The effect of chronic insulin therapy on phosphate metabolism in diabetes mellitus

Abstract

Plasma and urine phosphate concentrations were improved in 21 patients with diabetes mellitus during "optimal" metabolic control as compared with "suboptimal" control. During the "suboptimal" control phase the daily insulin dosage averaged 38 +/- 22 (SD) U/day and the mean plasma glucose levels averaged 17.1 +/- 1.8 mmol/l, while during the "optimal" control phase the daily insulin dosage averaged 84 +/- 59 U/day and the mean plasma glucose level was 6.2 +/- 1.4 mmol/l. The institution of rigid diabetic control over 4-10 days significantly raised serum phosphorus from 1.12 +/- 0.16 to 1.26 +/- 0.19 mmol/l (p less than 0.001), and decreased urinary phosphorus excretion from 686 +/- 125 to 588 +/- 88 mg/day (p less than 0.001). These changes were associated with significant reductions in urinary calcium, urinary glucose, plasma immunoreactive glucagon and serum parathyroid hormone. This diminution in urinary phosphorus loss may have been due to diminished glycosuria but equally could have been influenced by a direct action of insulin on the renal tubule or suppression of glucagon and parathyroid hormone secretion. Under the conditions of this study, reduced urinary phosphorus may have been sufficient to cause a rise in serum phosphorus despite the known effects of insulin on the cellular influx of phosphorus.

Systemic bone marker expression induced by grey and white mineral trioxide aggregate in normal and diabetic conditions

“…The authors proposed that higher concentration of Fe 2 O 3 in GMTA may have an influence on Ca 2+ release. At the same time, an increase in the serum phosphorus level in diabetes has been reported (Raskin & Pak 1981). However, studies have shown that the phosphorus ions released after CaP precipitation reduced with time (Reyes-Carmona et al 2009).…”

“…Similarly, normal plasma calcium levels were reported in diabetic rats, despite an increase in renal calcium excretion (Anwana & Garland 1990). Raskin & Pak (1981) reported that an increase in the rate of renal phosphate reabsorption, coupled with a decrease in the urinary phosphorus loss, could be the reason behind the increase in the phosphorus levels in diabetes. In contrast, phosphorus levels of the WMTA group of healthy rats were higher than those of the diabetic group on day 7.…”

Effect of Glycemic Control on Calcium and Phosphorus Handling and Parathyroid Hormone Level in Patients with Non-Insulin-Dependent Diabetes Mellitus.

“…Our results revealed that urinary excretion of calcium and phosphorus increased relatively when the patients were poor in metabolic control. The enhanced urinary loss of calcium and phosphorus, related to urinary glucose excretion [11][12][13], became reduced in parallel with the improvement in glycemic control. The lowered serum phosphorus levels on admission were d ue to urinary loss of phosphorus, since they were positively correlated with the renal threshold for phosphorus excretion.…”

“…Also, serum osteocalcin concentrations are low in diabetic animals and human patients [7][8][9][10]. Urinary loss of minerals can be corrected by appropriate blood glucose control [11][12][13], but it remains unclear whether glycemic control has any effect on PTH secretion or bone turnover. The present study …”

Calciotrophic hormones during experimental hypocalcaemia and hypercalcaemia in spontaneously diabetic rats

“…In those studies in which ionised calcium (Ca 2+ ) was measured, a small but significant decrease has been documented in both diabetic children and adults (Fogh-Andersen et al 1983, Saggese et al 1988, Schwarz et al 1992; this decrease persisted during a calcium infusion (Amado et al 1987). Serum P concentrations were reported to be normal (Saggese et al 1988, Schwarz et al 1992, increased (Rødland et al 1985) or decreased (Auwerx et al 1988); intensifying the insulin therapy raised serum P levels (Raskin & Pak 1981). PTH concentrations, measured by immunoassays that detect the intact hormone, were found to be within the normal range in diabetic adults (Schwarz et al 1992, Gallacher et al 1993, but a rise in PTH levels was noted after improvement of glycaemic control (Thalassinos et al 1993); decreased levels of intact PTH were reported in diabetic children, with a sluggish response to a low-Ca diet (Saggese et al 1988).…”