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Regulation of Appetite and Obesity · Journal article
Frontiers in Synaptic Neuroscience · August 10, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review that proposes zebrafish as a translational platform for investigating synaptic dysfunction in obesity and screening peptide-based therapeutics. The source synthesizes conceptual rationale and technological capabilities but does not report empirical findings, effect sizes, or clinical validation; it raises mechanistic hypotheses rather than answering them.
Journal article. Conceptual; zebrafish as a model organism proposed for mechanistic and therapeutic studies related to obesity and neurodegeneration..
Zebrafish offer optical transparency, genetic tractability, and high-throughput screening capacity for studying neuronal circuitry Obesity-driven synaptic dysfunction is proposed as a key mechanism linking metabolic disorders to neurodegenerative diseases including Parkinson's and Alzheimer's disease Pathophysiological processes implicated include central hormone resistance, oxidative stress, and chronic neuroinflammation
Efficacy and safety of candidate peptides (GLP-1 analogs, BDNF molecules) in zebrafish or humans not empirically demonstrated in this source.
This review does not provide evidence for clinical decision-making. It articulates a rationale for using zebrafish in preclinical research on obesity and neuroprotection, but does not report outcomes applicable to patient care or establish efficacy of any therapeutic intervention.
This is a narrative review proposing zebrafish as a model system for studying obesity-related synaptic dysfunction and peptide therapeutics, without reporting original experimental data or clinical outcomes.
This review does not provide evidence for clinical decision-making. It articulates a rationale for using zebrafish in preclinical research on obesity and neuroprotection, but does not report outcomes applicable to patient care or establish efficacy of any therapeutic intervention.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Obesity-driven synaptic dysfunction is increasingly recognized as a key mechanism linking metabolic disorders to neurodegenerative diseases. This review aims to explore the utility of zebrafish ( Danio rerio ) as a translational model to investigate these mechanisms and screen peptide-based therapeutic strategies. Owing to their optical transparency, genetic tractability, and suitability for high-throughput screening, zebrafish provide a powerful platform for studying neuronal circuitry and evaluating bioactive peptides in vivo. Current evidence on pathophysiological processes underlying obesity-related synaptic impairment, including central resistance to metabolic hormones, oxidative stress, and the chronic inflammatory state, which promotes persistent immune activation and neuroinflammation. In addition, the persistence of these disturbances in the organism can lead to dysfunctions and pathologies, such as Parkinson’s and Alzheimer’s diseases, both of which are discussed in more detail in this review. Also, particular emphasis is placed on the roles of glial cells and the gut–brain axis in modulating synaptic integrity. We highlight how cutting-edge technologies, such as live neural imaging and single-cell transcriptomics, are accelerating peptide discovery and mechanism-of-action studies in zebrafish. Furthermore, we discuss emerging therapeutic peptides such as GLP-1 analogs and BDNF-based molecules that modulate inflammatory pathways, restore insulin signaling, and enhance neuronal resilience. Collectively, the evidence positions zebrafish as a robust model not only for elucidating disease mechanisms but also for advancing peptide-based interventions targeting synaptic dysfunction in obesity.
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