Does Exogenous Hypermagnesaemia Inhibit Insulin Secretion in Patients with Impaired Glucose Tolerance or Non-Insulin-Dependent Diabetes Mellitus?

Summary

Acute exogenous hypermagnesaemia in healthy subjects retards glucose assimilation (K_g) and inhibits B cell function. The glycoregulatory effect of hypermagnesaemia was investigated in the course of the intravenous glucose tolerance test (IVGTT) in 16 subjects, incl. eight with impaired glucose tolerance (IGT) and eight with noninsulin dependent diabetes mellitus (NIDDM). Hypermagnesaemia was induced by intravenous infusion of 6g MgSO₄. The secretory response of insulin (IRI) and C-peptide were expressed as the incremental area (IA of S-IRI and IA of S-C-peptide). The results were compared with control IVGTT following infusion of saline. Hypermagnesaemia did not affect glucose assimilation in subjects with IGT as compared with control values nor in subjects with NIDDM. Hypermagnesaemia did not change IA of S-IRI nor of S-C-peptide in IGT as compared with control values (IA of S-IRI were 4308±1126 vs 3309±610 μU/ml × min and IA of S-C-peptide 191±43 vs 177±46 ng/ml × min) (means±SEM). In NIDDM there was no significant difference between the response of C-peptide during hypermagnesaemia and the response during control IVGTT (IA were 72 ±20 ng/ml × min vs 73.5 ±22.4 ng/ml × min). As no significant insulin response to glucose was obtained after saline or magnesium in NIDDM, the effect of hypermagnesaemia was not possible to evaluate. In conclusion, no significant decline of glucose assimilation and B-cell function in IGT and NIDDM can be proved in the course of exogenous hypermagnesaemia. Intravenous administration of pharmacological amounts of magnesium does not involve the risk of deteriorated metabolic compensation in these patients.

Key words

Magnesium - Assimilation of Glucose - Insulin Secretion - Impaired Glucose Tolerance - NonInsulin-Dependent Diabetes Mellitus