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The effect of trimethylamine N-oxide on the metabolism of visceral white adipose tissue in spontaneously hypertensive rat

ABSTRACT: The effect of trimethylamine N-oxide on the metabolism of visceral white adipose tissue in spontaneously hypertensive rat

PROVIDER: PRJNA778395 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16832253_1.fastq.gz	Fastqsanger.gz
	SRR16832253_2.fastq.gz	Fastqsanger.gz
	SRR16832254_1.fastq.gz	Fastqsanger.gz
	SRR16832254_2.fastq.gz	Fastqsanger.gz
	SRR16832255_1.fastq.gz	Fastqsanger.gz

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Excessive leukotriene B4 in nucleus tractus solitarii is pro-hypertensive in spontaneously hypertensive rats.

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The effect of trimethylamine N-oxide on the metabolism of visceral white adipose tissue in spontaneously hypertensive rat.

Project description:Strong links have been reported among trimethylamine N-oxide (TMAO), visceral white adipose tissue (vWAT), and cardiometabolic diseases. However, the effects of TMAO on vWAT in hypertension remained incompletely explored. The impact of a chronic 22-week-long treatment with 1 g/L TMAO on vWAT, and its transcriptional and metabolic changes in spontaneously hypertensive rats (SHRs) were evaluated by serum cytokine measurements, histological analysis, fatty acid determinations, and co-expression network analyses. TMAO increased the serum interleukin-6 levels and insulin secretion in SHRs. The adipocyte size was diminished in the SHR 1 g/L TMAO group. In addition, one kind of monounsaturated fatty acids (cis-15-tetracosenoate) and four kinds of polyunsaturated fatty acids (cis-11,14,17-eicosatrienoic acid, docosatetraenoate, docosapentaenoate n-3, and docosapentaenoate n-6) were elevated by TMAO treatment. Three co-expression modules significantly related to TMAO treatment were identified and pathway enrichment analyses indicated that phagosome, lysosome, fatty acid metabolism, valine, leucine, and isoleucine degradation and metabolic pathways were the most significantly altered biological pathways. This study shed new light on the metabolic roles of TMAO on the vWAT of SHRs. TMAO regulated the metabolic status of vWAT, including reduced lipogenesis and an improved specific fatty acid composition. The mechanisms underlying these effects likely involve phagosome and lysosome pathways.

| S-EPMC9387326 | biostudies-literature

Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Trimethylamine N-oxide (TMAO), a metabolite derived from intestine microbial flora, enhances vascular inflammation in a variety of cardiovascular disease, and the bacterial communities associated with trimethylamine N-oxide (TMAO) metabolism is higher in pulmonary hypertension (PH) patients. The effects of TMAO on PH, however, has not been elucidated. In the present study, we found that circulating TMAO is elevated in intermediate to high-risk PH patients when compared to healthy control or low-risk PH patients. In monocrotaline-induced rat PH models, circulating TMAO is elevated; and reduction of TMAO using 3,3-dimethyl-1-butanol (DMB) significantly decreased right ventricle systolic pressure, pulmonary vascular muscularization in both monocrotaline-induced rat PH and hypoxia induced mice PH models. RNA sequencing of rat lungs on DMB revealed significant suppression of pathways involved in cytokine-cytokine receptor interaction, and cytokine and chemokine signaling. Protein-protein interaction analysis of the differentially expressed transcripts regulated by DMB showed 5 hub genes with a strong connectivity of proinflammatory cytokines and chemokines including Kng1, Cxcl1, Cxcl2, CxcL6 and Il6. In vivo, TMAO significantly increased the expression of Kng1, Cxcl1, Cxcl2, CxcL6 and Il6 in bone marrow derived macrophage. And TMAO-treated conditioned medium from macrophage increased the proliferation and migration of pulmonary artery smooth muscle cells; but TMAO treatment did not change the proliferation or migration of pulmonary artery smooth muscle cells. In conclusion, our study demonstrates that TMAO is increased in severe PH, and the reduction of TMAO using DMB reduces pulmonary vascular muscularization and alleviates PH via suppressing the macrophage production of chemokines and cytokines.

2022-06-07 | GSE190203 | GEO

The effect of trimethylamine N-oxide on the metabolism of visceral white adipose tissue in spontaneously hypertensive rat

Project description:Male SHRs and normotensive Wistar-Kyoto(WKY) rats were purchased from Vital River (Vital River Laboratory Animal Technology Co., Ltd, Beijing, China). Briefly, eightteen SHRs aged seven to eight weeks old were randomly assigned to one of three groups: water group (drinking tap water), water containing 333 mg/L or 1g/L TMAO group (TMAO, product number: T1362, Tokyo Chemical Industry, Japan). Six WKY rats of the same age were used as normotensive controls. In this study, WKY rats (n=6), SHR (n=6), and SHR treated with 1g/L TMAO (n=6) were uesd for experiments.

2022-08-17 | GSE188336 | GEO

Quantitative TMT proteomics of brainstem in spontaneously hypertensive rats

Project description:The brainstem, the core of the central nervous system, plays a vital role in controlling arterial blood pressure and its elevation of hypertension subtypes, especially essential hypertension. Integrative metabolic and proteomic profiling was performed on the brainstem samples of 11-week-old spontaneously hypertensive rats (SHRs) and age-matched normotensive Wistar rats, using hydrophilic interaction liquid chromatography-quadrupole/time-of-flight mass spectrometry (HILIC-Q/TOFMS) and nano-liquid chromatography-high-resolution-mass spectrometry (nano-LC-high-resolution-MS) combined with quantitative tandem mass tags (TMT).

2020-09-24 | PXD021210 | Pride

Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

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Time-dependent specific molecular signatures of inflammation and remodelling are associated with Trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction

Project description:Cardiovascular diseases (CVDs) are leading causes of death worldwide. Endothelial dysfunction is a critical initiating factor contributing to CVDs, which progression involves the gut microbiome-derived metabolite Trimethylamine N-oxide (TMAO). Here, we aim to clarify the time-dependent pathways by which TMAO mediates endothelial dysfunction.

2023-11-23 | GSE235204 | GEO

Genome-wide Profiling of Long Noncoding RNA Expression Patterns in Thoracic Aorta from Spontaneously Hypertensive Rats.

Project description:We used lncRNA-mRNA micro-array to analyze the transcriptome in the thoracic aorta tissue of 24 wees-old WKY and spontaneously hypertensive rats (SHRs).

2021-01-01 | GSE145854 | GEO

Transcription profiling of rat kidney from spontaneously hypertensive rats vs. controls

Project description:Development of renal transcriptome in spontaneously hypertensive rats (SHR) as compared to normotensive wistar kyoto rats (WKY) from birth to old age.

2008-04-30 | E-MEXP-1550 | biostudies-arrayexpress

Excessive leukotriene B4 in nucleus tractus solitarii is pro-hypertensive in spontaneously hypertensive rats.

Project description:We have used Affymetrix microarray-driven gene profiling to comprehensively describe the expression of mRNAs in the nucleus tractus solitarii (NTS) in the adult male spontaneously hypertensive rat (SHR) as compared to its normotensive parental Wistar-Kyoto (WKY) strain. Keywords: Gene expression NTS was dissected from hypertensive (SHR) and normotensive (WKY) strains of rat. For each structure, 10 independent Affymetrix Genechip 230 2.0 experiments were performed (5 SHR, 5 WKY), with each chip representing an independent biological replication (n=5).

2013-03-01 | E-GEOD-8796 | biostudies-arrayexpress

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