Produção Nacional
Revisado por pares
Early onset and progression of non-alcoholic fatty liver disease in young monosodium l-glutamate-induced obese mice
2018; Cambridge University Press; Volume: 10; Issue: 02 Linguagem: Inglês
10.1017/s2040174418000284
ISSN2040-1752
AutoresCaio Fernando Ferreira Coêlho, Lucas Martins França, Johnny Ramos do Nascimento, Alcione Miranda dos Santos, Ana Paula Silva de Azevedo dos Santos, Flávia Raquel Fernandes do Nascimento, Antonio Marcus de Andrade Paes,
Tópico(s)Diet and metabolism studies
ResumoAbstract Monosodium l -glutamate (MSG)-induced obesity is a useful model for non-alcoholic fatty liver disease (NAFLD) studies. However, there is limited data on its initiation and progression. Thus, this study aimed to characterize the onset of metabolic and histopathological features of NAFLD and its progression to non-alcoholic steatohepatitis (NASH) in this model. To perform this study, Swiss mice pups were neonatally injected with MSG (4 g/kg/day, s.c.) or equiosmolar saline and followed up to 60, 120 or 180 days old. At each age, blood, liver, as well as periepididymal and retroperitoneal fat pads were collected for morphometric, biochemical and histological analyses, the later according to NAFLD activity score. MSG mice presented hypertriglyceridemia and central obesity at all ages, but peripheral insulin-resistance was verified only in 120- and 180-day-old mice. Hepatic total fat and triglycerides content were higher in MSG mice at all ages. Accordingly, histopathological analysis showed that 60-day-old MSG mice had microvesicular steatosis with occasional ballooning, which evolved into NASH from 120 days old. Retroperitoneal fat accumulation was the only variable to independently correlate with NAFLD activity total score upon multivariate analysis ( R 2 =71.45%). There were no differences in IL-6 and TNF-α serum levels among groups. Overall, this study shows that NAFLD is a precocious outcome in MSG-obese mice, whereas the period comprised between 60 and 120 days old seems to be a crucial metabolic window for comprehending pathophysiological events involved in NAFLD-to-NASH progression in this model.
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