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Liver metabolism in adult male mice offspring: consequences of a maternal, paternal or both maternal and paternal high-fructose diet

Published online by Cambridge University Press:  17 April 2018

P. V. Carapeto
Affiliation:
Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, University of the State of Rio de Janeiro, Rio de Janeiro, Brazil
F. Ornellas
Affiliation:
Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, University of the State of Rio de Janeiro, Rio de Janeiro, Brazil
C. A. Mandarim-de-Lacerda*
Affiliation:
Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, University of the State of Rio de Janeiro, Rio de Janeiro, Brazil
M. B. Aguila
Affiliation:
Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, University of the State of Rio de Janeiro, Rio de Janeiro, Brazil
*
Address for correspondence: C. A. Mandarim-de-Lacerda, Laboratório de Morfometria, Metabolismo e Doenças Cardiovasculares, Centro Biomédico, Instituto de Biologia, Universidade do Estado do Rio de Janeiro. Av 28 de Setembro 87 fds, 20551-030 Rio de Janeiro, RJ, Brazil. E-mail: mandarim@uerj.br

Abstract

The study aimed to evaluate the consequences of the consumption of a high-fructose diet (HFR; fructose was responsible for 45% of the energy from carbohydrates) by the mother, the father, or both on C57BL/6 adult male offspring. Non-consanguineous parents received the diet (HFR or control, C) from 8 weeks before mating until weaning (n=10 fathers and n=10 mothers on each diet). After weaning, only the C diet was offered to offspring. The groups were formed by one male randomly taken from each litter. The offspring groups were identified according to the mother’s diet (the first letter), then the father’s diet (the second letter), that is, C/C, C/HFR, HFR/C, HFR/HFR (n=10 per group). The parents exhibited the following characteristics: compared with those of the C group, the HFR parents had higher blood pressure (BP), enlarged liver, increased hepatic triacylglycerol content, hypercholesterolemia, hypertriglyceridemia, high plasma leptin and low adiponectin. The offspring exhibited the following characteristics: compared with the C/C group, the HFR/HFR group had high BP. The C/HFR, HFR/C and HFR/HFR showed elevated uric acid and leptin levels and diminished adiponectin. The HFR/HFR group showed liver inflammation (increased NFκB, SOCS3, JNK, TNF-α, IL1-β and IL6 levels). Likewise, SREBP-1c and FAS were upregulated. In conclusion, the consumption of a HFR by the mother and/or father is associated with adverse effects on liver metabolism in adult male offspring. When both mother and father are fed a HFR, the adverse effects on the offspring are more severe.

Type
Original Article
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2018 

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