DOES INSULIN-RESISTANCE PARTICIPATE IN AN IMPAIRED GLUCOSE-TOLERANCE IN PRIMARY ALDOSTERONISM

It has been reported that glucose intolerance is occasionally found in primary aldosteronism. In this study, we measured insulin sensitivity by the euglycaemic hyperinsulinaemic glucose clamp technique and ability to release insulin by 75 g oral glucose tolerance test (OGTT) in primary aldosteronism. Seven patients with primary aldosteronism (PA) (53.7 +/- 3.4 years; mean +/- SEM) and eight normotensive subjects (NS) (57.5 +/- 2.6 years) were employed in this study. The two-hour euglycemic hyperinsulinaemic glucose clamp technique was performed in seven PA before adrenalectomy, six PA after adrenalectomy and eight NS. The 75 g OGTT was also done in five PA before and after adrenalectomy and eight NS. The mean rate of glucose infusion to maintain euglycemia for the last 30 minutes of the clamp technique was used as an indicator of insulin sensitivity (M-value). The total blood glucose levels during 75 g OGTT (area under the curves) (SIGMA blood glucose) were significantly higher in PA than those in NS, and the total insulin levels during 75 g OGTT (area under the curves) (SIGMA IRI) were significantly lower in PA than those in NS. After adrenalectomy in PA, blood glucose levels were significantly decreased and IRI were significantly increased compared with the normal range. There was a significant positive correlation (P < 0.05, r = 0.71) between serum potassium levels and IRI in PA which were determined before and after adrenalectomy. In PA, M-values (240.7 +/- 14.6 mg/m2/min). After adrenalectomy, M-values (188.7 +/- 17.1 mg/m2/min) decreased significantly compared with basal M-values (246.3 +/- 15.9 mg/m2/min), and returned to the normal ranges. These findings demonstrate that: (1) glucose intolerance in PA is caused by the suppression of insulin release related to hypopotassaemia, (2) compensatory increase of insulin sensitivity is observed in PA, and insulin sensitivity does not influence glucose intolerance in PA, and (3) elevated BP does not induce insulin resistance.