Endocrine Abstracts

Adiponectin, a recently discovered protein which is secreted by the adipose tissue, exerts anti-inflammatory and anti atherogenic properties, but also promotes glucose uptake by skeletal muscle and fatty acids oxidation. Patients with hypertension and obesity have reduced plasma levels of adiponectin so that they lack its beneficial metabolic effects. However no data are available in patients with primary aldosteronism (PA). In order to investigate the role of the adiponectin gene variants on glucose and lipids metabolism in patients with PA, we analysed data from 89 patients: 23 with aldosterone producing adenoma (APA) and 66 with idiopathic hyperaldosteronism (IHA). Two single nucleotide polimorphysms were studied, the T45G in exon 2 and the T276G in intron 2, using enzymatic restriction analysis. The same SNPs were also evaluated in 45 patients with essential hypertension (EH). No differences in genotype distribution were observed between PA and EH patients. Allele and genotype frequency distributions were in Hardy-Weinberg equilibrium for both SNPs in both PA and EH. Genotype distribution for T45G was: TT=63, GT=25, GG=1. No significant correlations were observed between genotype and allele distribution and blood pressure values nor glucose and lipid profiles. The G allele was associated with lower values of HOMA-IR (1.7±1.2 vs 3.9±4.7 P<0.05). Although not significantly different, the G allele was also associated to lower waist circumference values, lower serum aldosterone levels, plasma glucose and insulin after OGTT. Genotype distribution for T276G was: GG=51, GT=33, TT=5. The genotype 276 T/T was associated with higher levels of both systolic and diastolic blood pressure levels (P<0.005), tryglicerides (P<0.05), and fasting plasma glucose (P<0.005) and insulin levels (P<0.05). Moreover, the T allele was associated with higher values of HOMA-IR index (3.9±5.5 vs 2.6±1.8, P<0.05).

In conclusion, our data show that the genotype 45G/G-G/T has a protective role against the development of metabolic complications in PA patients, while the genotype 276 T/T defines PA patients with a worse glucose and lipids profiles.