PTH and primary hyperparathyroidism: In detail, in vitro data suggest a negative regulatory effect of both short-term (3 h) and long-term (6 days) treatment with PTH on FNDC5mRNA and protein expression in myotubes, by acting through the PTH receptor, which subsequently activates Erk1/2 phosphorylation, whereas plasma irisin has been shown to be lower among post-menopausal females with primary hyperparathyroidism than controls [34].