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Mediators of Inflammation
Volume 2014 (2014), Article ID 736506, 9 pages
Research Article

Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood

1Mestrado em Biociências, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, Brazil
2Laboratório de Avaliação Biológica de Alimentos, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, Brazil
3Departamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, Brazil
4Faculdade de Ciências Aplicadas da Universidade Estadual de Campinas, Campinas, SP, Brazil

Received 23 May 2014; Accepted 26 June 2014; Published 31 August 2014

Academic Editor: Fabio Santos Lira

Copyright © 2014 Hellen Barbosa Farias Silva et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We evaluated whether protein restriction in fetal life alters food intake and glucose homeostasis in adulthood by interfering with insulin signal transduction through proinflammatory mechanisms in the hypothalamus and peripheral tissues. Rats were divided into the following: a control group (C); a recovered group (R); and a low protein (LP) group. Relative food intake was greater and serum leptin was diminished in LP and R compared to C rats. Proinflammatory genes and POMC mRNA were upregulated in the hypothalamus of R group. Hypothalamic NPY mRNA expression was greater but AKT phosphorylation was diminished in the LP than in the C rats. In muscle, AKT phosphorylation was higher in restricted than in control animals. The HOMA-IR was decreased in R and C compared to the LP group. In contrast, the Kitt in R was similar to that in C and both were lower than LP rats. Thus, nutritional recovery did not alter glucose homeostasis but produced middle hyperphagia, possibly due to increased anorexigenic neuropeptide expression that counteracted the hypothalamic inflammatory process. In long term protein deprived rats, hyperphagia most likely resulted from increased orexigenic neuropeptide expression, and glucose homeostasis was maintained, at least in part, at the expense of increased muscle insulin sensitivity.