{{Rsnum
|rsid=6902123
|Gene=PPARD
|Chromosome=6
|position=35362644
|Orientation=plus
|GMAF=0.213
|Assembly=GRCh38
|GenomeBuild=38.1
|dbSNPBuild=141
|geno1=(C;C)
|geno2=(C;T)
|geno3=(T;T)
|Gene_s=PPARD
}}{{ population diversity
| geno1=(C;C)
| geno2=(C;T)
| geno3=(T;T)
| CEU | 0.0 | 15.4 | 84.6
| HCB | 0.0 | 11.1 | 88.9
| JPT | 0.0 | 9.3 | 90.7
| YRI | 59.0 | 36.1 | 4.9
| ASW | 0.0 | 0.0 | 0.0
| CHB | 0.0 | 11.1 | 88.9
| CHD | 0.0 | 0.0 | 0.0
| GIH | 0.0 | 0.0 | 0.0
| LWK | 0.0 | 0.0 | 0.0
| MEX | 0.0 | 0.0 | 0.0
| MKK | 0.0 | 0.0 | 0.0
| TSI | 0.0 | 0.0 | 0.0
| HapMapRevision=28
}}

{{PMID|18252792}} [[rs1053049]], [[rs6902123]], and [[rs2267668]] in PPARD affect Lifestyle Intervention induced changes in overall adiposity, hepatic fat storage, and relative muscle mass. Our findings provide a mechanistic explanation for the involvement of these genetic variations in the development of insulin resistance and [[type-2 diabetes]].

{{PMID|16804087}} Single nucleotide polymorphisms of PPARD in combination with the Gly482Ser substitution of PGC-1A and the Pro12Ala substitution of PPARG2 predict the conversion from impaired glucose tolerance to type 2 diabetes: the STOP-NIDDM trial.

{{PMID|18401448|OA=1
}} PPAR Genomics and Pharmacogenomics: Implications for Cardiovascular Disease.

{{on chip | 23andMe v3}}
{{on chip | 23andMe v4}}
{{on chip | HumanOmni1Quad}}