{{Rsnum
|rsid=1053049
|Gene=PPARD
|Chromosome=6
|position=35427841
|Orientation=plus
|GMAF=0.3214
|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 | 7.1 | 36.3 | 56.6
| HCB | 6.6 | 38.2 | 55.1
| JPT | 3.5 | 38.1 | 58.4
| YRI | 44.1 | 43.4 | 12.4
| ASW | 49.1 | 35.1 | 15.8
| CHB | 6.6 | 38.2 | 55.1
| CHD | 13.9 | 42.6 | 43.5
| GIH | 3.1 | 39.6 | 57.3
| LWK | 47.3 | 34.5 | 18.2
| MEX | 0.0 | 21.1 | 78.9
| MKK | 37.8 | 49.4 | 12.8
| TSI | 8.8 | 36.3 | 54.9
| 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|21331343|OA=1
}} The myocyte expression of adiponectin receptors and PPARdelta is highly coordinated and reflects lipid metabolism of the human donors.

{{on chip | 23andMe v1}}
{{on chip | 23andMe v2}}
{{on chip | 23andMe v3}}
{{on chip | 23andMe v4}}
{{on chip | FTDNA2}}
{{on chip | HumanOmni1Quad}}
{{on chip | Illumina Human 1M}}