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ABSTRACT: Intestinal alkaline phosphatase (IAP, IAP enhancer) attenuates intestinal inflammation and alleviates insulin resistance

PROVIDER: PRJNA833108 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18965042.fastq.gz	Fastqsanger.gz
	SRR18965043.fastq.gz	Fastqsanger.gz
	SRR18965044.fastq.gz	Fastqsanger.gz
	SRR18965045.fastq.gz	Fastqsanger.gz
	SRR18965046.fastq.gz	Fastqsanger.gz

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Project description:Metabolic alterations relevant to postprandial dyslipidemia were previously identified in the intestine of obese subjects with systemic insulin resistance. These dysregulations were closely associated with an amplification of intestinal lipogenesis and lipoprotein output, which was triggered by insulin resistance likely sustained by oxidative stress and inflammation. The aim of the study was to identify the genes deregulated by the presence of systemic insulin resistance in the intestine of severely obese subjects. Transcripts from duodenal samples of insulin-sensitive (HOMA-IR<3, n=9) and insulin-resistant (HOMA-IR>7, n=9) obese subjects were assayed by microarray (Illumina HumanHT-12). The small intestine exhibits a highly specific mRNA expression profile that was similar between insulin-sensitive and insulin-resistant individuals. A total of 195 annotated genes were identified as differentially expressed between these two groups with a fold change higher than 1.2. Metabolic pathway analysis revealed that 36 differently expressed genes were directly involved in known intestinal functions, including digestion, extracellular matrix, endocrine system, immunity, inflammation/oxidative stress and cholesterol metabolism. Several signaling pathways involved in immunity and inflammation were significantly enriched in differently expressed genes and were predicted to be activated in the intestine of insulin-resistant subjects. Using stringent criteria (Fold change>1.5; FDR<0.05), only three genes were found to be significantly and differently expressed in the intestine of insulin-resistant compared to insulin-sensitive subjects: the transcripts of the insulinotropic glucose-dependant peptide (GIP) and of the β-microseminoprotein (MSMB) were significantly reduced, but that of the humanin like-1 (HNL1) protein was significantly increased. These results underline that systemic insulin resistance is associated with an amplification of local inflammatory process and remodeling of key intestinal functions. Genes identified in this study are potentially triggered throughout the development of intestinal metabolic alterations, which could contribute to dyslipidemia, a component of metabolic syndrome and diabetes.

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