Ordoñez Llanos, Jorge

Rechi Lasala, Anna

Universitat Autònoma de Barcelona. Facultat de Biociències

Ordóñez, J. (Jordi)

Diposit Digital de Documents de la UAB

Legend             B48, APOB: apolipoprotein B48 IDL-C: Intermediate Density Lipoprotein-Cholesterol LPL: lipoprotein lipase B100, APOB: apolipoprotein B100 VLDL-C: Very Low Density Lipoprotein-Cholesterol HL, LIPC: hepatic lipase A1, APOA1: apolipoprotein A1 LDL-C: Low Density Lipoprotein-Cholesterol FA: fatty acids A4, APOA4: apolipoprotein A4 HDL: High Density Lipoprotein SFA: saturated fatty acids E, APOE: apolipoprotein E TAGs: Tryacylglycerides PUFA: polyunsaturated fatty acids CM: chylomicrons LDLR: Low Density Lipoprotein receptor MUFA: monounsaturated fatty acids rCM: remnant chylomicrons LDL-ox: oxidated Low Density Lipoprotein CHO: Carbohidrates RESULTS                                         Figure 2. Polymorphisms associated with cardiovascular risk (CV risk) described in lipoprotein metabolism genes. CV risk vary depending on diet interventions.             Variants conferring more CV risk: APOE: -219G/T, ε2/ε2 and ε4/ε4 APOA4: Thr347Ser APOB: -516C/T and Gly4154Leu + Ala3611Gly            Variants conferring less CV risk: APOA1: -75G/A APOA4: Thr347Ser and Gln360His APOA1 and APOA4 (combined): -75G/A and Thr347Ser,respectively             Figure 1. Lipoprotein metabolism pathway. In orange, apolipoproteins whose genetic variations has been described. HL variations also described. Enterocytes get dietary fat, then cholesterol is transported to the liver by chylomicrons and to peripheral tissues by LDL particles. Cholesterol reverse transport allow its elimination by the liver through the HDL particles. CONCLUSIONS  APOE, APOA1, APOA4 and APOB genes showed responses to different diet interventions, but LIPC gene did not.  There are evidences associating polymorphisms with diet compounds, which is traduced in changes in lipid metabolism, but it is needed more information to consider nutrigenomics for the clinical practise. Genomic studies have to be performed, but also it is important not to set aside other factors, to determine CV risk and set a personalized medicine in each case, focusing  specially in genetic individual variations.  It is still far reducing CV risk and, as a consequence, the morbidity and mortality of CVD, applying nutrigenomics. However, the knowledge of variants and interactions will allow to treat patients, reducing their risk factors by performing different diet interventions depending on the genotype. Variation in cardiovascular risk due to polymorphisms in lipoproteins and application of nutrigenomics Anna Rechi Lasala, Biomedical Sciences, Biosciences School, Universitat Autònoma de Barcelona.  INTRODUCTION  Cardiovascular risk (CV risk) is determined by genetic and acquired factors. They both involve hypertension, dyslipemia and diabetes, key factors to develop cardiovascular diseases (CVD). In addition to other risk factors, lipoprotein levels are used to determine  the CV risk on an individual. However, it exists variability between individuals with the same profile. This can be explained by genetic variations that modify CV risk. Diet is an environmental factor that involve individual variation. Different studies have been performed to analyse individual response to different diet interventions, depending on the genotype. This review collects the most relevant information about APOE, APOA, APOB and LIPC genes involving lipoprotein level variations. STATE OF THE ART  In the last two decades, it has been described the role of diet in individual variations, depending on the genetic profile. However, to consolidate this information, it is necessary to replicate these studies with more patients. This will clarify some contradictory results produced for the low number of subjects with uncommon variations. Currently, the knowledge is lack of soundness.  Expected short term goals:  To discriminate those SNPs that drive to functional protein alterations in order to reduce wrong associations.  To predict interactions: several genes interacting with several diet compounds lead to different phenotypes. Use of transcriptomics, proteomics and metabolomics to progress in the field of nutrigenomics.  To standardize study designs to make data collection easier, classifying the subjects depending on their characteristics.  To create consortiums to increase the number of subjects GOALS  • To analyze the connection between polymorphisms in genes involved in lipoprotein metabolism and CV risk.  • To evaluate the implication of nutrigenomics in the prevention or treatment of CVD in high risk individuals.  METHODS  The search of the bibliography has been performed in the data base Medline using the key words: polymorphisms, lipoproteins and cardiovascular biomarkers. Among the 28 papers found, 12 has been used. AKNOWLEDGMENTS                 Thanks to Dr. Jordi Ordóñez. 

Variation in cardiovascular risk due to polymorphisms in lipoproteins and application of nutrigenomics

http://ddd.uab.cat/pub/tfg/2013/113451/TFG_annarechilasala.pdf

Variation in cardiovascular risk due to polymorphisms in lipoproteins and application of nutrigenomics

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