The effect of calcium and other salts upon the release of glucagon-like immunoreactivity from the gut.

It has been suggested that glucagon-like immunoreactivity (GLI) of gastrointestinal tissues might, like pancreatic glucagon, have calcium-lowering activity. Studies were designed, therefore, to determine if calcium absorption was associated with GLI release from the gut. The intraduodenal administration of 4.5 mmoles of calcium chloride per kg of body weight to conscious dogs was associated with a prompt rise in plasma GLI from a base line of 2.2 ng/ml (SEM +/-0.2) to a peak of 4.3 ng/ml (SEM +/-0.3) at 45 and 60 min, in association with a rise of plasma calcium from 8.6 to 10.4 mg/100 ml. Neither pancreatic glucagon, insulin, nor glucose changed. Smaller calcium loads had progressively diminishing effects on GLI release. Calcium lactate also appeared to stimulate effectively GLI release. Both magnesium chloride and sodium chloride given intraduodenally were associated with a significant though modest increase in GLI. To determine if stimulation of GLI release by substances other than calcium would lower serum calcium, glucose was administered intraduodenally. Despite a marked increase in GLI, plasma calcium fell only 9%, a decline which could be entirely accounted for by hemodilution. Although the physiologic significance of this demonstration that the absorption of calcium salts is associated with GLI release is open to serious question, the findings are not incompatible with the concept that glucagon-like polypeptides are released from the gut during the absorption of certain salts, possibly to alert appropriate homeostatic regulators so as to avoid major changes in electrolyte concentration after the ingestion of large salt loads.