Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

التفاصيل البيبلوغرافية
العنوان: Vitamin A supplementation in early life affects later response to an obesogenic diet in rats
المؤلفون: Joan Ribot, H Musinovic, J. von Lintig, Jaume Amengual, E. Ceresi, Andreu Palou, M L Bonet, Nuria Granados
المصدر: International Journal of Obesity. 37:1169-1176
بيانات النشر: Springer Science and Business Media LLC, 2012.
سنة النشر: 2012
مصطلحات موضوعية: Male, Vitamin, Retinyl Esters, medicine.medical_specialty, Adipose Tissue, White, Endocrinology, Diabetes and Metabolism, Medicine (miscellaneous), Adipose tissue, 030209 endocrinology & metabolism, Weaning, White adipose tissue, Diet, High-Fat, Real-Time Polymerase Chain Reaction, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Adipocyte, Retinyl palmitate, Internal medicine, medicine, Animals, Rats, Wistar, Vitamin A, Adiposity, 030304 developmental biology, 2. Zero hunger, 0303 health sciences, Nutrition and Dietetics, business.industry, Leptin, Body Weight, Retinol, Gene Expression Regulation, Developmental, Immunohistochemistry, Animals, Suckling, Rats, PPAR gamma, Endocrinology, Animals, Newborn, chemistry, Dietary Supplements, Female, Diterpenes, business
الوصف: 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. 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. 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. 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. This paper reports that rats that are given excess vitamin A (three times normal requirement) in early life become more obese than control animals when given a high-fat diet later in life. Although this is an animal study, it is worth considering the implications for humans. Some children are given extra vitamins in early life and modern civilization provides a high fat, obesogenic environment throughout life. Further research in humans is needed to identify individuals who were given excess vitamin A in early life to determine if they are at higher risk of subsequent obesity.
تدمد: 1476-5497
0307-0565
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4a755d98c26f1ac4d44efd3f2877cd10
https://doi.org/10.1038/ijo.2012.190
حقوق: CLOSED
رقم الأكسشن: edsair.doi.dedup.....4a755d98c26f1ac4d44efd3f2877cd10
قاعدة البيانات: OpenAIRE