title: A possible association between primary aldosteronism and a lower beta-cell function.
abstract: 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.
  
  
  METHODS
  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), 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-betaF) 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, P = 0.854) were similar in both groups. HOMA-betaF 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 in both groups. Negative correlations between serum aldosterone/plasma renin activity (SA/PRA) ratio and HOMA-betaF, 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-betaF.
  
  
  CONCLUSIONS
  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.
authors: Department of Nutrition and Diabetes, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
authors: Lorena M
authors: LM
authors: Mosso
authors: Cristian A
authors: CA
authors: Carvajal
authors: Alberto
authors: A
authors: Maiz
authors: Eugenia H
authors: EH
authors: Ortiz
authors: Carmen R
authors: CR
authors: Castillo
authors: Rocío A
authors: RA
authors: Artigas
authors: Carlos E
authors: CE
authors: Fardella
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D006973:Hypertension / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D012083:Renin / Q000097:blood; D013148:Spironolactone / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin; D000451:Mineralocorticoid Receptor Antagonists; D014280:Triglycerides; D013148:Spironolactone; D000450:Aldosterone; D002784:Cholesterol; D012083:Renin