Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood

• Main Authors: Hellen Barbosa Farias Silva (Author), Ana Paula Carli de Almeida (Author), Katarine Barbosa Cardoso (Author), Letícia Martins Ignacio-Souza (Author), Silvia Regina de Lima Reis (Author), Marise Auxiliadora de Barros Reis (Author), Márcia Queiroz Latorraca (Author), Marciane Milanski (Author), Vanessa Cristina Arantes (Author)
• Format: Book
• Published: Hindawi Limited, 2014-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

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.

Item Description

0962-9351
1466-1861
10.1155/2014/736506