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Supplementation with methyl donors during lactation to high-fat-sucrose-fed dams protects offspring against liver fat accumulation when consuming an obesogenic diet

Published online by Cambridge University Press:  01 August 2014

P. Cordero
Affiliation:
Department of Nutrition, Food Science and Physiology, University of Navarra, Pamplona, Spain
F. I. Milagro
Affiliation:
Department of Nutrition, Food Science and Physiology, University of Navarra, Pamplona, Spain CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain
J. Campion
Affiliation:
Department of Nutrition, Food Science and Physiology, University of Navarra, Pamplona, Spain CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain
J. A. Martinez*
Affiliation:
Department of Nutrition, Food Science and Physiology, University of Navarra, Pamplona, Spain CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain
*
*Address for correspondence: Prof. J. Alfredo Martinez, Department of Nutrition, Food Science and Physiology, University of Navarra, Irunlarrea Street 1, 31008 Pamplona, Spain. Email:jalfmtz@unav.es

Abstract

Methyl donor supplementation has been reported to prevent obesity-induced liver fat accumulation in adult rats. We hypothesized that this protection could be mediated by perinatal nutrition. For this purpose, we assessed the response to an obesogenic diet (high-fat-sucrose, HFS) during adulthood depending on maternal diet during lactation. Female Wistar rats fed control diet during pregnancy were assigned to four postpartum dietary groups: control, control supplemented with methyl donors (choline, betaine, folic acid, vitamin B12), HFS and HFS supplemented with methyl donors. At weaning, the male offspring was transferred to a chow diet and at week 12th assigned to a control or a HFS diet during 8 weeks. The offspring whose mothers were fed HFS during lactation showed increased adiposity (19%, P<0.001). When fed the HFS diet as adults, offspring whose mothers were HFS supplemented had more body fat (23%, P<0.001) than those from HFS non-supplemented. However, they showed lower liver fat accumulation (−18%, P<0.001). Srebf1, Dnmt1 and Lepr liver mRNA levels increased after adulthood HFS feeding. In those animals HFS fed during adulthood, previous maternal HFS decreased Lepr and Dnmt1 expression levels when compared with c-HFS offspring, while the supplementation of control and HFS-fed dams, respectively, induced higher hepatic Mme and Lepr mRNA levels after adult HFS intake compared with hfs-HFS offspring. In conclusion, maternal HFS diet during lactation influenced the response to an obesogenic diet in the adult progeny. Interestingly, dietary methyl donor supplementation in lactating mothers fed an obesogenic diet reduced liver fat accumulation, but increased adipose tissue storage in adult HFS-fed offspring.

Type
Original Article
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2014 

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