More specifically, an in vivo study, based on chronic 40-day peripheral administration of lixisenatide to high-fat fed mice with established obesity, insulin resistance and impaired cognition, found that lixisenatide significantly upregulated expression of the neurotrophic tyrosine kinase receptor type 2 (NTRK2) gene and of the mammalian target of rapamycin (mTOR) gene in the hippocampus, which are involved in regulating synaptic plasticity [100]. The gene discussed is MTOR; the disease is obesity due to melanocortin 4 receptor deficiency.