RESUMO
We investigated the insulin release induced by glucose, the Ca2+ oscillatory pattern, and the cyclic AMP (cAMP)/protein kinase A (PKA) and phospholipase C (PLC)/protein kinase C (PKC) pathways in islets from adult rats that were reared under diets with 17% protein (C) or 6% protein (LP) during gestation, suckling, and after weaning and in rats receiving diets with 6% protein during gestation and 17% protein after birth (R). First-phase glucose-induced insulin secretion was reduced in LP and R islets, and the second phase was partially restored in the R group. Glucose stimulation did not modify intracellular Ca2+ concentration, but it reduced the Ca2+ oscillatory frequency in the R group compared with the C group. Intracellular cAMP concentration was higher and PKA-Cα expression was lower in the R and LP groups compared with the C group. The PKCα content in islets from R rats was lower than that in C and LP rats. Thus, nutritional recovery from a low-protein diet during fetal life did not repair the kinetics of insulin release, impaired Ca2+ handling, and altered the cAMP/PKA and PLC/PKC pathways.
Assuntos
Cálcio/metabolismo , Dieta com Restrição de Proteínas , Secreção de Insulina/fisiologia , Transdução de Sinais/fisiologia , Animais , AMP Cíclico/metabolismo , Proteínas Quinases Dependentes de AMP Cíclico/metabolismo , Feminino , Masculino , Estado Nutricional/fisiologia , Gravidez , Ratos , Ratos Wistar , Fosfolipases Tipo C/metabolismoRESUMO
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Assuntos
Animais , Feminino , Gravidez , Comunicação Celular/fisiologia , Dieta com Restrição de Proteínas , Diabetes Gestacional/dietoterapia , Junções Intercelulares/metabolismo , Ilhotas Pancreáticas/metabolismo , RNA Mensageiro/metabolismo , Análise de Variância , Actinas/metabolismo , Junções Aderentes/metabolismo , Glicemia/análise , /metabolismo , Conexinas/metabolismo , Diabetes Gestacional/prevenção & controle , Junções Comunicantes/metabolismo , Glucose/administração & dosagem , Insulina/metabolismo , Insulina , Ratos Wistar , Reação em Cadeia da Polimerase em Tempo Real , beta Catenina/metabolismoRESUMO
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.