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BACKGROUND/OBJECTIVE: Blood proportions of fatty acids (FAs) and FA-ratios reflecting desaturase activity are associated with the risk of chronic diseases like type 2 diabetes mellitus or cardiovascular diseases. Biomarkers of dyslipidemia are considered as potential mediators of this association. We evaluated associations of erythrocyte membrane proportions of individual disease-related polyunsaturated fatty acids (PUFAs), trans-FAs, dairy-derived saturated FAs (SFAs) (15:0, 17:0) and FA-ratios with biomarkers of dyslipidemia (high-density lipoprotein (HDL)- cholesterol, low-density lipoprotein (LDL)-cholesterol, non-HDL-cholesterol, triglycerides). SUBJECTS/METHODS: We conducted a cross-sectional analysis of a subsample (n = 1759) of the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam study. Associations of individual FAs and FA-ratios with plasma biomarkers of dyslipidemia were evaluated by linear multivariable regression. RESULTS: Most notably, FA-ratios reflecting activity of Δ6-desaturase (D6D) and stearoyl-coenzyme A- desaturase (SCD) were positively associated with triglyceride and LDL-cholesterol concentrations (adjusted means (95% confidence interval (CI)) of triglycerides (mg/dl) across D6D tertiles: men--102 (94.7-110), 111 (104-120), 144 (134- 156) and women--73.5 (70.0-77.2), 82.9 (79.0-86.9), 94.2 (89.7-98.9));across SCD tertiles: men--99.0 (91.8-107), 115 (107-124), 144 (134-156) and women--72.4 (69.0-76.0), 81.5 (77.8-85.5), 97.2 (92.6-102)), whereas inverse associations with triglycerides were observed for the estimated A5-desaturase (D5D) activity (adjusted means (95% CI) of triglycerides (mg/dl) across D5D tertiles: men--128 (119-138), 121 (113-131), 106 (97.9-114) and women--92.0 (87.6- 96.6), 82.8 (78.9-86.9), 75.3 (71.6-79.1), P-values for trend at least 0.0006). Furthermore, we observed generally weaker and less consistent associations of dairy-derived SFAs (mainly 17:0) with triglycerides and HDL-cholesterol. Individual PUFAs and frans-FAs were, if at all, only weakly associated with dyslipidemia markers. CONCLUSIONS: Our findings suggest that triglyceride and LDL-cholesterol concentrations may be mediators that link intake and metabolism of FAs to metabolic risk. European Journal of Clinical Nutrition (2014) 68, 517-525; doi: 10.1038/ejcn.2014.18; published online 26 February 2014, INTRODUCTION The dietary intake and metabolism of fatty acids (FAs) is believed to have an important role in the etiology of chronic diseases such as type 2 diabetes mellitus (T2DM) [...]

Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle--triglyceride and--cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults., Introduction Studies investigating the effects of fructose consumption in humans and animals have been comprehensively reviewed (1), (2), (3), (4), and while strong evidence exists that consumption of diets high [...]

People who have the apolipoprotein (apo) E4 allele may have an increased risk of coronary heart disease (CHD). Apo E is a blood protein that can take different forms as determined by genetics. Alleles are alternative forms of a gene. Researchers examined and took blood samples from 1034 men and 916 women to evaluate the association between apo E alleles, abnormal blood fat levels, and CHD. Female patients with the apo E4 allele were more likely than male patients with the allele to have high total cholesterol levels and high low density lipoprotein levels than patients with the apo E2 allele. Both the E2 and E4 alleles were associated with moderately elevated triglyceride levels in men. Excessively high triglyceride levels were rare and occurred most often in men with the E2 allele. Fewer women over age 60 had the E4 allele compared to their younger counterparts. The E4 allele was associated with an increased risk of CHD in both men and women independent of CHD risk factors and blood lipid levels., Objective. - To describe the association between apolipoprotein E alleles ([epsilon]2, [epsilon]3, and [epsilon]4), dyslipidemias, and coronary heart disease (CHD). Design. - Cross-sectional prevalence study. Setting and Participants. - Community-based sample of men (n=1034) and women (n=916) aged 40 to 77 years who are participating in a long-term study of cardiovascular disease. Study participants underwent fasting lipid measurements, coronary risk factor determinations, and a comprehensive evaluation for the presence of current or previous CHD. Results. - Compared with the [epsilon]3 allele, the [epsilon]4 allele was associated with elevated low-density lipoprotein cholesterol values ([greater than or equal to]4.14 mmol/L [160 mg/dL]) in women, the [epsilon]2 and [epsilon]4 alleles were associated with moderately elevated triglyceride values ([greater than or equal to]2.82 mmo/L [250 mg/dL]) in men, and the [epsilon]2 allele was associated with severely elevated triglyceride values ([greater than or equal to]5.64 mmo/L [500 mg/dL]) in men. The apolipoprotein E alleles were not associated with hypertension, obesity, smoking, or diabetes, but the [epsilon]4 allele frequency was reduced in women after 60 years of age. The age-adjusted prevalence of CHD was associated when the [epsilon]4 allele in both men (relative odds=1.53, P=.04) and women (relative odds=1.99, P=.05). In analyses for women and for both sexes combined, this relation persisted after adjustment by hypertension, smoking, obesity, diabetes, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Conclusions. - Apolipoprotein E alleles are important genetic markers for dyslipidemia and CHD. The estimated CHD odds associated with the [epsilon]4 allele appears to be greater than that for any other known genetic lipid abnormality, and the association of the [epsilon]4 allele with CHD remains significant in women and both sexes combined after adjustment by traditional coronary desk factors and lipids.

Recent research has emphasized the importance of the metabolic cluster, which includes glucose intolerance, dyslipidemia, and high blood pressure, as a strong predictor of the obesity-related morbidities and premature mortality. Fundamental to this association, commonly referred to as the metabolic syndrome, is the close interaction between abdominal fat patterning, total body adiposity, and insulin resistance. As the initial step in identifying major genetic loci influencing these phenotypes, we performed a genomewide scan by using a 10-centiMorgan map in 2,209 individuals distributed over 507 nuclear Caucasian families. Pedigree-based analysis using a variance components linkage model demonstrated a quantitative trait locus (QTL) on chromosome 3 (3q27) strongly linked to six traits representing these fundamental phenotypes [logarithm of odds (lod) scores ranged from 2.4 to 3.5]. This QTL exhibited possible epistatic interaction with a second QTL on chromosome 17 (17p12) strongly linked to plasma leptin levels (lod = 5.0). Situated at these epistatic QTLs are candidate genes likely to influence two biologic precursor pathways of the metabolic syndrome.