However additive effects between any of the two chemical and HFD were not

However additive effects between any of the two

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not observed. Although this model showed an increase in blood vessel lipids for a HFD in a short period of time, thisresult does not reflect obesity as a chronic disease, because differences in the accumulation of lipids in the visceralWAT between SD and HFD animals or increase in weight and size of HFD larvae were not observed. Perhaps a longerexposure period to the HFD would affect these parameters.Progatzky et al[111], showed that the exposure to a HF diet or a high-cholesterol diet (HCD) in zebrafish larvaeinduced an inflammatory response in hours, with infiltration of myeloid cells in the intestine, dependent oninflammasome activation by IECs. They demonstrated that the inflammation was directly induced by cholesterolbinding to the Niemann-Pick C1-like receptor, with the participation of the apoptosis-associated speck-like proteincontaining a CARD (ASC) and activation of caspase-1, which is part of the inflammasome complex[112]that produceshigh levels of active IL-1. Furthermore, this inflammation was dependent on the microbiota and NFB activation.Finally, extended feeding with a HCD produced the accumulation of visceral fat, liver steatosis, sustainedinflammation in the intestine, and impaired peristalsis. This study verified a direct link between inflammation andhigh-fat diets, specifically the activation of the inflammasome complex by cholesterol in the intestine, and opened anew window to the study of innate inflammation in the context of obesity and its influence in other chronicinflammatory diseases.By last, a study analyzing two flame retardants, tetrabromobisphenol-A and tetrachlorobisphenol-A, as possibleobesogens using zebrafish larvae[113] showed lipid accumulation in larval stage and late-onset weight gain in juvenileanimals, which was most likely caused by the compounds’ activity as a PPARagonist. This method could beinteresting for the analysis of the inflammatory state under such conditions, using these substances as agonists ofPPAR.The zebrafish models related to obesity maybe are not so well known as mice models, nonetheless, the examplespresented here (Table 2) are evidence of the conserved signals that control lipids metabolism and the flexibility of thezebrafish as model of metabolic diseases.CONCLUSION
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The models presented in this review exhibit the utility of zebrafish as a model of diseases and demonstrate thatthis animal as an intermediate between models involving simpler invertebrates and more complex highermammals and can be used as an alternative or a complement to pre-clinical and drug screening studies thatinvolve conserved metabolic and inflammatory pathways. Furthermore, the characteristics of zebrafish such asphysiological homology, rapid development and a low cost of production, make this animal a great option forresearch on new therapies for inflammatory diseases.
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