Parathyroid hormone and calcitonin may modulate hepatic IGF-I production in calves.

Four young milk-fed calves were fitted with catheters chronically implanted in the mesenteric, portal and hepatic veins and in the hepatic artery, and with electromagnetic blood flow probes in the portal vein and hepatic artery, allowing continuous measurement of IGF-I hepatic production. According to a latin square design, these calves received iv mesenteric infusion of calcium (Ca2+; 5 mg/kg) or synthetic salmon calcitonin (sCT; 1 microgram/kg), or synthetic bovine parathyroid hormone (1-34) (bPTH; 1 microgram/kg), or solvent alone (1.2 ml/kg). Ca2+, sCT or bPTH had no significant effect on portal vein or hepatic artery blood flow. Hypercalcemia observed following Ca2+ infusion did not significantly modify hepatic IGF-I production. sCT decreased plasma Ca2+, inorganic phosphorus and GH concentrations and hepatic IGF-I production. bPTH induced a slight hypercalcemia and hypophosphatemia. It had no significant effect on plasma GH concentration, but increased significantly hepatic IGF-I production. Thus, the anabolic effects of PTH on bone may be partly mediated through an increase in hepatic IGF-I production.