Institute, Washington, DC, USA.
Background: Prenatally transmitted viruses can cause severe damage to the developing brain. There is unexplained variability in prenatal brain injury and postnatal neurodevelopmental outcomes, suggesting disease modifiers. Of note, prenatal Zika infection can cause a spectrum of neurodevelopmental disorders, including congenital Zika syndrome.
View Article and Find Full Text PDFIncreased Prevalence of Skeletal Anomalies on Ultrasound Evaluation of Buprenorphine-Exposed Human Fetuses.
South Med J
January 2025
Department of Obstetrics and Gynecology, East Tennessee State University, Johnson City.
Objectives: In this study, buprenorphine was the primary source of maternal opioid exposure at the time of initial prenatal evaluation. Current recommendations advise that level II ultrasounds be performed in patients with substance use disorders. For some patients, distance, transportation, and costs associated with obtaining ultrasounds from a specialist pose significant barriers.
View Article and Find Full Text PDFCIROZ is dispensable in ancestral vertebrates but essential for left-right patterning in humans.
Am J Hum Genet
December 2024
Laboratory of Human Genetics & Therapeutics, Genome Institute of Singapore (GIS), A(∗)STAR, Singapore, Singapore; Laboratory of Human Genetics & Therapeutics, BESE, KAUST, Thuwal, Saudi Arabia; Department of Physiology, Cardiovascular Disease Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. Electronic address:
Four genes-DAND5, PKD1L1, MMP21, and CIROP-form a genetic module that has specifically evolved in vertebrate species that harbor motile cilia in their left-right organizer (LRO). We find here that CIROZ (previously known as C1orf127) is also specifically expressed in the LRO of mice, frogs, and fish, where it encodes a protein with a signal peptide followed by 3 zona pellucida N domains, consistent with extracellular localization. We report 16 individuals from 10 families with bi-allelic CIROZ inactivation variants, which cause heterotaxy with congenital heart defects.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!