The aim of this study was to elucidate the diabetic hypocalcemia and PTH responsiveness, investigated by measuring blood ionized calcium and serum intact parathyroid hormone (S-PTH(1–84)) concentrations, before and during an induced and maintained controlled hypocalcemia. In 15 patients with insulin-dependent diabetes mellitus and 19 healthy volunteers the blood ionized calcium concentration was lowered by about 0.20 mmol/l and maintained at this level by blood ionized calcium controlled tri-sodium-citrate infusion. In patients vs controls, baseline measurements averaged for blood ionized calcium (mmol/l) 1.18±0.08 vs 1.24±0.03 (p<0.01), for S-magnesium (mmol/l) 0.73±0.07 vs 0.81±0.07 (p<0.01) and for S-PTH (1–84) (pmol/l) 3.0±1.0 vs 3.1±1.0 (p>0.75). During the clamp. S-PTH (1–84) peaked to comparable maximums after 5–10 min in both groups and then declined to constant concentrations two to three times above their control levels. In conclusion, we found a diabetic hypocalcemia and hypomagnesemia, though baseline levels of PTH and PTH responsiveness were normal. This may be taken to indicate a mild shift downwards in the set-point for PTH secretion in patients with insulin-dependent diabetes mellitus.
The aim of the present study was to test a mathematical model of the biochemical processes in the parathyroid glands responsible for the secretion of parathyroid hormone resulting from extracellular calcium reduction. A double exponential curve described the parathyroid hormone secretion induced by rapid lowering of blood-ionized calcium in humans with normal as well as abnormal parathyroid tissue. Our data show that it was possible to establish a simple mathematical model of the parathyroid hormone response to blood-ionized calcium lowering, sufficient to fit experimental data obtained from patients with abnormal and normal parathyroid tissue. The fitted parameters showed no significant differences between patients with insulin-dependent diabetes mellitus and controls. In primary hyperparathyroidism, the parathyroid hormone production and steady-state transport across the cell membrane were increased, probably due to the larger amount of parathyroid tissue in these patients. These observations reveal a striking functional similarity between abnormal and normal parathyroid tissue. Furthermore, an apparently linear relationship between the rate of parathyroid hormone elimination from the blood plasma and the rate of cellular production/secretion was observed. This could be interpreted as an adaptation of the parathyroid gland's ability to produce parathyroid hormone depending on the average demand from the body.
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