{"id":{"repo_id":"sherbrooke","oai_identifier":"oai:usherbrooke.scholaris.ca:11143/18383"},"canonical_url":"https://search.dev.ndltd.org/etd/sherbrooke/oai:usherbrooke.scholaris.ca:11143/18383","repository":{"repo_id":"sherbrooke","name":"Université de Sherbrooke","base_url":"https://usherbrooke.scholaris.ca/server/oai/request"},"display":{"title":"Metabolism of omega-3 fatty acids in carriers of apolipoprotein E epsilon 4","abstract":"According to world health organization, 50 million individuals live with dementia, where Alzheimer’s disease represents 60 to 70% of those cases. Carrying the apolipoprotein E epsilon 4 allele (APOE4) is the main genetic risk factor for late onset Alzheimer’s disease. Studies have found that consuming a diet rich in omega-3 fatty acids such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) can decrease the risk of developing Alzheimer’s disease. However, the benefit of consuming omega-3 fatty acids is not seen in APOE4 carriers. Additionally, studies have demonstrated that brain can take-in fatty acids in the lysophosphatidylcholine (LPC) and free fatty acid (FFA) compartments. Therefore, we hypothesized that after consuming omega-3 fatty acid supplements for six months, APOE4 carriers’ plasma omega-3 fatty acid levels would not increase in the LPC and FFA plasma lipid compartments compared to non-carriers of the APOE4. To investigate this, we analysed DHA and EPA concentrations in the following plasma lipid compartments: LPC, phosphatidylcholine (PC), phosphatidylethanolamine (PE), FFA, triglyceride (TG) and cholesteryl esters (CE). Firstly, lipids were extracted from the plasma and then separated into CE, TG, FFA, and PL using thin layer chromatography. PL were further separated into PE, PC and LPC using a second thin layer chromatography plate. The fatty acids in the separated lipid compartments were converted to fatty acid methyl ester to be analysed using gas chromatography. In the current study, post-omega-3 fatty acid supplementation for six months, plasma DHA and EPA levels increased in all the lipid compartments analyzed. Additionally, there was a genotype trend for DHA in CE, where APOE4 carriers had higher levels of DHA compared to non-carriers before and after omega-3 supplementation. When comparing ΔDHA and ΔEPA (pre – post concentration) in the different lipid compartments between low and high body mass index (BMI) groups (<25.2 kg/m2 and >25.2 kg/m2, respectively) and genotype, plasma concentration of DHA and EPA in LPC of individuals in the high BMI group did not increase as much as those in the low BMI group after taking omega-3 fatty acids. Therefore, individuals in the high BMI group had less DHA available in the lipid compartment the brain can take-in. In conclusion, our research hypothesis is rejected as our results suggests supplementation with omega-3 fatty acids could benefit APOE4 carriers since DHA and EPA levels are higher in the plasma compartments where uptake of omega-3 fatty acids are possible by the brain.","abstract_html":"According to world health organization, 50 million individuals live with dementia, where Alzheimer’s disease represents 60 to 70% of those cases. Carrying the apolipoprotein E epsilon 4 allele (APOE4) is the main genetic risk factor for late onset Alzheimer’s disease. Studies have found that consuming a diet rich in omega-3 fatty acids such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) can decrease the risk of developing Alzheimer’s disease. However, the benefit of consuming omega-3 fatty acids is not seen in APOE4 carriers. Additionally, studies have demonstrated that brain can take-in fatty acids in the lysophosphatidylcholine (LPC) and free fatty acid (FFA) compartments. Therefore, we hypothesized that after consuming omega-3 fatty acid supplements for six months, APOE4 carriers’ plasma omega-3 fatty acid levels would not increase in the LPC and FFA plasma lipid compartments compared to non-carriers of the APOE4. To investigate this, we analysed DHA and EPA concentrations in the following plasma lipid compartments: LPC, phosphatidylcholine (PC), phosphatidylethanolamine (PE), FFA, triglyceride (TG) and cholesteryl esters (CE). Firstly, lipids were extracted from the plasma and then separated into CE, TG, FFA, and PL using thin layer chromatography. PL were further separated into PE, PC and LPC using a second thin layer chromatography plate. The fatty acids in the separated lipid compartments were converted to fatty acid methyl ester to be analysed using gas chromatography. In the current study, post-omega-3 fatty acid supplementation for six months, plasma DHA and EPA levels increased in all the lipid compartments analyzed. Additionally, there was a genotype trend for DHA in CE, where APOE4 carriers had higher levels of DHA compared to non-carriers before and after omega-3 supplementation. When comparing ΔDHA and ΔEPA (pre – post concentration) in the different lipid compartments between low and high body mass index (BMI) groups (&lt;25.2 kg/m2 and &gt;25.2 kg/m2, respectively) and genotype, plasma concentration of DHA and EPA in LPC of individuals in the high BMI group did not increase as much as those in the low BMI group after taking omega-3 fatty acids. Therefore, individuals in the high BMI group had less DHA available in the lipid compartment the brain can take-in. In conclusion, our research hypothesis is rejected as our results suggests supplementation with omega-3 fatty acids could benefit APOE4 carriers since DHA and EPA levels are higher in the plasma compartments where uptake of omega-3 fatty acids are possible by the brain.","abstract_has_math":false,"creators":["Balakrishnan, Janani"],"institution":"Université de Sherbrooke","degree_name":"M. Sc.","degree_level":"Maîtrise","degree_discipline":"Physiologie","degree_department":null,"school":null,"contributors":[],"advisors":["Plourde, Mélanie"],"committee_chairs":[],"committee_members":[],"year":2021,"date_issued":"2021","date_published":"2021","updated_at":"2026-07-27T21:07:32Z","subjects":["Omega-3 fatty acids","Fatty acid metabolism","APOE4","Cognitive decline","Alzheimer's disease","Acides gras oméga-3","Métabolisme des acides gras","Déclin cognitive"],"languages":["en"],"rights":[],"rights_urls":["http://creativecommons.org/licenses/by-nc-nd/2.5/ca/"],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/11143/18383","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Plourde, Mélanie"]},{"key":"dc:creator","label":"Author","values":["Balakrishnan, Janani"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2021-05-20T18:05:46Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2021-05-20T18:05:46Z"]},{"key":"dc:date.issued","label":"Date","values":["2021"]},{"key":"dc:publisher","label":"Institution","values":["Université de Sherbrooke"]},{"key":"dc:type","label":"Dc Type","values":["Mémoire de maîtrise"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Physiologie"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Maîtrise"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M. 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Carrying the apolipoprotein E epsilon 4 allele (APOE4) is the main genetic risk factor for late onset Alzheimer’s disease. Studies have found that consuming a diet rich in omega-3 fatty acids such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) can decrease the risk of developing Alzheimer’s disease. However, the benefit of consuming omega-3 fatty acids is not seen in APOE4 carriers. Additionally, studies have demonstrated that brain can take-in fatty acids in the lysophosphatidylcholine (LPC) and free fatty acid (FFA) compartments. Therefore, we hypothesized that after consuming omega-3 fatty acid supplements for six months, APOE4 carriers’ plasma omega-3 fatty acid levels would not increase in the LPC and FFA plasma lipid compartments compared to non-carriers of the APOE4. To investigate this, we analysed DHA and EPA concentrations in the following plasma lipid compartments: LPC, phosphatidylcholine (PC), phosphatidylethanolamine (PE), FFA, triglyceride (TG) and cholesteryl esters (CE). Firstly, lipids were extracted from the plasma and then separated into CE, TG, FFA, and PL using thin layer chromatography. PL were further separated into PE, PC and LPC using a second thin layer chromatography plate. The fatty acids in the separated lipid compartments were converted to fatty acid methyl ester to be analysed using gas chromatography. In the current study, post-omega-3 fatty acid supplementation for six months, plasma DHA and EPA levels increased in all the lipid compartments analyzed. Additionally, there was a genotype trend for DHA in CE, where APOE4 carriers had higher levels of DHA compared to non-carriers before and after omega-3 supplementation. When comparing ΔDHA and ΔEPA (pre – post concentration) in the different lipid compartments between low and high body mass index (BMI) groups (<25.2 kg/m2 and >25.2 kg/m2, respectively) and genotype, plasma concentration of DHA and EPA in LPC of individuals in the high BMI group did not increase as much as those in the low BMI group after taking omega-3 fatty acids. Therefore, individuals in the high BMI group had less DHA available in the lipid compartment the brain can take-in. In conclusion, our research hypothesis is rejected as our results suggests supplementation with omega-3 fatty acids could benefit APOE4 carriers since DHA and EPA levels are higher in the plasma compartments where uptake of omega-3 fatty acids are possible by the brain.","Selon l’organisation mondiale de la santé, 50 millions de personnes vivent avec la démence, où la maladie d’Alzheimer représente 60 à 70% de ces cas. Être porteur de l’allèle epsilon 4 de l’apolipoprotéine E (APOE4) est le principal facteur de risque génétique de la maladie d’Alzheimer tardive. Des études ont montré qu'une alimentation riche en acides gras (AG) oméga-3 comme l'acide docosahexaénoïque (DHA) et l'acide eicosapentaénoïque (EPA) peut réduire le risque de développer la maladie d'Alzheimer tardive. Cependant, l'avantage de la consommation d'AG oméga-3 n'est pas observé chez les porteurs de l'APOE4. De plus, des études ont démontré que le cerveau peut capter les AG lorsqu’ils sont estérifiés sous forme de lysophosphatidylcholine (LPC) ou lorsqu’ils ne sont pas estérifiés (FFA). Ainsi, notre hypothèse de recherche est qu’après avoir consommé des suppléments d’AG oméga-3 pendant six mois, l’augmentation de la concentration d’AG oméga-3 plasmatiques des porteurs de l’APOE4 n’augmente pas dans les LPC et FFA plasmatique par rapport aux non-porteurs de l’APOE4. Pour étudier cette hypothèse, nous avons analysé les concentrations plasmatiques de DHA et d'EPA dans les LPC, les phosphatidylcholines (PC), les phosphatidyléthanolamines (PE), les FFA, les triglycérides (TG) et les esters de cholestérol (CE). Les lipides totaux dans le plasma ont été extraits, puis séparés en CE, TG, FFA et phospholipides totaux en utilisant une chromatographie sur couche mince (CCM). Les PL ont par la suite été séparés en PE, PC et LPC en utilisant une deuxième plaque de CCM. Après avoir été convertis en ester méthylique d'AG, les AG méthylés ont été analysés par chromatographie en phase gazeuse. Après six mois de supplémentation en AG oméga-3, les concentrations plasmatiques de DHA et d'EPA ont augmenté dans tous les compartiments plasmatiques analysés. De plus, il y avait une tendance à ce que le DHA dans les CE soit plus élevé chez les porteurs de l'APOE4 comparativement aux non-porteurs. L’indice de masse corporelle a également affecté la réponse à la supplémentation. En effet, le ΔDHA et ΔEPA (pré - post concentration) n'a pas augmenté autant dans la LPC des individus ayant un indice de masse corporelle (IMC) élevé (>25,2 kg/m2) comparativement à ceux avec un IMC <25,2 kg/m2. Par conséquent, les participants du groupe à IMC élevé avaient moins de DHA disponible dans le compartiment plasmatique que le cerveau peut capter. En conclusion, notre hypothèse de recherche est infirmée ce qui suggère qu’une supplémentation en AG omega-3 pourrait bénéficier les porteurs de l’APOE4 puisque le DHA et l’EPA augmentent dans les compartiments plasmatiques qui permet la capture des AG omega-3 par le cerveau."]},{"key":"dc:title","label":"Title","values":["Metabolism of omega-3 fatty acids in carriers of apolipoprotein E epsilon 4"]}]}],"canonical_facts":{"dc:contributor.advisor":["Plourde, Mélanie"],"dc:creator":["Balakrishnan, Janani"],"dc:date.accessioned":["2021-05-20T18:05:46Z"],"dc:date.available":["2021-05-20T18:05:46Z"],"dc:date.issued":["2021"],"dc:description.abstract":["According to world health organization, 50 million individuals live with dementia, where Alzheimer’s disease represents 60 to 70% of those cases. Carrying the apolipoprotein E epsilon 4 allele (APOE4) is the main genetic risk factor for late onset Alzheimer’s disease. Studies have found that consuming a diet rich in omega-3 fatty acids such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) can decrease the risk of developing Alzheimer’s disease. However, the benefit of consuming omega-3 fatty acids is not seen in APOE4 carriers. Additionally, studies have demonstrated that brain can take-in fatty acids in the lysophosphatidylcholine (LPC) and free fatty acid (FFA) compartments. Therefore, we hypothesized that after consuming omega-3 fatty acid supplements for six months, APOE4 carriers’ plasma omega-3 fatty acid levels would not increase in the LPC and FFA plasma lipid compartments compared to non-carriers of the APOE4. To investigate this, we analysed DHA and EPA concentrations in the following plasma lipid compartments: LPC, phosphatidylcholine (PC), phosphatidylethanolamine (PE), FFA, triglyceride (TG) and cholesteryl esters (CE). Firstly, lipids were extracted from the plasma and then separated into CE, TG, FFA, and PL using thin layer chromatography. PL were further separated into PE, PC and LPC using a second thin layer chromatography plate. The fatty acids in the separated lipid compartments were converted to fatty acid methyl ester to be analysed using gas chromatography. In the current study, post-omega-3 fatty acid supplementation for six months, plasma DHA and EPA levels increased in all the lipid compartments analyzed. Additionally, there was a genotype trend for DHA in CE, where APOE4 carriers had higher levels of DHA compared to non-carriers before and after omega-3 supplementation. When comparing ΔDHA and ΔEPA (pre – post concentration) in the different lipid compartments between low and high body mass index (BMI) groups (<25.2 kg/m2 and >25.2 kg/m2, respectively) and genotype, plasma concentration of DHA and EPA in LPC of individuals in the high BMI group did not increase as much as those in the low BMI group after taking omega-3 fatty acids. Therefore, individuals in the high BMI group had less DHA available in the lipid compartment the brain can take-in. In conclusion, our research hypothesis is rejected as our results suggests supplementation with omega-3 fatty acids could benefit APOE4 carriers since DHA and EPA levels are higher in the plasma compartments where uptake of omega-3 fatty acids are possible by the brain.","Selon l’organisation mondiale de la santé, 50 millions de personnes vivent avec la démence, où la maladie d’Alzheimer représente 60 à 70% de ces cas. Être porteur de l’allèle epsilon 4 de l’apolipoprotéine E (APOE4) est le principal facteur de risque génétique de la maladie d’Alzheimer tardive. Des études ont montré qu'une alimentation riche en acides gras (AG) oméga-3 comme l'acide docosahexaénoïque (DHA) et l'acide eicosapentaénoïque (EPA) peut réduire le risque de développer la maladie d'Alzheimer tardive. Cependant, l'avantage de la consommation d'AG oméga-3 n'est pas observé chez les porteurs de l'APOE4. De plus, des études ont démontré que le cerveau peut capter les AG lorsqu’ils sont estérifiés sous forme de lysophosphatidylcholine (LPC) ou lorsqu’ils ne sont pas estérifiés (FFA). Ainsi, notre hypothèse de recherche est qu’après avoir consommé des suppléments d’AG oméga-3 pendant six mois, l’augmentation de la concentration d’AG oméga-3 plasmatiques des porteurs de l’APOE4 n’augmente pas dans les LPC et FFA plasmatique par rapport aux non-porteurs de l’APOE4. Pour étudier cette hypothèse, nous avons analysé les concentrations plasmatiques de DHA et d'EPA dans les LPC, les phosphatidylcholines (PC), les phosphatidyléthanolamines (PE), les FFA, les triglycérides (TG) et les esters de cholestérol (CE). Les lipides totaux dans le plasma ont été extraits, puis séparés en CE, TG, FFA et phospholipides totaux en utilisant une chromatographie sur couche mince (CCM). Les PL ont par la suite été séparés en PE, PC et LPC en utilisant une deuxième plaque de CCM. Après avoir été convertis en ester méthylique d'AG, les AG méthylés ont été analysés par chromatographie en phase gazeuse. Après six mois de supplémentation en AG oméga-3, les concentrations plasmatiques de DHA et d'EPA ont augmenté dans tous les compartiments plasmatiques analysés. De plus, il y avait une tendance à ce que le DHA dans les CE soit plus élevé chez les porteurs de l'APOE4 comparativement aux non-porteurs. L’indice de masse corporelle a également affecté la réponse à la supplémentation. En effet, le ΔDHA et ΔEPA (pré - post concentration) n'a pas augmenté autant dans la LPC des individus ayant un indice de masse corporelle (IMC) élevé (>25,2 kg/m2) comparativement à ceux avec un IMC <25,2 kg/m2. Par conséquent, les participants du groupe à IMC élevé avaient moins de DHA disponible dans le compartiment plasmatique que le cerveau peut capter. En conclusion, notre hypothèse de recherche est infirmée ce qui suggère qu’une supplémentation en AG omega-3 pourrait bénéficier les porteurs de l’APOE4 puisque le DHA et l’EPA augmentent dans les compartiments plasmatiques qui permet la capture des AG omega-3 par le cerveau."],"dc:identifier.uri":["http://hdl.handle.net/11143/18383"],"dc:language.iso":["en"],"dc:publisher":["Université de Sherbrooke"],"dc:rights.uri":["http://creativecommons.org/licenses/by-nc-nd/2.5/ca/"],"dc:subject":["Omega-3 fatty acids","Fatty acid metabolism","APOE4","Cognitive decline","Alzheimer's disease","Acides gras oméga-3","Métabolisme des acides gras","Déclin cognitive"],"dc:title":["Metabolism of omega-3 fatty acids in carriers of apolipoprotein E epsilon 4"],"dc:type":["Mémoire de maîtrise"],"thesis:degree_discipline":["Physiologie"],"thesis:degree_level":["Maîtrise"],"thesis:degree_name":["M. Sc."],"thesis:institution_name":["Faculté de médecine et des sciences de la santé"]},"updated_at":"2026-07-27T21:07:32Z"}