Azza M. Abdel-Latif

Several environmental and genetic factors are associated with high levels of lipids in obese patients. Apolipoprotein B (ApoB) is the major protein component of low-density lipoproteins (LDL), very-low density lipoproteins (VLDL) and chylomicrons and plays a central role in lipid metabolism. Several apoB restriction fragment length polymorphisms (XbaI, EcoRI, MspI) have been reported to be associated with variation in lipid levels and obesity. To date, no data are available on the relationship between XbaI polymorphism and lipid levels in Egyptian populations. Following clinical profiling, 178 obese (body mass index [BMI] >25 kg/m2) and 178 age-matched non-obese (BMI ≤ 25 kg/m2) subjects were included in this case–control study. All samples were analysed for total cholesterol, triglycerides and HDL-cholesterol. Genetic analysis of apoB XbaI (X) was performed using Polymerase Chain Reaction-Restriction Fragment Length polymorphism (PCR-RFLP). The aim of this study was to assess the association of apoB XbaI gene polymorphism (X) and lipid profiles in obese and non-obese Egyptian populations. Obese subjects demonstrated significantly higher values of waist-to-hip ratio, blood pressure, and total lipid. However, in our sample we did not find significant differences in apoB XbaI gene polymorphism (X) genotype or allele frequencies. Moreover, none of the studied lipid parameters showed any association with the gene polymorphism. This study reveals no significant association of apoB XbaI gene polymorphism (X) with obesity or lipid profiles in an Egyptian population.

Background: Dipeptidyl Peptidase I (DPPI) is one of the essential components which initiate chain reaction for triggering the inflammatory response mediated allergic diseases such as asthma. Previous studies have reported that several mutations have been detected within the dipeptidyl peptidase I gene (CTSC) cause Papillon-Lefévre syndrome. It has been suggested that a mutation in this gene could give protection against the inflammatory response in allergic diseases. The aim of this study was to investigate wither the polymorphism (rs217086 (T153I)) in the gene for DPPI may be protective in asthma. Methods: To examine possible associations of DPP1 polymorphism with asthma susceptibility, we performed this study. 341 families with at least two siblings with asthma were genotyped for a CTSC polymorphism using high resolution melting curve analysis. Genetic association analysis was analysed using family based association tests (FBAT) and resultant called genotypes were sequenced. Results: DNA sequence data confirmed all variant genotypes. Analysis by FBAT showed no significant association between this polymorphism and asthma susceptibility or with any of asthma-related phenotypes tested. Conclusions: Our data proved that DPPI does not contribute substantially to susceptibility for asthma. Further studies examining both genotypes and environmental factors will be necessary to elucidate the role of DPPI in the development of allergic diseases.