In conclusion, we have reported here a novel mechanism by which gut dysbiosis associated with late‐stage muscular dystrophy in mdx mice may participate in some of the features of this disorder through the reduced release of SCFAs in the blood and impaired GPR109A and PPARγ activation in skeletal muscle, with subsequent disinhibition of endocannabinoid signaling at CB1 receptors and exacerbation of inflammation and autophagy deficit in this tissue. Here, HCAR2 is linked to muscular dystrophy.