<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>20(2)</volume><submitter>Hashemian L</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Type 2 diabetes (T2DM) prevalence has been rapidly increasing in the last decades. T2DM pathogenesis is related to insulin resistance and beta-cell dysfunction. &lt;i>Peroxisome proliferator-activated receptor gamma (PPARG)&lt;/i> is concerned about T2DM risk through the involvement in adipocyte differentiation and energy homeostasis. The present study aimed to find the risk associated with a common genetic variant (Pro12Ala) of the &lt;i>PPARG&lt;/i> gene in the development of T2DM in a group of the Iranian population.&lt;h4>Methods&lt;/h4>Totally, 149 patients with T2DM and 96 healthy individuals were recruited in this case-control study. The genotyping of the genetic variant was carried out using the polymerase chain reaction (PCR) followed by Sanger sequencing.&lt;h4>Results&lt;/h4>No significant difference is observed between the CG and GG genotypes frequency of the &lt;i>PPARG&lt;/i> variant (&lt;i>P&lt;/i> = 0.17) in T2DM patient and the control groups. Furthermore, the frequency of the G allele was similar between case and control groups. The Pro12Ala variant may decrease the risk of diabetic retinopathy (DR) which was not statistically significant. Furthermore, the Pro12Ala variant caused a 27% increase in the risk of diabetes nephropathy (DN) among patients with T2DM but was not significant.&lt;h4>Conclusions&lt;/h4>Our findings showed that the &lt;i>PPARG&lt;/i> variant could not impact on T2DM development and its complications.</pubmed_abstract><journal>Journal of diabetes and metabolic disorders</journal><pagination>1385-1390</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8630345</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The role of the PPARG (Pro12Ala) common genetic variant on type 2 diabetes mellitus risk.</pubmed_title><pmcid>PMC8630345</pmcid><pubmed_authors>Hasanzad M</pubmed_authors><pubmed_authors>Sarhangi N</pubmed_authors><pubmed_authors>Aghaei Meybodi HR</pubmed_authors><pubmed_authors>Afshari M</pubmed_authors><pubmed_authors>Hashemian L</pubmed_authors></additional><is_claimable>false</is_claimable><name>The role of the PPARG (Pro12Ala) common genetic variant on type 2 diabetes mellitus risk.</name><description>&lt;h4>Background&lt;/h4>Type 2 diabetes (T2DM) prevalence has been rapidly increasing in the last decades. T2DM pathogenesis is related to insulin resistance and beta-cell dysfunction. &lt;i>Peroxisome proliferator-activated receptor gamma (PPARG)&lt;/i> is concerned about T2DM risk through the involvement in adipocyte differentiation and energy homeostasis. The present study aimed to find the risk associated with a common genetic variant (Pro12Ala) of the &lt;i>PPARG&lt;/i> gene in the development of T2DM in a group of the Iranian population.&lt;h4>Methods&lt;/h4>Totally, 149 patients with T2DM and 96 healthy individuals were recruited in this case-control study. The genotyping of the genetic variant was carried out using the polymerase chain reaction (PCR) followed by Sanger sequencing.&lt;h4>Results&lt;/h4>No significant difference is observed between the CG and GG genotypes frequency of the &lt;i>PPARG&lt;/i> variant (&lt;i>P&lt;/i> = 0.17) in T2DM patient and the control groups. Furthermore, the frequency of the G allele was similar between case and control groups. The Pro12Ala variant may decrease the risk of diabetic retinopathy (DR) which was not statistically significant. Furthermore, the Pro12Ala variant caused a 27% increase in the risk of diabetes nephropathy (DN) among patients with T2DM but was not significant.&lt;h4>Conclusions&lt;/h4>Our findings showed that the &lt;i>PPARG&lt;/i> variant could not impact on T2DM development and its complications.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2024-11-15T20:17:15.932Z</modification><creation>2024-11-15T20:17:15.932Z</creation></dates><accession>S-EPMC8630345</accession><cross_references><pubmed>34900790</pubmed><doi>10.1007/s40200-021-00872-6</doi></cross_references></HashMap>