Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12742450.fastq.gz	Fastqsanger.gz
	SRR12742451.fastq.gz	Fastqsanger.gz
	SRR12742452.fastq.gz	Fastqsanger.gz
	SRR12742453.fastq.gz	Fastqsanger.gz
	SRR12742454.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

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:Atypical antipsychotics such as risperidone cause drug-induced metabolic syndrome. However, the underlying mechanisms remain largely unknown. Here, we report a new mouse model that reliably reproduces risperidone-induced weight gain, adiposity, and glucose intolerance. We found that risperidone treatment acutely altered energy balance in C57BL/6 mice and that hyperphagia accounted for most of the weight gain. Transcriptomic analyses in the hypothalamus of risperidone-fed mice revealed that risperidone treatment reduced the expression of Mc4r. Furthermore, Mc4r in Sim1 neurons was necessary for risperidone-induced hyperphagia and weight gain. Moreover, we found that the same pathway underlies the obesogenic effect of olanzapine-another commonly prescribed antipsychotic drug. Remarkably, whole-cell patch-clamp recording demonstrated that risperidone acutely inhibited the activity of hypothalamic Mc4r neurons via the opening of a postsynaptic potassium conductance. Finally, we showed that treatment with setmelanotide, an MC4R-specific agonist, mitigated hyperphagia and obesity in both risperidone- and olanzapine-fed mice.

| S-EPMC8126977 | biostudies-literature

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.

2021-09-08 | GSE180473 | GEO

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.

2022-05-11 | GSE198053 | GEO

Antipsychotic Weight Gain

Project description:Altered Gene Expression in Antipsychotic Induced Weight Gain

| PRJEB31532 | ENA

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

2015-04-09 | E-GEOD-67723 | biostudies-arrayexpress

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

2015-04-09 | GSE67723 | GEO

Assess the effects of antipsychotic use on gene expression changes in dementia

Project description:In order to elucidate mechanisms underlying adverse effects of antipsychotic use in dementia we generated gene expression signatures for three antipsychotics representing a range of mechanisms of action relevant to the current landscape of drug development and clinical use in dementia: amisulpride (primarily a D2/D3 antagonist), risperidone (primarily a 5HT2A/D2 antagonist) and volinanserin (highly selective 5HT2A inverse agonist). We reported that the antipsychotic signatures would be score positively with conditions and diseases related to known side effects of their use in dementia such as cardiovascular and infectious diseases.

2020-04-30 | GSE149611 | GEO

Microarray profiling of rats treated for 21 days with haloperidol (0.25 mg/kg/d), risperidone (5 mg/kg/d) or vehicle

Project description:SD rats were dosed with gold standard antipsychotic therapies, haloperidol or risperidone, at doses aimed at achieving therapeutically relevant drug exposures. Tissues were collected after 21 days of delivery to examine the impact of this treatment on gene expression in frontal cortex, hippocampus and striatum.

2015-03-16 | GSE66275 | GEO

Classification of Antipsychotic Drugs by Gene Expression in the Frontal Cortex of Mice

Project description:Antipsychotic drugs are classified as typical and atypical based on extrapyramidal effects. However, since the frontal cortex is one of the most important regions for antipsychotic actions, this study attempted to classify antipsychotic drugs based on gene expression in the frontal cortex. Chlorpromazine and thioridazine were selected as typical antipsychotics, and olanzapine and quetiapine as atypical antipsychotics. Since these drugs have similar chemical structures, the effect of the basic structure on gene expression can be eliminated. Cluster analysis of microarray experiments showed thioridazine and olanzapine constituted a robust cluster. K-means clustering separated 4-drug-administered mice into chlorpromazine-quetiapine and thioridazine-olanzapine groups. This classification scheme is different from that which is based on criteria currently used to group the typical and atypical drugs and suggests that antipsychotic drugs can be further separated into multiple groups. Keywords: repeat sample

2004-09-24 | GSE1501 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data