AI Article Synopsis
- Previous research highlights the role of IL-17A in regulating gut microbiota and overall metabolic functions, but the specific site of IL-17RA signaling has not been explored.
- Using specific mouse models that lack IL-17RA in either the intestines or liver, the study found that gut IL-17RA signaling is crucial for managing metabolic functions when exposed to a high-fat diet.
- Mice lacking intestinal IL-17RA exhibited negative effects like poor glucose metabolism, abnormal hormone levels, increased body fat, and greater liver fat accumulation, linking changes in gut microbiota to systemic glucose regulation.
Article Abstract
Previous studies indicate that IL-17A plays an important role in mediating the intestinal microbiota and systemic metabolic functions. However, it is not known where IL-17RA signaling occurs to mediate these effects. To investigate this question, we used intestinal epithelial-specific ( ) and liver-specific ( ) IL-17RA knockout mice as well as littermate control mice. Our results indicate that intestinal IL-17RA signaling helps mediate systemic metabolic functions upon exposure to prolonged high-fat diet. mice display impaired glucose metabolism, altered hormone and adipokine levels, increased visceral adiposity, and greater hepatic lipid deposition when compared with their littermate controls. We show that IL-17RA-driven changes in microbiota composition are responsible for regulating systemic glucose metabolism. Altogether, our data elucidate the importance of intestinal IL-17RA signaling in regulating high-fat diet-mediated systemic glucose and lipid metabolism.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8556717 | PMC |
| http://dx.doi.org/10.4049/jimmunol.2000986 | DOI Listing |
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