Nutritional recovery promotes hypothalamic inflammation in rats during adulthood.

Autor: Silva HB; Mestrado em Biociências, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, Brazil., de Almeida AP; Mestrado em Biociências, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, Brazil., Cardoso KB; Laboratório de Avaliação Biológica de Alimentos, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Cuiabá, MT, Brazil., Ignacio-Souza LM; Departamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, Brazil., Reis SR; Departamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, Brazil., Reis MA; Departamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, Brazil., Latorraca MQ; Departamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, Brazil., Milanski M; Faculdade de Ciências Aplicadas da Universidade Estadual de Campinas, Campinas, SP, Brazil., Arantes VC; Departamento de Alimentos e Nutrição, Faculdade de Nutrição, Universidade Federal de Mato Grosso, Avenida Fernando Correa da Costa, 2367. Bairro Boa Esperança, Cuiabá, MT, Brazil.
Jazyk: angličtina
Zdroj: Mediators of inflammation [Mediators Inflamm] 2014; Vol. 2014, pp. 736506. Date of Electronic Publication: 2014 Aug 31.
DOI: 10.1155/2014/736506
Abstrakt: 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.
Databáze: MEDLINE