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The Atypical Antipsychotic Risperidone Targets Central Melanocortin 4 Receptors to Cause Weight

ABSTRACT: The Atypical Antipsychotic Risperidone Targets Central Melanocortin 4 Receptors to Cause Weight

PROVIDER: PRJNA666420 | ENA |

REPOSITORIES: ENA

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The Atypical Antipsychotic Risperidone Targets Central Melanocortin 4 Receptors to Cause Weight

Project description:hypothalami from female C57BL/6 mice fed either the risperidone or the control diet for 28 days, along with those from a third group of “pair-fed” mice that were given the risperidone diet, but limited to the same amount that Ctrl_ Ad lib mice had consumed.

2021-01-01 | GSE158751 | GEO

The atypical antipsychotic risperidone targets hypothalamic melanocortin 4 receptors to cause weight gain.

Project description: Not available

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Effects of antipsychotics risperidone and olanzapine on the striatum, liver, pancreas and adipose tissue

Project description:Analysis of gene expression in the striatum, the liver, the pancreas, and the visceral adipose tissue of mice treated for 28 days with a daily dose of an atypical antipsychotic: risperidone (1 mg/kg) or olanzapine (3.5 mg/kg). Results provide new insights into the molecular mechanisms underlying antipschotic effects, particularly in tissues relevant for antipsychotic-induced metabolic dysregulation. Antipsychotics are associated with weight gain and other metabolic abnormalities such as hyperglycemia, dyslipidemia and metabolic syndrome. We used microarrays to uncover the underlying molecular mechanisms and identify the key genes involved in AP-induced metabolic effects.

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Deciphering risperidone-induced lipogenesis by network pharmacology and molecular validation

Project description:Risperidone is an atypical antipsychotic that can cause substantial weight gain. The pharmacological targets and molecular mechanisms related to risperidone-induced lipogenesis (RIL) remain to be elucidated. Therefore, network pharmacology and further experimental validation were undertaken to explore the action mechanisms of RIL. In this study, RIL was systematically analyzed using integrating multiple databases through integrated network pharmacology, transcriptomics, molecular docking, and molecular experiment analysis. The potential signaling pathways for RIL were identified and experimentally validated using Gene Ontology (GO) enrichment and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Our experimental data showed that Risperidone promotes adipocyte differentiate and lipid accumulation. And network pharmacology and GO analyses showed that risperidone induced adipocyte metabolism, differentiation, and lipid accumulation related functions. Intersecting analysis, molecular docking, and pathway validation analysis indicated that risperidone activated adipocytokine signaling pathway related genes by targeting MAPK14 (Mitogen-activated protein kinase 14), MAPK8 (Mitogen-activated protein kinase 8), and RXRA (Retinoic acid receptor RXR-alpha), thereby inhibiting long-chain fatty acid beta-oxidation by suppressing STAT3 (Signal transducer and activator of transcription 3) expression and phosphorylation. This study suggested that Risperidone increases adipocyte lipid accumulation by plausible inhibiting long-chain fatty acid beta-oxidation through targeting MAPK14, MAPK8, and RXRA.

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Antipsychotic Weight Gain

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Network analysis of gene expression in mice provides new evidence of involvement of the mTOR pathway in antipsychotic-induced extrapyramidal symptoms

Project description:To identify potential candidate genes for future pharmacogenetic studies of antipsychotic (AP)-induced extrapyramidal symptoms (EPS), we used gene expression arrays to analyze changes induced by risperidone in mice strains with different susceptibility to EPS This study is a part of a convergent functional genomic approach that plans to integrate the data presented here with: data from gene expression analysis of neuroblastoma cell line under treatment with risperidone; and data from gene expression analysis of peripheral blood from first psychotic patients treated with risperidone. Gene expression was assessed by microarray (Affymetrix GeneChip® Arrays MG 430 PM) in mice treated with risperidone 1mg/kg for three consecutive days

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Network analysis of gene expression in mice provides new evidence of involvement of the mTOR pathway in antipsychotic-induced extrapyramidal symptoms

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