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J Nutr Biochem ; 86: 108485, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-32828899

RESUMO

We have previously demonstrated that ascorbic acid (AsA) deficiency causes inflammatory changes in the liver and intestine in Osteogenic Disorder Shionogi (ODS) rats, which are unable to synthesize AsA. We have suggested that AsA deficiency increased intestinal interleukine (IL)-6 production, stimulating hepatic acute phase proteins (APPs) expression via the portal vein. In this study, we determined whether these hepatic and intestinal inflammatory changes by AsA deficiency are induced in germ-free (GF) ODS rats. For 18 days, male specific pathogen-free (SPF) ODS rats were fed the basal diet containing 600 mg AsA/kg (control group) or the AsA-free diet (AsA-deficient group) in SPF conditions, while male GF ODS rats were fed the basal diet (control group) or the AsA-free diet (AsA-deficient group) in GF conditions. Firstly, AsA deficiency significantly elevated the hepatic expression of APPs in both SPF and GF rats. In hepatic mRNA levels of some APPs, significant interaction between GF and AsA-deficiency effects was observed. Secondly, AsA deficiency elevated intestinal IL-6 and IL-1ß mRNA levels in both SPF and GF rats, and significant interaction between GF and AsA-deficiency effects was observed in these mRNA levels of jejunum and cecum. In SPF and GF rats, AsA deficiency elevated portal IL-6 concentration. These results show that AsA deficiency caused hepatic and intestinal inflammatory changes in both the GF and SPF ODS rats and indicate that AsA deficiency could directly induce intestinal inflammatory changes without the involvement of gut microbiota.


Assuntos
Deficiência de Ácido Ascórbico/metabolismo , Perfilação da Expressão Gênica , Inflamação/metabolismo , Mucosa Intestinal/metabolismo , Fígado/metabolismo , Proteínas de Fase Aguda/metabolismo , Animais , Peso Corporal , Citocinas/metabolismo , Microbioma Gastrointestinal , Interleucina-6/metabolismo , Masculino , Tamanho do Órgão , Veia Porta/metabolismo , Ratos , Distribuição Tecidual
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