Open AccessA role for methanogens and methane in the regulation of GLP ‐1
Author(s) -
Laverdure Rose,
Mezouari Ania,
Carson Michael A.,
Basiliko Nathan,
Gag Jeffrey
Publication year - 2018
Publication title -
endocrinology, diabetes and metabolism
Language(s) - English
Resource type - Journals
ISSN - 2398-9238
DOI - 10.1002/edm2.6
Subject(s) - methanogen , secretion , butyrate , biology , intracellular , microbiology and biotechnology , medicine , endocrinology , methane , biochemistry , ecology , fermentation
Summary Introduction The gastrointestinal ( GI ) microbiome has emerged as a potential regulator of metabolism. However, the precise mechanisms of how microorganisms may influence physiology remain largely unknown. Interestingly, GI microorganisms, including methanogens, are localized within the same regions as the glucagon‐like peptide‐1 ( GLP ‐1) secreting L cells. GLP ‐1 plays key roles appetite and glucose regulation. Furthermore, both methane and GLP ‐1 levels are altered in obese humans with metabolic disease. We predict that high‐fat diet‐induced obesity alters the abundance of GI methanogens and that methane may play a role in the GLP ‐1 secretory response from the L cell. Methods To demonstrate this, GLP ‐1 secretion response and faecal methanogens were examined in mice given a high‐fat diet for 14 weeks. In addition, the direct effect of methane on GLP ‐1 secretion was assessed in two L‐cell models ( NCI ‐H716 and GLUT ag). Results High‐fat diet caused a significant increase in both GLP ‐1 secretion and faecal methanogen content. There was a direct correlation between GLP ‐1 secretion response and faecal methanogen levels. In L cells, methane stimulated GLP ‐1 secretion and enhanced intracellular cAMP content. Conclusion These results indicate that alterations in the methanogen communities occurring in obesity may play a vital role in directly enhancing GLP ‐1 secretion, and that methane can directly stimulate the secretion of GLP ‐1.