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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Main Authors: Hellen Barbosa Farias Silva, Ana Paula Carli de Almeida, Katarine Barbosa Cardoso, Letícia Martins Ignacio-Souza, Silvia Regina de Lima Reis, Marise Auxiliadora de Barros Reis, Márcia Queiroz Latorraca, Marciane Milanski, Vanessa Cristina Arantes
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/736506
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author Hellen Barbosa Farias Silva
Ana Paula Carli de Almeida
Katarine Barbosa Cardoso
Letícia Martins Ignacio-Souza
Silvia Regina de Lima Reis
Marise Auxiliadora de Barros Reis
Márcia Queiroz Latorraca
Marciane Milanski
Vanessa Cristina Arantes
author_facet Hellen Barbosa Farias Silva
Ana Paula Carli de Almeida
Katarine Barbosa Cardoso
Letícia Martins Ignacio-Souza
Silvia Regina de Lima Reis
Marise Auxiliadora de Barros Reis
Márcia Queiroz Latorraca
Marciane Milanski
Vanessa Cristina Arantes
author_sort Hellen Barbosa Farias Silva
collection DOAJ
description 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.
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series Mediators of Inflammation
spelling doaj-art-39fc6f202d4344a99ad83b07eaef33a12025-08-20T02:24:13ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/736506736506Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during AdulthoodHellen Barbosa Farias Silva0Ana Paula Carli de Almeida1Katarine Barbosa Cardoso2Letícia Martins Ignacio-Souza3Silvia Regina de Lima Reis4Marise Auxiliadora de Barros Reis5Márcia Queiroz Latorraca6Marciane Milanski7Vanessa Cristina Arantes8Mestrado em Biociências, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, BrazilMestrado em Biociências, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, BrazilLaboratório de Avaliação Biológica de Alimentos, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, BrazilDepartamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, BrazilDepartamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, BrazilDepartamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, BrazilDepartamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, BrazilFaculdade de Ciências Aplicadas da Universidade Estadual de Campinas, Campinas, SP, BrazilDepartamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, BrazilWe 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.http://dx.doi.org/10.1155/2014/736506
spellingShingle Hellen Barbosa Farias Silva
Ana Paula Carli de Almeida
Katarine Barbosa Cardoso
Letícia Martins Ignacio-Souza
Silvia Regina de Lima Reis
Marise Auxiliadora de Barros Reis
Márcia Queiroz Latorraca
Marciane Milanski
Vanessa Cristina Arantes
Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood
Mediators of Inflammation
title Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood
title_full Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood
title_fullStr Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood
title_full_unstemmed Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood
title_short Nutritional Recovery Promotes Hypothalamic Inflammation in Rats during Adulthood
title_sort nutritional recovery promotes hypothalamic inflammation in rats during adulthood
url http://dx.doi.org/10.1155/2014/736506
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