Leptin as an important link between obesity and cardiovascular risk factors in men with acute myocardial infarction.

OBJECTIVE: The levels of leptin, a major regulator of lipid metabolism, may increase in obesity, and contribute to the development of metabolic syndrome. Leptin is produced by adipose tissue and is a peptide hormone, which has strong association with obesity, elevated cardiovascular risk, and morbidity. The present study was designed to evaluate the relationships between leptin levels, obesity, and cardiovascular risk factors in men with acute myocardial infarction. METHODS AND RESULTS: Twenty-four obese and twenty-three nonobese male patients, who had experienced their first myocardial infarction, were included in the study. Their leptin levels, biochemical parameters, and anthropometric measures were obtained. Mean leptin levels were significantly higher in the obese group compared to the nonobese group (2.53ng/mL versus 1.23ng/mL; p<0.01). Leptin levels correlated positively with anthropometric measurements, triglyceride, fasting glucose, C-reactive protein, and uric acid levels, and negatively with high-density lipoprotein cholesterol levels. CONCLUSION: Findings indicate high leptin levels to be positively correlated with obesity and diastolic blood pressure in male patients with myocardial infarction.

Serum visfatin and fetuin-a levels and glycemic control in patients with obese type 2 diabetes mellitus.

BACKGROUND: Visfatin is an adipokine produced by visceral adipose tissue and has insulin-mimicking effects. Fetuin-A is a hepatic secretory protein that binds the insulin receptor and inhibits insulin action both in vivo and in vitro. The authors of the present study aimed to investigate the levels of serum visfatin and fetuin-A and their correlation with hemoglobin A1c (HbA1c) and urine albumin levels in patients with type 2 diabetes mellitus (T2DM). METHODS: A total of 40 obese patients with T2DM (11 males and 29 females; age, 54.47±10.83 years and 23 obese nondiabetic controls (8 males and 15 females; age, 53.04±11.33 years) were included in the study. Age, sex, and body mass index were similar in the 2 groups. Serum visfatin and fetuin-A levels were measured by enzyme-linked immunosorbent assay. HbA1c and urine albumin levels were measured by high performance liquid chromatography and nephelometric method, respectively. RESULTS: Serum levels of visfatin in patients with T2DM (4.03±2.44 ng/mL) were similar to the control group (3.65±3.02 ng/mL). Serum fetuin-A levels were significantly lower in patients with T2DM than the controls (298.75±78.86 and 430.73±94.46 µg/mL, respectively). HbA1c levels were significantly higher in the T2DM group compared with controls (7.33±1.32 and 5.44±0.84%, respectively). Correlations between visfatin, fetuin-A and HbA1c levels were not observed. CONCLUSION: The present study suggests fetuin-A may play a role in the pathogenesis of T2DM.