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dc.date.accessioned2013-03-12T12:39:32Z
dc.date.available2013-03-12T12:39:32Z
dc.date.issued2005en_US
dc.date.submitted2005-07-28en_US
dc.identifier.citationTøgersen, Kristine Elise. PRO12ALA POLYMORFISME I PPARg-GENET HOS DIABETIKERE. Prosjektoppgave, University of Oslo, 2005en_US
dc.identifier.urihttp://hdl.handle.net/10852/29511
dc.description.abstractBackground: The prevalence of type 2 diabetes mellitus has increased dramatically in the western societies over the last few decades. This is probably a result of increasing prevalence of obesity. Nevertheless, the ilness seems to have an important genetic component as well, being more frequent among certain ethnic groups and occurring more often in certain families. A Pro12Ala polymorphism has been detected in the gene coding for the receptor PPARg, which plays a significant role in adipocytt differentiation. Enhanced stimulation of PPARg seems to increase insulin sensitivity. The substitution of prolin to alanin probably results in conformational changes in the protein and thereby changes its activity. The frequency of the pro- allel in the population is 85%, where as the ala- allel represents 16%. We wanted to find out if people carrying the ala- allel where somehow protected against some of the co- factors known to accelerate the development of type 2 diabetes. Methods: We extracted DNA from 49 people with known type 2 diabetes and used PCR and gel electrophoresis to detect the genotypes. 40 people had the genotype pro/pro and 9 people had the genotype pro/ala. We then compared this information to quantified variables like waightgain, urinary albumin excretion, diastolic blood pressure, the presence of lipids in the blood and fat around the waistline. Then we used the student`s t- test to find out if the two groups differed significantly. Results and conclusions: We found no significant correlations between the presence of an ala- allel to protection against waightgain, increased diastolic blood pressure, higtened amounts of lipids in the blood and increased urinary albumin excretion. This might be due to our small sample and reduced statistical strength, or that there actually aro no difference between the two genotypes. Future research will probably highlight this issue to a greater extent.nor
dc.language.isonoben_US
dc.subjectmedisinsk genetikk
dc.titlePRO12ALA POLYMORFISME I PPARg-GENET HOS DIABETIKEREen_US
dc.typeMaster thesisen_US
dc.date.updated2005-09-08en_US
dc.creator.authorTøgersen, Kristine Eliseen_US
dc.subject.nsiVDP::714en_US
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft.au=Tøgersen, Kristine Elise&rft.title=PRO12ALA POLYMORFISME I PPARg-GENET HOS DIABETIKERE&rft.inst=University of Oslo&rft.date=2005&rft.degree=Prosjektoppgaveen_US
dc.identifier.urnURN:NBN:no-36966
dc.type.documentProsjektoppgaveen_US
dc.identifier.duo29003en_US
dc.contributor.supervisorPer Thorsbyen_US


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