Lipoprotein lipase gene polymorphism and lipid profile in coronary artery disease.

CONTEXT: Lipoprotein lipase (LPL) plays a central role in lipid metabolism, hydrolyzing triglyceride in chylomicrons and very-low-density lipoproteins. The PvuII polymorphic variant of LPL gene is common and might affect risk of coronary artery disease (CAD). OBJECTIVE: Our aim was to determine whether LPL- PvuII polymorphism can be considered to be an independent risk factor or a predictor for CAD in Turkish subjects. DESIGN: We used polymerase chain reaction and restriction enzyme digestion to determine the distribution of the previously described C-->T transition that causes a PvuII polymorphism in intron 6 among healthy blood donors of Turkish origin and among angiographically confirmed CAD patients with comparable ethnic backgrounds. RESULTS: For the PvuII genotypes, within the CAD group (n = 80), the +/- genotype was found in 39 individuals (48.8%), whereas 25 (31.3%) carried the +/+ genotype, and 14 (17.5%) carried the -/- genotype. Within the control group (n = 49), the -/- genotype was found in 19 individuals (38.8%), 16 (32.7%) carried the +/- genotype, and 14 (28.6%) carried the +/+ genotype. The genotype frequency distribution was significantly different (P =.049) in the CAD and control study groups. The most frequent genotype among CAD patients was +/-; this genotype was more frequent in patients than in control subjects. However, the -/- genotype was more prevalent in the control group. Lipoprotein lipase-PvuII polymorphism was found to be associated with fasting total cholesterol and low-density lipoprotein cholesterol levels. The +/+ genotype was found to have higher levels of total cholesterol and low-density lipoprotein cholesterol in both the CAD and control groups. CONCLUSION: There was a difference in the distribution of LPL-PvuII genotypes between the healthy subjects and the patients with CAD. Lipoprotein lipase-PvuII polymorphisms were not detected as independent risk factors for CAD in this study group, but had associations with lipid levels.

Effect of abdominal obesity on insulin resistance and the components of the metabolic syndrome: evidence supporting obesity as the central feature.

BACKGROUND: Metabolic syndrome includes abdominal obesity, diabetes type 2, hypertension, dyslipidemia, derangements of fibrinolysis, and atherosclerosis. Since abdominal obesity is one of the major components of the insulin resistance syndrome (IRS), an attempt was made to evaluate the interrelationships between the magnitude of obesity and the components of the syndrome. METHODS: A cross-sectional study of 123 subjects with type 2 diabetes, of whom 31 were normal body weight and 92 had varying degrees of obesity was conducted. The participants were investigated in terms of clinical and laboratory findings of IRS. Fasting and 30-min (early) plasma glucose and serum insulin excursions in response to oral glucose challenge (75 g) were determined. The peripheral and hepatic insulin resistance (insensitivity) was calculated by homeostasis model assessment (HOMA). RESULTS: Clinical and biochemical findings were compared with the components of the IRS, and demonstrated that a rise in fasting as well as 30-min insulin secretion increases as abdominal body fat (obesity) increases. There was also a significant and proportional correlation between the magnitude of abdominal obesity and the components of metabolic syndrome. CONCLUSION: Abdominal adiposity appears to have a pivotal role in the development of IRS.

The interrelationship between insulin secretion and action in type 2 diabetes mellitus with different degrees of obesity: evidence supporting central obesity.

This paper investigates the relative role of the impairment of insulin secretion and action in the pathogenesis of Type 2 diabetes mellitus (T2DM). The parameters indicating insulin secretion and action were calculated from the data obtained during oral glucose tolerance test (OGTT), in 156 age- and sex-matched T2DM patients divided in 4 groups according to their body mass index (BMI, I = 20.0-24.9, II = 25.0-29.9, III = 30.0-39.9 and IV > 40.0 kg/m2). After obtaining baseline biomedical parameters (plasma glucose, serum insulin, cholesterol, HDL-cholesterol, triglycerides, BMI, and amount of fat tissue), the rates of insulin secretory capacity and insulin action were obtained from OGTT and compared between the T2DM patients with normal body weight and different grades of obesity. Beta-cell secretory capacity of the participants was found to be proportionally and significantly higher in graded obese than that of the normal body weight patients. The rates of hepatic as well as peripheral insulin resistance in obese groups proportionally and significantly rise in comparison with that of non-obese diabetics. In addition, these parameters are shown to be related to the body fat, presumably visceral in origin. In conclusion, hyperglycemia-hyperinsulinemia observed in obese and T2DM patients might be due, in part, to increased capacity of insulin secretion, and to exaggerated hepatic glucose production because of hepatic insulin resistance, respectively.