Influence of serum adiponectin level and SNP +45 polymorphism of adiponectin gene on myocardial fibrosis

Adiponectin plays an important role in the development of hypertension, atherosclerosis, and cardiomyocyte hypertrophy, but very little was known about the influence of serum adiponectin or the adiponectin gene polymorphism on myocardial fibrosis. Our study investigates the influence of the SNP +45 polymorphism of the adiponectin gene and serum levels of adiponectin on myocardial fibrosis in patients with essential hypertension. A case-control study was conducted on 165 hypertensive patients and 126 normotensive healthy controls. The genotypes of adiponectin gene polymorphisms were detected by the polymerase chain reaction (PCR) method. Serum concentrations of procollagen were measured by a double antibody sandwich enzyme-linked immunosorbent assay (ELISA) in all subjects. The integrated backscatter score (IBS) was measured in the left ventricular myocardium using echocardiography. The serum levels of adiponectin in hypertensive patients were significantly lower than those in the normal control group ((2.69±1.0) μg/ml vs. (4.21±2.89) μg/ml, respectively, P<0.001). The serum levels of type-I procollagen carboxyl end peptide (PICP) and type-III procollagen ammonia cardinal extremity peptide (PIIINP) in the hypertension group were significantly higher than those in the control group. In the hypertension group, serum levels of adiponectin were significantly and negatively related to the average acoustic intensity and corrected acoustic intensity of the myocardium (r=0.46 and 0.61, respectively, P<0.05 for both). The serum levels of PICP and PIIINP were significantly different among the three genotypes of SNP +45 (P<0.01). Logistic regression analyses showed that sex and genotype (GG+GT) were the major risk factors of myocardial fibrosis in hypertensive patients (OR=5.343 and 3.278, respectively, P<0.05). These data suggest that lower levels of adiponectin and SNP +45 polymorphism of the adiponectin gene are likely to play an important role in myocardial fibrosis in hypertensive patients.

Adiponectin plays an important role in the development of hypertension, atherosclerosis, and cardio- myocyte hypertrophy, but very little was known about the influence of serum adiponectin or the adiponectin gene polymorphism on myocardial fibrosis. Our study investigates the influence of the SNP ＋45 polymorphism of the adi- ponectin gene and serum levels of adiponectin on myocardial fibrosis in patients with essential hypertension. A case-control study was conducted on 165 hypertensive patients and 126 normotensive healthy controls. The geno- types of adiponectin gene polymorphisms were detected by the polymerase chain reaction （PCR） method. Serum concentrations of procollagen were measured by a double antibody sandwich enzyme-linked immunosorbent assay （ELISA） in all subjects. The integrated backscatter score （IBS） was measured in the left ventricular myocardium using echocardiography. The serum levels of adiponectin in hypertensive patients were significantly lower than those in the normal control group （（2.69±1.0） μg/ml vs. （4.21±2.89） μg/ml, respectively, P〈0.001）. The serum levels of type-Ⅰ procoilagen carboxyl end peptide （PiCP） and type-Ⅲprocollagen ammonia cardinal extremity peptide （PIIINP） in the hypertension group were significantly higher than those in the control group. In the hypertension group, serum levels of adiponectin were significantly and negatively related to the average acoustic intensity and corrected acoustic intensity of the myocardium （t=0.46 and 0.61, respectively, P〈0.05 for both）. The serum levels of PICP and PIIINP were sig- nificantly different among the three genotypes of SNP ＋45 （P〈0.01）. Logistic regression analyses showed that sex and genotype （GG＋GT） were the major risk factors of myocardial fibrosis in hypertensive patients （OR=5.343 and 3.278, respectively, P〈0.05）. These data suggest that lower levels of adiponectin and SNP ＋45 polymorphism of the adi- ponectin gene are likely to play an important role in myocardial fibrosis in hypertensive patients.