Adiponectin and Insulin Sensitivity in Primary Aldosteronism

• Published in: American journal of hypertension 2007-08, Vol.20 (8), p.855-861
• Main Authors: Fallo, Francesco, Della Mea, Paolo, Sonino, Nicoletta, Bertello, Chiara, Ermani, Mario, Vettor, Roberto, Veglio, Franco, Mulatero, Paolo
• Format: Article
• Language: English
• Subjects: Adiponectin; Adiponectin - blood; Adrenals. Adrenal axis. Renin-angiotensin system (diseases); Aldosterone - blood; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Biomarkers - blood; Blood and lymphatic vessels; Cardiology. Vascular system; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Female; Follow-Up Studies; Humans; Hyperaldosteronism - blood; Hyperaldosteronism - complications; Insulin - blood; insulin resistance; Insulin Resistance - physiology; Luminescent Measurements; Male; Medical sciences; Metabolic Syndrome - blood; Metabolic Syndrome - epidemiology; Metabolic Syndrome - etiology; Middle Aged; Non tumoral diseases. Target tissue resistance. Benign neoplasms; Potassium - blood; Prevalence; primary aldosteronism; Prognosis; Prospective Studies; Radioimmunoassay; Regression Analysis; Risk Factors
• ISSN: 0895-7061; 1879-1905; 1941-7225
• DOI: 10.1016/j.amjhyper.2007.03.012

A high prevalence of metabolic syndrome has been reported in primary aldosteronism. Low levels of adiponectin, an adipokine with insulin-sensitizing properties, are considered a hallmark of the metabolic syndrome. We evaluated the relationship between adiponectin and insulin sensitivity in primary aldosteronism, with and without metabolic syndrome, compared with essential hypertension. Forty patients with primary aldosteronism and 40 matched patients with low-renin essential hypertension (LREH) were studied. Patients with type 2 diabetes were excluded. Each group was divided into two subsets: one including patients with metabolic syndrome and one including patients without metabolic syndrome (ie, hypertension alone or associated with another component of the syndrome). Insulin resistance, defined by increased homeostasis model assessment (HOMA index), was higher in patients with primary aldosteronism than in those with LREH only in the absence of metabolic syndrome ( P < .01), whereas in the subsets bearing the syndrome it was similar. Adiponectin levels were lower in primary aldosteronism than in patients with LREH ( P < .01). Like HOMA index, the difference was maintained ( P < .01) only in the subsets without metabolic syndrome. Adiponectin levels were inversely correlated with HOMA index and positively correlated with potassium levels both in primary aldosteronism ( P < .001) or in LREH ( P < .05) groups. Lower adiponectin as well as lower insulin sensitivity in primary aldosteronism compared with LREH seem to result from both direct (aldosterone excess) and indirect (hypokalemia) mechanisms. Therapeutic interventions aimed at correcting both potassium and adiponectin levels by specific antihypertensive agents might improve insulin sensitivity, providing better cardiovascular protection in primary aldosteronism.