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Vitamin A supplementation in early life affects later response to an obesogenic diet in rats
N Granados1, J Amengual, J Ribot
1Laboratory of Molecular Biology, Nutrition and Biotechnology-Nutrigenomics, University of the Balearic Islands and CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Palma de Mallorca, Spain.
Insights
Early life vitamin A supplementation programs white adipose tissue (WAT) for increased adiposity when exposed to a high-fat diet later in life, mediated by retinoic acid (RA).
Area of Science:
- Nutritional Science
- Developmental Biology
- Endocrinology
Background:
- Early life nutrition significantly influences long-term metabolic health.
- Vitamin A is crucial for development, but its excess during sensitive periods may have adverse effects.
- Adipose tissue development in early life can predispose individuals to obesity.
Purpose of the Study:
- To investigate the long-term impact of early-life vitamin A supplementation on adipose tissue development.
- To determine if early vitamin A exposure alters the response to a high-fat diet later in life.
- To elucidate the mechanisms underlying vitamin A's influence on adiposity.
Main Methods:
- Rat pups received daily oral doses of retinyl palmitate during the suckling period.
- White adipose tissue (WAT) was analyzed for gene expression and morphology post-weaning.
- Rats were subsequently fed either a normal-fat or high-fat diet for 16 weeks to assess long-term effects.
Main Results:
- Early vitamin A exposure led to smaller adipocytes with reduced adipogenic markers but increased cell proliferation potential in young rats.
- Vitamin A-treated rats exhibited significantly higher adiposity, increased WAT mass, and larger adipocytes when fed a high-fat diet.
- These effects were attributed to adipocyte hyperplasia and were not observed on a normal-fat diet.
Conclusions:
- Early-life vitamin A supplementation promotes high-fat diet-induced adiposity gain later in life.
- The observed effects are likely mediated by retinoic acid (RA) and involve alterations in adipose tissue development.
- This highlights a critical window for vitamin A intake regarding long-term metabolic health.
Objective:
To assess the influence of supplementation with a moderate dose of vitamin A in early life on adipose tissue development and the response to an obesogenic diet later in life.
Methods:
During the suckling period, rat pups received a daily oral dose of retinyl palmitate corresponding to three times the vitamin A ingested daily from maternal milk. Control rats received the vehicle (olive oil). Short-term effects of treatment on gene expression and morphology of white adipose tissue (WAT) were analyzed in animals on the day after weaning (day 21). To study long-term effects, control and vitamin A-treated rats were fed, after weaning, a normal fat or a high-fat (HF) diet for 16 weeks.
Results:
WAT of vitamin A-treated young rats (day 21) was enriched in small adipocytes with a reduced expression of adipogenic markers (peroxisome proliferator-activated receptor γ and lipoprotein lipase) and an increased cell proliferation potential as indicated by increased expression of proliferating cell nuclear antigen. Increased retinoic acid (RA)-induced transcriptional responses were present in the tissues of vitamin A-treated young rats (day 21) including WAT. Vitamin A-treated rats developed higher adiposity than control rats on a HF diet as indicated by body composition analysis and increased WAT depot mass, adipocyte diameter, WAT DNA content, leptinemia and adipose leptin gene expression. Excess adiposity gain in vitamin A-treated rats developed in the absence of changes in body weight and was attributable to excess adipocyte hyperplasia. No differences in adiposity were observed between vitamin A-treated rats and control rats on a normal fat diet. Total retinol levels in WAT of vitamin A-treated rats were elevated at weaning (day 21) and normalized by day 135 of age.
Conclusion:
Vitamin A intake in the early stages of postnatal life favors subsequent HF diet-induced adiposity gain through mechanisms that may relate to changes in adipose tissue development, likely mediated by RA.
