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Sus scrofa

ABSTRACT: Hepatic transcriptome changes in testosterone-deficient pigs fed a high-fat diet

PROVIDER: PRJNA264829 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1628661_1.fastq.gz	Fastqsanger.gz
	SRR1628661_2.fastq.gz	Fastqsanger.gz
	SRR1628662_1.fastq.gz	Fastqsanger.gz
	SRR1628662_2.fastq.gz	Fastqsanger.gz
	SRR1628663_1.fastq.gz	Fastqsanger.gz

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Hepatic transcriptome changes in testosterone-deficient pigs fed a high-fat diet

Project description:To gain insight into the role of testosterone in modulating hepatic fat accumulation, we collected liver tissues from high fat diet-fed intact male pigs, castrated male pigs, and castrated male pigs with testosterone replacement. RNA-Seq was employed to profile hepatic gene expression in pigs with different testosterone levels. Liver mRNA profiles of intact male pigs fed a HFC diet, castrated male pigs fed a HFC diet, and castrated male pigs treated with testosterone fed a HFC diet were generated by deep sequencing, using Illumina HiSeq 2000.

2015-01-08 | E-GEOD-62696 | biostudies-arrayexpress

Hepatic transcriptome changes in testosterone-deficient pigs fed a high-fat diet

2015-01-08 | GSE62696 | GEO

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Project description:Testosterone deficiency induces changes of the transcriptomes of visceral adipose tissue in miniature pigs fed a high-fat and high-cholesterol diet

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Renal transcriptome changes in testosterone deficient-pigs fed a high-fat diet

Project description:Renal transcriptome changes in testosterone deficient-pigs fed a high-fat diet

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Renal transcriptome changes in testosterone deficient-pigs fed a high-fat diet

Project description:Purpose: Obesity and dyslipidemia are associated with increased risk of renal disease.Testosterone deficiency aggravated high-fat diet-induced obesity and hypercholeterolemia. However,whether testosterone deficiency or testosterone deficiency-induced dyslipidemia aggravate the progression of renal disease is not clear. To gain insight into the role of testosterone in modulating renal lipid metabolism, we profiled renal gene expression by RNA-Seq in HFC-fed intact male pigs (IM), castrated male pigs (CM), and castrated male pigs with testosterone replacement (CMT). Methods: Sexually mature male miniature pigs were either surgical castrated or sham-operated, and castrated with testosterone replacement. We administrated to pigs a high-fat and high-cholesterol (HFC) diet for twelve weeks. RNA-Seq was employed to profile renal gene expression in pigs with different testosterone levels. Conclusions: This study demonstrated that testosterone deficiency aggravated renal lipid accumulation in pigs fed an HFC diet and that these effects could be reversed by testosterone replacement therapy. Impaired metabolic processes, bile acid secretion,estrogen signaling pathway and enhanced triglyceride synthesis may contribute to the increased renal lipid accumulation induced by testosterone deficiency and an HFC diet.

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Testosterone deficiency induces changes of the transcriptomes of visceral adipose tissue in miniature pigs fed a high-fat and high-cholesterol diet

Project description:Testosterone deficiency causes fat deposit, particularly in the visceral region, and its replacement might reverse fat accumulation, but the underlying mechanisms of such processes are largely unclear. To gain insights into the genome-wide role of testosterone on visceral adipose tissue (VAT), RNA-Seq was used to investigate testosterone deficiency induced changes of VAT in miniature pigs fed a high-fat and high-cholesterol (HFC) diet among intact male pigs (IM), castrated male pigs (CM), and castrated male pigs with testosterone replacement (CMT) treatments. The results showed that testosterone deficiency induced VAT deposit and increased serum leptin level. Moreover, a total of 1,732 differentially expressed genes (DEGs) were identified between different two groups. Compared with gene expression profiles in IM and CMT pigs, upregulated genes in CM pigs, i.e., LOC100520753 (CD68), LCN2, EMR1, NCF1 (p47phox), and NOX2 (GP91-PHOX), were mainly enriched in inflammatory response, oxidation-reduction process, and response to oxidative stress, while downregulated genes in CM pigs, i.e., DIO3, PCK1, and ABHD5, mainly focused on small molecule metabolic process. Taken together, our study provides a novel genome-wide view on the role of testosterone on VAT deposit under HFC diet, thus improving our understanding of the molecular mechanisms involved in VAT changes induced by testosterone deficiency.

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