Abstract
The circulating level of vitamin A (VA; retinol) was reported to be lower in obese adults. It is unknown if maternal obesity influences the VA status of offspring. The objective of the study was to determine the VA status and deposition of neonatal and weanling rats reared by mothers consuming a normal or high-fat diet (NFD or HFD) with or without supplemented VA. Pregnant Sprague-Dawley rats were randomized to an NFD or HFD with 2.6 mg/kg VA. Upon delivery, half of the rat mothers in the NFD or HFD cohort were switched to an NFD or HFD with supplemented VA at 129 mg/kg (NFD+VA and HFD+VA group). The other half remained on their original diet (NFD and HFD group). At postnatal day 14 (P14), P25, and P35, pups (n = 4 or 3/group/time) were euthanized. The total retinol concentration in the serum, liver, visceral white adipose tissue (WAT), and brown adipose tissue (BAT) was measured. At P14, the HFD+VA group showed a significantly lower serum VA than the NFD+VA group. At P25, both the VA concentration and total mass in the liver, WAT, and BAT were significantly higher in the HFD+VA than the NFD+VA group. At P35, the HFD group exhibited a significantly higher VA concentration and mass in the liver and BAT compared with the NFD group. In conclusion, maternal HFD consumption resulted in more VA accumulation in storage organs in neonatal and/or weanling rats, which potentially compromised the availability of VA in circulation, especially under the VA-supplemented condition.
Highlights
Vitamin A (VA, retinol) is an essential nutrient required for the development of newborns and infants (1 month to 2 years), in terms of growth, hematopoiesis, lung maturation, and immunity [1]
Maternal HFD consumption resulted in more vitamin A (VA) accumulation in storage organs in neonatal and/or weanling rats, which potentially compromised the availability of VA in circulation, especially under the VA-supplemented condition
Previous studies have documented the beneficial effects of VA on obesity-related metabolic and developmental conditions in adult or young rodent models [47,48,49], the current study provides novel information on how maternal obesity alters the deposition of VA from a VA-adequate or -supplemented maternal diet in the offspring
Summary
Vitamin A (VA, retinol) is an essential nutrient required for the development of newborns (birth to1 month) and infants (1 month to 2 years), in terms of growth, hematopoiesis, lung maturation, and immunity [1]. VA is critical for the postnatal development of the lung [3]. Rapid utilization of the storage form of VA, i.e., retinyl esters, and of the production of retinoic acid, the active metabolite of VA, in newborn rats during lung development was reported [4]. In spite of the significance of VA for infants, they are born with low stores of VA, partly due to limited placental transfer. They rely on breast milk to build up this crucial nutrient [5]. VA levels are even lower in low birth weight or preterm newborns [9,10]. Maternal VA intake is critical to establishing an optimal VA status during infancy
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