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Coronavirus disease 2019 severity in obesity:Metabolic dysfunctionassociated fatty liver disease in the spotlight

World Journal of Gastroenterology 2021年第16期27卷 1738-1750页

作者： isabela macedo lopes vasques-monteiro Vanessa Souza-Mello Anatomy Rio de Janeiro State UniversityRio de Janeiro 20551030Brazil Food Science and Technology Federal University of the State of Rio de JaneiroRio de Janeiro 22290250Brazil Laboratory of Morphometry Metabolismand Cardiovascular DiseasesBiomedical CenterInstitute of BiologyAnatomy DepartmentRio de Janeiro State UniversityRio de Janeiro 20551030Brazil

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 *** dysfunction-associated fatty liver disease(MAFLD)emerges as a surrogate for COVID-19 severity due to the constellation of metabolic alterations it *** review outlines the impact MAFLD exerts on COVID-19 severity in obese subjects,besides the possible mechanistic links to the poor *** data collected showed that MAFLD patients had poorer COVID-19 outcomes than non-MAFLD obese *** is generally accompanied by impaired glycemic control and systemic arterial hypertension,both of which can decompensate during the COVID-19 clinical ***,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 *** conclusion,MAFLD represents a higher risk than obesity for COVID-19 severity,resulting in poor outcomes and even progression to non-alcoholic *** should include MAFLD subjects in the high-risk group,intensify preventive measurements,and prioritize their vaccination.

关键词： Metabolic dysfunction-associated fatty liver disease Obesity COVID-19 Severity Cytokine storm syndrome

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Peroxisome proliferator-activated receptor-alpha activation and dipeptidyl peptidase-4 inhibition target dysbiosis to treat fatty liver in obese mice

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World Journal of Gastroenterology 2022年第17期28卷 1814-1829页

作者： Flavia Maria Silva-Veiga Carolline Santos Miranda isabela macedo lopes vasques-monteiro Henrique Souza-Tavares Fabiane Ferreira Martins Julio Beltrame Daleprane Vanessa Souza-Mello Department of Anatomy Institute of BiologyState University of Rio de JaneiroLaboratory of MorphometryMetabolism and Cardiovascular DiseasesRio de Janeiro 20551-030Brazil Department of Clinical and Toxicology Analysis State University of Rio de JaneiroNutrition InstituteState University of Rio de JaneiroNutrition InstituteUniversity of Sao PauloRio de Janeiro 20551-030Brazil

BACKGROUND Obesity and comorbidities onset encompass gut dysbiosis,altered intestinal permeability,and *** that target gut dysbiosis can cope with obesity and nonalcoholic fatty liver disease(NAFLD)*** proliferator-activated receptor(PPAR)-alpha activation and dipeptidyl-peptidase-4(DPP-4)inhibition alleviate NAFLD,but the mechanism may involve gut microbiota modulation and merits further *** To address the effects of PPAR-alpha activation and DPP-4 inhibition(isolated or combined)upon the gut-liver axis,emphasizing inflammatory pathways in NAFLD management in high-fat-fed C57BL/6J *** Male C57BL/6J mice were fed a control diet(C,10%of energy as lipids)or a highfat diet(HFD,50%of energy as lipids)for 12 wk,when treatments started,forming the groups:C,HF,HFA(HFD+PPAR-alpha agonist WY14643,2.5 mg/kg body mass),HFL(HFD+DPP-4 inhibitor linagliptin,15 mg/kg body mass),and HFC(HFD+the combination of WY14643 and linagliptin).RESULTS The HFD was obesogenic compared to the C *** treatments elicited significant body mass loss,and the HFC group showed similar body mass to the C *** treatments tackled oral glucose intolerance and raised plasma glucagon-like peptide-1 *** metabolic benefits restored Bacteroidetes/Firmicutes ratio,resulting in increased goblet cells per area of the large intestine and reduced lipopolysaccharides concentrations in treated *** the gene level,treated groups showed higher intestinal Mucin 2,Occludin,and Zo-1 expression than the HFD *** reduced endotoxemia suppressed inflammasome and macrophage gene expression in the liver of treated *** observations complied with the mitigation of liver steatosis and reduced hepatic triacylglycerol,reassuring the role of the proposed treatments on NAFLD *** PPAR alpha activation and DPP-4 inhibition(isolated or combined)tackled NAFLD in dietinduced obese mice by restoration of gut-liver axis

关键词： Nonalcoholic fatty liver disease High-fat diet Peroxisome proliferator-activated receptor-alpha Dipeptidyl-peptidase-4-inhibitor Dysbiosis Inflammation

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Peroxisome proliferator-activated receptors as targets to treat metabolic diseases:Focus on the adipose tissue,liver,and pancreas

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World Journal of Gastroenterology 2023年第26期29卷 4136-4155页

作者： Henrique Souza-Tavares Carolline Santos Miranda isabela macedo lopes vasques-monteiro Cristian Sandoval Daiana Araujo Santana-Oliveira Flavia Maria Silva-Veiga Aline Fernandes-da-Silva Vanessa Souza-Mello Department of Anatomy Rio de Janeiro State UniversityRio de Janeiro 20551030Brazil Escuela de Tecnología Médica Facultad de SaludUniversidad Santo TomásOsorno 5310431Chile Departamento de Ciencias Preclínicas Universidad de la FronteraTemuco 4780000Chile

The world is experiencing reflections of the intersection of two pandemics:Obesity and coronavirus disease *** prevalence of obesity has tripled since 1975 worldwide,representing substantial public health costs due to its *** adipose tissue is the initial site of obesity *** excessive energy intake,it undergoes hyperplasia and hypertrophy until overt inflammation and insulin resistance turn adipocytes into dysfunctional cells that send lipotoxic signals to other *** pancreas is one of the organs most affected by *** lipotoxicity becomes chronic,there is an increase in insulin secretion by pancreatic beta cells,a surrogate for type 2 diabetes mellitus(T2DM).These alterations threaten the survival of the pancreatic islets,which tend to become dysfunctional,reaching exhaustion in the long *** for the liver,lipotoxicity favors lipogenesis and impairs beta-oxidation,resulting in hepatic *** silent disease affects around 30%of the worldwide population and can evolve into end-stage liver *** therapy for hepatic steatosis remains to be defined,peroxisome proliferator-activated receptors(PPARs)activation copes with T2DM *** PPARs are transcription factors found at the intersection of several metabolic pathways,leading to insulin resistance relief,improved thermogenesis,and expressive hepatic steatosis mitigation by increasing mitochondrial *** review aimed to update the potential of PPAR agonists as targets to treat metabolic diseases,focusing on adipose tissue plasticity and hepatic and pancreatic remodeling.

关键词： Obesity Insulin resistance Peroxisome proliferator-activated receptors Pancreas Hepatic steatosis Adipose tissue

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Time-dependent impact of a high-fat diet on the intestinal barrier of male mice

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World Journal of Methodology 2024年第1期14卷 114-123页

作者： Carolline Santos Miranda Daiana Araujo Santana-Oliveira isabela lopes vasques-monteiro Nathan Soares Dantas-Miranda Jade Sancha de Oliveira Glauser Flavia Maria Silva-Veiga Vanessa Souza-Mello Department of Anatomy Rio de Janeiro State UniversityRio de Janeiro 20551030Brazil

BACKGROUND Excessive saturated fat intake compromises the integrity of the intestinal mucosa,leading to low-grade inflammation,impaired mucosal integrity,and increased intestinal permeability,resulting in the migration of lipopolysaccharide(LPS)to other *** To evaluate the chronic effects(at 10 and 16 wk)of a high-fat diet(HFD)(with 50%energy as fat)on the phylogenetic gut microbiota distribution and intestinal barrier structure and protection in C57BL/6 *** Forty adult male mice were divided into four nutritional groups,where the letters refer to the type of diet(control and HFD or HF)and the numbers refer to the period(in weeks)of diet administration:Control diet for 10 wk,HFD for 10 wk,control diet for 16 wk,and HFD for 16 *** sacrifice,biochemical,molecular,and stereological analyses were *** The HF groups were overweight,had gut dysbiosis,had a progressive decrease in occludin immunostaining,and had increased LPS *** progression reduced the number of goblet cells per large intestine area and Mucin2 expression in the HF16 group,consistent with a completely disarranged intestinal ultrastructure after 16 wk of HFD *** Chronic HFD intake causes overweight,gut dysbiosis,and morphological and functional alterations of the intestinal barrier after 10 or 16 ***-dependent reductions in goblet cell numerical density and mucus production have emerged as targets for countering obesity-driven intestinal damage.

关键词： High-fat diet Intestine Ultrastructure Goblet cells Gut microbiota

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