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http://purl.uniprot.org/citations/27069866http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Objective

Insulin-like peptide 5 (INSL5) is a recently identified gut hormone that is produced predominantly by L-cells in the colon, but its function is unclear. We have previously shown that colonic expression of the gene for the L-cell hormone GLP-1 is high in mice that lack a microbiota and thus have energy-deprived colonocytes. Our aim was to investigate if energy deficiency also affected colonic Insl5 expression and to identify a potential role of INSL5.

Methods

We analyzed colonic Insl5 expression in germ-free (GF), conventionally raised (CONV-R), conventionalized (CONV-D) and antibiotic-treated mice, and also assessed the effect of dietary changes on colonic Insl5 expression. In addition, we characterized the metabolic phenotype of Insl5-/-mice.

Results

We showed that colonic Insl5 expression was higher in GF and antibiotic-treated mice than in CONV-R mice, whereas Insl5 expression in the brain was higher in CONV-R versus GF mice. We also observed that colonic Insl5 expression was suppressed by increasing the energy supply in GF mice by colonization or high-fat feeding. We did not observe any differences in food intake, gut transit or oral glucose tolerance between Insl5-/- and wild-type mice. However, we showed impaired intraperitoneal glucose tolerance in Insl5-/-mice. We also observed improved insulin tolerance and reduced hepatic glucose production in Insl5-/-mice.

Conclusions

We have shown that colonic Insl5 expression is regulated by the gut microbiota and energy availability. We propose that INSL5 is a hormone that could play a role in promoting hepatic glucose production during periods of energy deprivation."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.org/dc/terms/identifier"doi:10.1016/j.molmet.2016.01.007"xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/author"Lee Y.S."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/author"Wichmann A."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/author"Backhed F."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/author"De Vadder F."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/author"Mithieux G."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/author"Tremaroli V."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/name"Mol Metab"xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/pages"263-270"xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/title"Insulin-like peptide 5 is a microbially regulated peptide that promotes hepatic glucose production."xsd:string
http://purl.uniprot.org/citations/27069866http://purl.uniprot.org/core/volume"5"xsd:string
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