Hyperlipidemias: Schrezenmeir J

Pfeuffer M, Schrezenmeir J. · Institute for Physiology and Biochemistry of Nutrition, Federal Research Centre for Nutrition and Food, Kiel, Germany. · Obes Rev. · Pubmed #17300277 No free full text.

Abstract: The metabolic syndrome is a cluster of metabolic disorders, namely dyslipidaemia, hypertension, obesity and glucose intolerance. Insulin resistance is the core phenomenon. Co-occurrence is associated with increased cardiovascular disease (CVD) risk. Observational studies found no increased CVD risk with increasing consumption of milk and other dairy products. In several studies dairy consumption was inversely associated with the occurrence of one or several facets of the metabolic syndrome. Many dairy components may contribute to the beneficial effects. Milk and particularly whey appeared insulinotropic when given in a single meal, but not in longer-term intervention. Medium chain fatty acids improve insulin sensitivity. Whey proteins, amino acids, medium chain fatty acids and in particular calcium and other minerals may contribute to the beneficial effect of dairy products on body weight and body fat. Peptides, calcium and other minerals reduce blood pressure. Fermented products and probiotic bacteria decrease absorption of cholesterol, sphingomyelin of cholesterol and fat, calcium of cholesterol, bile acids and fat. Proteins, peptides and bacteria may also reduce plasma cholesterol. Lactose, citrate, proteins and peptides improve weight control, blood pressure and plasma lipids indirectly, by improving calcium bioavailability. Furthermore, dairy consumption improves the bioavailability of folate and other secondary plant components.

Steinmetz A, Fenselau S, Schrezenmeir J. · St. Nikolaus-Stiftshospital, Teaching Hospital, University of Bonn at Andernach, Germany. Armin.Steinmetz@Stiftshospital-Andernach · Exp Clin Endocrinol Diabetes. · Pubmed #11453042 No free full text.

Abstract: The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk to develop cardiovascular disease. The metabolic syndrome is characterized by atherogenic dyslipidemia (elevated triglycerides, increased small dense low-density lipoproteins, and decreased high-density lipoproteins), hypertension, insulin resistance and obesity. To decrease the risk of cardiovascular disease events decreasing body weight by ingesting a healthy diet, increasing physical activity, cessation of smoking and managing dyslipidemia are recommended. Pharmacological treatment of dyslipidemia is based on different drug classes. For LDL-cholesterol-lowering mainly statins and for triglyceride-lowering mainly fibrates are used. In primary and secondary prevention trials of heart disease they have shown to reduce the incidence of coronary artery disease or coronary events by 25-60 percent. Statins reduce mainly LDL-cholesterol levels by competitive inhibition of HMG-CoA reductase but have also shown to reduce fasting and postprandial triglyceride levels. Fibrates effectively reduce fasting and postprandial lipemia, shift the distribution of LDL particles towards less dense particles and increase HDL-cholesterol. Thus fibrates particularly address components of the metabolic syndrome and features of diabetic dyslipidemia. However studies still are needed showing definite evidence on differential therapy in lipid lowering based on prospective controlled trials with endpoints of macro- and microangiopathy in diabetic patients.

Helwig U, Rubin D, Klapper M, Li Y, Nothnagel M, Fölsch UR, Döring F, Schreiber S, Schrezenmeir J. · Institute of Physiology and Biochemistry of Nutrition, Federal Research Centre for Nutrition and Food, 24103 Kiel, Germany. <> · Metabolism. · Pubmed #17512303 No free full text.

Abstract: Studies on the association of fatty acid-binding protein 2 (FABP2) A54T and promoter polymorphism, and type 2 diabetes mellitus, insulin, and triglyceride levels are controversial. The aim of this study was to investigate the interfering effect of FABP2 A54T and promoter polymorphism on the postprandial response to a mixed meal and an oral glucose load. Seven hundred men from the Metabolic Intervention Cohort Kiel underwent a standard glucose tolerance test and a standardized mixed meal test and were genotyped by use of the Taqman method. When calculated independently from promoter variability, postprandial triglyceride levels were significantly higher and postprandial insulin sensitivity (homeostasis model assessment index) was lower in homozygous carriers of FABP2 T54T compared with carriers of the FABP2 exon wild-type allele (FABP2 A54A and A54T). This confirms previous findings. The effect of the exon T54T genotype on triglyceride levels and insulin sensitivity, however, was dependent on promoter variability. We found a significant increase in postprandial triglyceride levels and a decrease in insulin sensitivity due to T54T only in the presence of the homozygous B genotype at the promoter polymorphism. Similar results were obtained after oral glucose tolerance test. Reporter gene assays indicated a higher responsiveness to peroxisome proliferator-activating receptor-gamma (PPAR-gamma)/retinoid X receptor (RXR) of FABP2 promoter B vs promoter A. Synergism between a higher inducibility of FABP2 expression and a higher activity of T54 variant may explain higher postprandial triglycerides in case of combined genotype (promoter B + T54). This interference and different linkage disequilibrium between FABP2 exon and promoter polymorphisms may explain the different results obtained in different cohorts.