Publications by authors named "Isabela Macedo Lopes Vasques-Monteiro"

2 Publications

  • Page 1 of 1

A rise in Proteobacteria is an indicator of gut-liver axis-mediated nonalcoholic fatty liver disease in high-fructose-fed adult mice.

Nutr Res 2021 07 21;91:26-35. Epub 2021 May 21.

Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, Rio de Janeiro State University, Rio de Janeiro, Brazil. Electronic address:

Current evidence suggests that high fructose intake results in gut dysbiosis, leading to endotoxemia and NAFLD onset. Thus, the hypothesis of the study was that an enhanced Proteobacteria proportion in the cecal microbiota could be the most prominent trigger of NAFLD through enhanced endotoxin (LPS) in adult high-fructose-fed C57BL/6 mice. Male C57BL/6 mice received a control diet (n = 10, C: 76% of energy as carbohydrates, 0% as fructose) or high-fructose diet (n = 10, HFRU: 76% of energy as carbohydrate, 50% as fructose) for 12 weeks. Outcomes included biochemical analyses, 16S rDNA PCR amplification, hepatic stereology, and RT-qPCR. The groups showed similar body masses during the whole experiment. However, the HFRU group showed greater water intake and blood pressure than the C group. The HFRU group showed a significantly lower amount of Bacteroidetes and a predominant rise in Proteobacteria, implying increased LPS. The HFRU group also showed enhanced de novo lipogenesis (Chrebp expression), while beta-oxidation was decreased (Ppar-alpha expression). These results agree with the deposition of fat droplets within hepatocytes and the enhanced hepatic triacylglycerol concentrations, as observed in the photomicrographs, where the HFRU group had a higher volume density of steatosis than the C group. Thus, we confirmed that a rise in the Proteobacteria phylum proportion was the most prominent alteration in gut-liver axis-induced hepatic steatosis in HFRU-fed C57BL/6 mice. Gut dysbiosis and fatty liver were observed even in the absence of overweight in this dietary adult mouse model.
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July 2021

Coronavirus disease 2019 severity in obesity: Metabolic dysfunction-associated fatty liver disease in the spotlight.

World J Gastroenterol 2021 Apr;27(16):1738-1750

Anatomy, Rio de Janeiro State University, Rio de Janeiro 20551030, Brazil.

The coronavirus disease 2019 (COVID-19) outbreak has drawn the scientific community's attention to pre-existing metabolic conditions that could aggravate the infection, causing extended viral shedding, prolonged hospitalization, and high death rates. Metabolic dysfunction-associated fatty liver disease (MAFLD) emerges as a surrogate for COVID-19 severity due to the constellation of metabolic alterations it entails. This review outlines the impact MAFLD exerts on COVID-19 severity in obese subjects, besides the possible mechanistic links to the poor outcomes. The data collected showed that MAFLD patients had poorer COVID-19 outcomes than non-MAFLD obese subjects. MAFLD is generally accompanied by impaired glycemic control and systemic arterial hypertension, both of which can decompensate during the COVID-19 clinical course. Also, MAFLD subjects had higher plasma inflammatory marker concentrations than non-MAFLD subjects, which might be related to an intensified cytokine storm syndrome frequently associated with the need for mechanical ventilation and death. In conclusion, MAFLD represents a higher risk than obesity for COVID-19 severity, resulting in poor outcomes and even progression to non-alcoholic steatohepatitis. Hepatologists should include MAFLD subjects in the high-risk group, intensify preventive measurements, and prioritize their vaccination.
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April 2021