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Maternal Choline Intake Programs Hypothalamic Energy Regulation and Later‐Life Phenotype of Male Wistar Rat Offspring
Author(s) -
Hammoud Rola,
Pannia Emanuela,
Kubant Ruslan,
Liao ChihSheng,
Ho Mandy,
Yang Neil V.,
Chatterjee Diptendu,
Caudill Marie A.,
Malysheva Olga V.,
Pausova Zdenka,
Anderson G. Harvey
Publication year - 2020
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201901178
Subject(s) - offspring , endocrinology , medicine , choline , orexigenic , weaning , pregnancy , leptin , biology , hypothalamus , in utero , hormone , fetus , neuropeptide , obesity , neuropeptide y receptor , receptor , genetics
Scope: High‐folic‐acid diets during pregnancy result in obesity in the offspring, associated with altered DNA‐methylation of hypothalamic food intake neurons. Like folic acid, the methyl‐donor choline modulates foetal brain development, but its long‐term programing effects on energy regulation remain undefined. This study aims to describe the effect of choline intake during pregnancy on offspring phenotype and hypothalamic energy‐regulatory mechanisms. Methods and results: Wistar rat dams are fed an AIN‐93G diet with recommended choline (RC, 1 g kg −1 diet), low choline (LC, 0.5‐fold), or high choline (HC, 2.5‐fold) during pregnancy. Male pups are terminated at birth and 17 weeks post‐weaning. Brain 1‐carbon metabolites, body weight, food intake, energy expenditure, plasma hormones, and protein expression of hypothalamic neuropeptides are measured. HC pups have higher expression of the orexigenic neuropeptide‐Y neurons at birth, consistent with higher cumulative food intake and body weight gain post‐weaning compared to RC and LC offspring. LC pups have lower leptin receptor expression at birth and lower energy expenditure and activity during adulthood. Conclusion: Choline content of diets that are consumed by rats during pregnancy affects the later‐life phenotype of offspring, associated with altered in utero programing of hypothalamic food intake regulation.