Maternal genetics and diet modulate vitamin A homeostasis of the offspring and affect the susceptibility to obesity in adulthood in mice

Author:

Srinivasagan Ramkumar1,Galmés Sebastià234,Vasileva Denitsa2,Rubí Paula2,Palou Andreu234,Amengual Jaume5,Ribot Joan234ORCID,von Lintig Johannes1,Bonet M. Luisa234ORCID

Affiliation:

1. Department of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland, Ohio, United State

2. Laboratory of Molecular Biology, Nutrition, and Biotechnology (Group of Nutrigenomics, Biomarkers and Risk Evaluation), University of the Balearic Islands (UIB), Palma, Spain

3. Health Research Institute of the Balearic Islands (IdISBa), Palma, Spain

4. CIBER Fisiopatología de la Obesidad y Nutrición, Palma, Spain

5. Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, Champaign, Illinois, United States

Abstract

A genetic mouse model, deficient in intestine-specific homeobox (ISX) transcription factor, is used to show that a mildly increased maternal vitamin A supply from β-carotene feeding during late gestation and lactation programs energy and lipid metabolism in tissues and protects the offspring from diet-induced hypertrophic obesity and hepatic steatosis. This knowledge may have implications for human populations where polymorphisms in ISX and ISX target genes involved in vitamin A homeostasis are prevalent.

Funder

HHS | NIH | National Eye Institute

MEC | Agencia Estatal de Investigación

Publisher

American Physiological Society

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