| Autor: |
Laverdure, Rose, Mezouari, Ania, Carson, Michael A., Basiliko, Nathan, Gagnon, Jeffrey |
| Zdroj: |
Endocrinology, Diabetes & Metabolism; January 2018, Vol. 1 Issue: 1 |
| Abstrakt: |
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, GImicroorganisms, 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 GImethanogens and that methane may play a role in the GLP-1 secretory response from the L cell. 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 GLUTag). 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 cAMPcontent. 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. Diet-induced weight gain in mice led to higher levels of the methanogen Methanobrevibacter smithii and higher levels of GLP-1 response. A direct stimulatory effect of methane on GLP-1 secretion was demonstrated in 2 different L-cell lines. |
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