IFN-α-2b treatment protects against diet-induced obesity and alleviates non-alcoholic fatty liver disease in mice

Quiroga, Ariel D.; Comanzo, Carla G.; Barbini, Francisco J. Heit; Lucci, Alvaro; Vera, Marina C.; Lorenzetti, Florencia; Ferretti, Anabela C.; Ceballos, María Paula; Álvarez, María Clara; Carrillo, María C.

doi:10.1016/j.taap.2019.114650

Cited by 11 publications

(6 citation statements)

References 48 publications

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“…The mechanical difference in the effect of IFN therapy and DAAs on liver steatosis has been not clarified well; however, certain hypotheses exist. Recently, it has been reported that IFN could decrease hepatocyte lipid droplets by promoting β‐oxidation and decreasing cholesterol synthesis 44 . Thus, IFN‐based therapy could suppress increased prevalence of fatty liver following HCV eradication.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C virus eradication by direct‐acting antivirals causes a simultaneous increase in the prevalence of fatty liver and hyper low‐density lipoprotein cholesterolemia without an increase in body weight

Tokuchi

Suda

Kawagishi

et al. 2023

Hepatology Research

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Section: Discussionmentioning

confidence: 99%

Hepatitis C virus eradication by direct‐acting antivirals causes a simultaneous increase in the prevalence of fatty liver and hyper low‐density lipoprotein cholesterolemia without an increase in body weight

Tokuchi

Suda

Kawagishi

et al. 2023

Hepatology Research

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“…Additionally, IFN-α increased hepatic adipogenesis and VLDL secretion, which was obvious in cultured hepatocytes and in patients with IFN-αtherapy ( Shinohara et al, 1997 ; Feingold et al, 1992 ). Therefore, OPTN might act in the inflammatory mechanisms of NASH as it is involved in TNF and IFNalfa pathways ( Quiroga et al, 2019 ). Our results also suggest that OPTN expression is closely associated with adipogenesis.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of NAFLD and the Therapeutic Target Identified

Wen

Zhang

et al. 2021

Front. Cell Dev. Biol.

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Objective: Non-alcoholic fatty liver disease (NAFLD) is a serious health threat worldwide. The aim of this study was to comprehensively describe the metabolic and immunologic characteristics of NAFLD, and to explore potential therapeutic drug targets for NAFLD.Methods: Six NAFLD datasets were downloaded from the Gene Expression Omnibus (GEO) database, including GSE48452, GSE63067, GSE66676, GSE89632, GSE24807, and GSE37031. The datasets we then used to identify and analyze genes that were differentially expressed in samples from patients with NAFLD and normal subjects, followed by analysis of the metabolic and immunologic characteristics of patients with NAFLD. We also identified potential therapeutic drugs for NAFLD using the Connectivity Map (CMAP) database. Moreover, we constructed a prediction model using minimum depth random forest analysis and screened for potential therapeutic targets. Finally, therapeutic targets were verified in a fatty liver model stimulated by palmitic acid (PA).Results: A total of 1,358 differentially expressed genes (DEGs) were obtained, which were mainly enriched in carbohydrate metabolism, lipid metabolism, and other metabolic pathways. Immune infiltration analysis showed that memory B cells, regulatory T cells and M1 macrophage were significantly up-regulated, while T cells follicular helper were down regulated in NAFLD. These may provide a reference for the immune-metabolism interaction in the pathogenesis of NAFLD. Digoxin and helveticoside were identified as potential therapeutic drugs for NAFLD via the CMAP database. In addition, a five-gene prediction model based on minimum depth random forest analysis was constructed, and the receiver operating characteristic (ROC) curves of both training and validation set reached 1. The five candidate therapeutic targets were ENO3, CXCL10, INHBE, LRRC31, and OPTN. Moreover, the efficiency of hepatocyte adipogenesis decreased after OPTN knockout, confirming the potential use of OPTN as a new therapeutic target for NAFLD.Conclusion: This study provides a deeper insight into the molecular pathogenesis of NAFLD. We used five key genes to construct a diagnostic model with a strong predictive effect. Therefore, these five key genes may play an important role in the diagnosis and treatment of NAFLD, particularly those with increased OPTN expression.

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“…Consequently, IFN-β1 may be used as a potential target in immune-driven diseases [ 124 ]. A previous study also indicated that IFN-α-2b treatment could attenuate obesity development by decreasing body weight and improving dyslipidemia, which involved FAO and cholesterol decrement [ 142 ]. IFN-τ exhibits anti-inflammatory effects and low cell cytotoxicity even in high-dose treatment.…”

Section: Therapeutic Perspective Of Ifn In Obesity and Insulin Sensit...mentioning

confidence: 99%

Interferon Family Cytokines in Obesity and Insulin Sensitivity

Huang

Chiu

Hsing

et al. 2022

Cells

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Obesity and its associated complications are global public health concerns. Metabolic disturbances and immune dysregulation cause adipose tissue stress and dysfunction in obese individuals. Immune cell accumulation in the adipose microenvironment is the main cause of insulin resistance and metabolic dysfunction. Infiltrated immune cells, adipocytes, and stromal cells are all involved in the production of proinflammatory cytokines and chemokines in adipose tissues and affect systemic homeostasis. Interferons (IFNs) are a large family of pleiotropic cytokines that play a pivotal role in host antiviral defenses. IFNs are critical immune modulators in response to pathogens, dead cells, and several inflammation-mediated diseases. Several studies have indicated that IFNs are involved in the pathogenesis of obesity. In this review, we discuss the roles of IFN family cytokines in the development of obesity-induced inflammation and insulin resistance.

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IFN-α-2b treatment protects against diet-induced obesity and alleviates non-alcoholic fatty liver disease in mice

Cited by 11 publications

References 48 publications

Hepatitis C virus eradication by direct‐acting antivirals causes a simultaneous increase in the prevalence of fatty liver and hyper low‐density lipoprotein cholesterolemia without an increase in body weight

Hepatitis C virus eradication by direct‐acting antivirals causes a simultaneous increase in the prevalence of fatty liver and hyper low‐density lipoprotein cholesterolemia without an increase in body weight

Comprehensive Analysis of NAFLD and the Therapeutic Target Identified

Interferon Family Cytokines in Obesity and Insulin Sensitivity

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