Sterol regulatory element-binding protein cleavage-activating protein (SCAP) and apolipoprotein E (apo E) regulate cellular and plasma lipid metabolism. Therefore, variations in the corresponding genes might influence weight reduction and obesity-associated metabolic changes. We investigated the relationships of SCAP (Ile796Val) and apo E polymorphisms on metabolic changes during weight reduction by using a 12-week very low-energy diet. Body composition, serum lipids, plasma glucose, and insulin were assessed in 78 healthy premenopausal women (initial body mass index, 34 +/- 4 kg/m(2); age, 40 +/- 4 years) before and after the intervention. The SCAP genotype groups did not differ in the responses of any parameters measured during weight reduction. Apo E did not differentiate the weight loss, but the changes in total and low-density lipoprotein cholesterol for the genotype groups apo E epsilon2/3, epsilon3/3, as well as epsilon3/4 and epsilon4/4 combined were -0.94 +/- 0.56 and -0.59 +/- 0.32, -0.71 +/- 0.49 and -0.49 +/- 0.45, and -0.55 +/- 0.47 and -0.37 +/- 0.39 mmol/L, respectively (P < .05 for both). In conclusion, neither the SCAP Ile796Val nor the apo E polymorphism was associated with weight loss in obese premenopausal women. However, the apo E-but not SCAP genotype-seems to be one of the modifying factors for serum cholesterol concentrations during very low-energy diet in obese premenopausal women.

The -219G/T (rs405509) and +113G/C (rs440446) polymorphisms within the regulatory region of the apolipoprotein E (APOE) gene have been related to the transcriptional activity of the gene. We examined the effect of the stated polymorphisms and their construct haplotypes with the APOE ɛ2/ɛ3/ɛ4 polymorphism on lipid levels and insulin resistance in the Turkish Adult Risk Factor Study. Randomly selected 1774 adults (mean age, 55.0 ± 11.7 years; 51.2% women) participating in the population-based Turkish Adult Risk Factor Study were cross-sectionally analyzed for the -219G/T, +113G/C, and ɛ2/ɛ3/ɛ4 polymorphisms as well as their haplotypes. Insulin resistance was defined as the 70th percentile in the sample (>2.51) of the homeostatic model assessment (HOMA). The frequencies of the -219T and +113C alleles were 0.477 and 0.423, respectively; and those of haplotype 1 (GGɛ3) and haplotype 2 (TCɛ3) were 44.1% and 41.9%, respectively. The -219G/T and +113G/C genotypes (both P < .04) and diplotypes of haplotype 2 (TCɛ3) (P < .014) were inversely related to serum fasting insulin and the HOMA index, even after controlling for 8 relevant covariates, but not to serum lipids. Within the APOE3 group, haplotype 2 (TC-/TC+) heterozygotes had an odds ratio of 0.66 (95% confidence interval, 0.42-0.99) for HOMA of insulin resistance after adjusting for 8 covariates. APOE promoter polymorphisms and their diplotypes are independently related with serum fasting insulin levels and HOMA index among Turks.

Decrease in adiponectin level, a common feature in patients with type 2 diabetes mellitus, is considered to predict cardiovascular events. Elevated oxidized low-density lipoprotein (oxLDL), formed within the arterial wall, is commonly seen as part of the atherogenic profile. We investigated the association of adiponectin and oxLDL in 58 patients with type 2 diabetes mellitus and ischemic coronary artery disease. In addition to adiponectin, the serum lipid profile (including oxLDL), plasminogen activator inhibitor 1, high-sensitivity C-reactive protein, and whole-body glucose uptake determined by euglycemic-hyperinsulinemic clamp were evaluated. The average adiponectin level was 7.1 +/- 3.5 microg/mL and was higher in female than in male patients (P = .011). Adiponectin level correlated with whole-body glucose uptake (P = .037) and high-density lipoprotein (HDL) cholesterol concentration (P = .007) and was inversely associated with oxLDL (P = .005), triglycerides (P = .010), and plasminogen activator inhibitor 1 (P = .004). No association was found between adiponectin and high-sensitivity C-reactive protein or LDL cholesterol levels. In multiple linear regression analysis, adiponectin contributed to oxLDL concentration, whereas total cholesterol, LDL and HDL cholesterol, and triglycerides did not. In conclusion, our results suggest that low adiponectin concentration indicates increased oxidative state in the arterial wall, which further supports previous data on the role of adipose tissue in atherogenesis.