A high-fat diet induced depression-like phenotype <i>via</i> hypocretin-HCRTR1 mediated inflammation activation

Dong, Jingyi; Zhang, Jinghui; Cheng, Shangping; Qin, Bin; Jin, Kangyu; Chen, Bing; Zhang, Yuyan; Lu, Jing

doi:10.1039/d4fo00210e

Cited by 2 publications

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Fluoxetine Ameliorates Cognitive Deficits in High-Fat Diet Mice by Regulating BDNF Expression

Zuo,

Zhu,

Liu

et al. 2024

ACS Chem. Neurosci.

View full text Add to dashboard Cite

High-fat diet (HFD) induced obesity is associated with depression-related behavioral and neurogenic changes and may lead to cognitive impairment. Fluoxetine (FXT), the most commonly used antidepressant, may alleviate depressive symptoms by increasing neurogenesis, but the potential efficacy of FXT for HFD-induced cognitive deficits is unclear. In this study, we established an obese HFD mouse model by feeding three-week-old male C57BL/6N mice with a chronic HFD for 18 weeks, then assessed adipose tissue morphology by magnetic resonance imaging and histopathology, assessed cognitive function by Morris water maze and novel object recognition tests, and detected DCX + and BrdU + expression in the hippocampal dentate gyrus (DG) region by immunofluorescence bioassay. Western blot detected brain-derived neurotrophic factor (BDNF) levels and CREB-BDNF pathway-related genes were assayed by Quantitative RT-PCR. The results of the study showed that HFD contributes to obesity and cognitive deficits, and more importantly, it also reduces BDNF expression and neurogenesis levels in the hippocampus. Subsequently, we found that treatment with FXT (10 mg/kg/day) ameliorated chronic HFD-induced cognitive deficits and increased the expression of Nestin, BrdU + , and DCX + in the DG, restored BDNF expression in the hippocampus and increased the expression of genes related to CREB, BDNF, NGF, and MAPK1. In conclusion, our data elucidated that FXT ameliorates cognitive deficits and reduces chronic HFD-induced neurogenesis by restoring BDNF expression and CREB-BDNF signaling, this provides a good basis and scientific significance for future research on the clinical treatment of obesity.

show abstract

Fluoxetine Ameliorates Cognitive Deficits in High-Fat Diet Mice by Regulating BDNF Expression

Zuo,

Zhu,

Liu

et al. 2024

ACS Chem. Neurosci.

View full text Add to dashboard Cite

show abstract

Identification of novel key genes and signaling pathways in hypertrophic cardiomyopathy: evidence from bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

View full text Add to dashboard Cite

Hypertrophic cardiomyopathy (HCM) is a global health problem characterized by left ventricle become thick and stiff with effect of indication including chest pain, fluttering, fainting and shortness of breath. In this investigation, we aimed to identify diagnostic markers and analyzed the therapeutic potential of essential genes. Next generation sequencing (NGS) dataset GSE180313 was obtained from the Gene Expression Omnibus (GEO) database and used to identify differentially expressed genes (DEGs) in HCM. DEGs were screened using the DESeq2 Rbioconductor tool. Then, Gene Ontology (GO) and REACTOME pathway enrichment analyses were performed. Moreover, a protein-protein interaction (PPI) network of the DEGs was constructed, and module analysis was performed. Next, miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed and analyzed. Finally, diagnostic values of hub genes were assessed by by receiver operating characteristic (ROC) curve analysis. By performing DEGs analysis, total 958 DEGs ( 479 up regulated genes and 479 down regulated genes) were successfully identified from GSE180313, respectively. GO and REACTOME pathway enrichment analyses revealed that GO functions and signaling pathways were significantly enriched including response to stimulus, multicellular organismal process, metabolism and extracellular matrix organization. The hub genes of FN1, SOX2, TUBA4A, RPS2, TUBA1C, ESR1, SNCA, LCK, PAK1 and APLNR might be associated with HCM. The hub gens of FN1 and TPM3, together with corresponding predicted miRNAs (e.g., hsa-mir-374a-5p and hsa-miR-8052), and SH3KBP1 and ESR1 together with corresponding predicted TFs (e.g PRRX2 and STAT3) were found to be significantly correlated with HCM. This investigation could serve as a basis for further understanding the molecular pathogenesis and potential therapeutic targets of HCM.

show abstract

A high-fat diet induced depression-like phenotype via hypocretin-HCRTR1 mediated inflammation activation

Abstract: HFD tips gut microbiota balance via the gut-brain axis perturbs cerebral equilibrium, increases hypocretin levels, and triggers microglial activation. This leads to inflammation and may cause mental disorders like depression and anxiety.

Cited by 2 publications

References 49 publications

Fluoxetine Ameliorates Cognitive Deficits in High-Fat Diet Mice by Regulating BDNF Expression

Fluoxetine Ameliorates Cognitive Deficits in High-Fat Diet Mice by Regulating BDNF Expression

Identification of novel key genes and signaling pathways in hypertrophic cardiomyopathy: evidence from bioinformatics and next generation sequencing data analysis

Contact Info

Product

Resources

About