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The present study, for the first time, demonstrates an underlying mechanism for the activation of eNOS by BPC 157 on stimulating the Cav-1 phosphorylation and reducing the binding of eNOS to Cav-1

Activation of PPAR in mice that were also treated with the PPAR agonist, rosiglitazone, prevented rosiglitazone-mediated increase of Ppargc1a and FAO-related gene expression and decreased mitochondrial number

Additionally, the use of tripeptides derived from animal sources, such as bovine and porcine, may raise social, religious, and cultural concerns