کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3001553 1180649 2016 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Insulin-like peptide 5 is a microbially regulated peptide that promotes hepatic glucose production
ترجمه فارسی عنوان
پپتید شبه انسولین 5 یک پپتید میکروبی تنظیم است که باعث ارتقای تولید گلوکز در کبد می شود
کلمات کلیدی
پپتید شبه انسولین 5 (INSL5)؛ میکروبیولوژیک روده؛ کبد؛ کولون
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی سیستم های درون ریز و اتونومیک
چکیده انگلیسی


• INSL5 is a microbially regulated peptide hormone.
• Colonic INSL5 expression is suppressed by increased energy availability.
• INSL5 promotes hepatic glucose production.

ObjectiveInsulin-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.MethodsWe 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.ResultsWe 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.ConclusionsWe 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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Metabolism - Volume 5, Issue 4, April 2016, Pages 263–270
نویسندگان
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