A possible association between primary aldosteronism and a lower β-cell function

Objective Primary aldosteronism ( PA) is the most common secondary cause of hypertension and recently has been implicated as a cause of impaired glucose tolerance. We investigated the glucose insulin sensitivity and insulin secretion in patients with idiopathic primary aldosteronism. Design Thirty PA patients and 60 essential hypertensive ( EH) patients as controls were included, matched ( 1 : 2) by their body mass index ( BMI) ( 29.9 +/- 4.3 versus 29.8 +/- 5.8 m/ kg 2), age ( 53.7 +/- 9.4 versus 59.9 +/- 8.6 years old) and gender ( male/ female: 8/ 22 versus 17/ 43). In all patients, we measured insulin, total cholesterol, triglycerides, C- peptide and fasting glucose levels. Homeostasis model assessment for insulin resistance ( HOMA- IR) and HOMA of pancreatic beta- cell function ( HOMA- beta F) indexes were calculated. We also evaluated the response to spironolactone in 19 PA patients. Results PA patients had higher levels of glucose ( 5.2 +/- 0.7 versus 4.9 +/- 0.7 mmol/ l; P=0.017). Insulin levels ( 10.7 +/- 6.5 versus 11.5 +/- 5.8 uUI/ ml, P=0.525) and HOMA- IR ( 2.51 +/- 1.59 versus 2.45 +/- 1.29 uUI/ ml x mmol/ l, PU0.854) were similar in both groups. HOMA- bF index ( 138.9 +/- 89.8 versus 179.8 +/- 100.2%, P=0.049) and C- peptide ( 0.83 +/- 0.63 versus 1.56 +/- 0.84 ng/ dl, P=0.0001) were lower in PA patients. Potassium was normal inboth groups. Negative correlations between serum aldosterone/ plasma renin activity ( SA/ PRA) ratio and HOMA- beta F, and between C- peptide and SA levels were found in all patients. After the spironolactone treatment, we found an increase of C- peptide and insulin levels without changes in HOMA- IR or HOMA- beta F. Conclusion Our results showed differences in glucose metabolism between PA patients and those with hypertension suggesting that these findings could probably be determined by a lower beta- cell function influenced by aldosterone. These findings highlight the importance of aldosterone in glucose metabolism.