Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood

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 r...

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Bibliographic Details
Published in:Mediators of Inflammation 2014-01, Vol.2014 (7), p.264-272
Main Authors: Arantes, Vanessa Cristina, Milanski, Marciane, Reis, Marise Auxiliadora de Barros, Reis, Silvia Regina de Lima, Ignacio-Souza, Letícia Martins, Cardoso, Katarine Barbosa, de Almeida, Ana Paula Carli, Silva, Hellen Barbosa Farias, Latorraca, Márcia Queiroz
Format: Article
Language:English
Subjects:
Adipose Tissue, White - metabolism
Animals
Body Weight - physiology
Cellular signal transduction
Diet, Protein-Restricted
Eating - physiology
Female
Glucose
Glucose metabolism
Health aspects
Hypothalamus
Hypothalamus - immunology
Hypothalamus - metabolism
Identification and classification
Immunoblotting
Inflammation
Insulin
Insulin resistance
Male
Nutrition
Physiological aspects
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Wistar
Rodents
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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 K itt 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.
ISSN:0962-9351
1466-1861
DOI:10.1155/2014/736506