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| http://purl.uniprot.org/citations/35472412 | http://www.w3.org/2000/01/rdf-schema#comment | "The testis expresses peroxisome proliferator-activated receptor-γ (PPAR-γ), but its involvement in regulating diabetes-induced testicular dysfunction and DNA damage repair is not known. Pioglitazone-induced activation of PPAR-γ for 12 weeks in db/db obese diabetic mice increases bodyweights and reduces blood glucose levels, but PPAR-γ inhibition by 2-chloro-5-nitro-N-phenylbenzamide does not alter these parameters; instead, improves testis and epididymis weights and sperm count. Neither activation nor inhibition of PPAR-γ normalizes the diabetes-induced seminiferous epithelial degeneration. The PPAR-γ activation normalizes testicular lipid peroxidation, but its inhibition reduces lipid peroxidation and oxidative DNA damage (8-oxo-dG) in diabetic mice. As a response to diabetes-induced oxidative DNA damage, the base-excision repair (BER) mechanism proteins-8-oxoguanine DNA glycosylases (OGG1/2) and X-ray repair cross-complementing protein-1 (XRCC1) increase, whereas the redox-factor-1 (REF1), DNA polymerase (pol) δ and poly (ADP-ribose) polymerase-1 (PARP1) show a tendency to increase suggesting an attempt to repair the oxidative DNA damage. The PPAR-γ stimulation inhibits OGG2, DNA pol δ, and XRCC1 in diabetic mice testes, but PPAR-γ inhibition reduces oxidative DNA damage and normalizes BER protein levels. In conclusion, type 2 diabetes negatively affects testicular structure and function and increases oxidative DNA damage and BER protein levels due to increased DNA damage. The PPAR-γ modulation does not significantly affect the structural changes in the testis. The PPAR-γ stimulation aggravates diabetes-induced effects on testis, including oxidative DNA damage and BER proteins, but PPAR-γ inhibition marginally recovers these diabetic effects indicating the involvement of the receptor in the reproductive effects of diabetes."xsd:string |
| http://purl.uniprot.org/citations/35472412 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cbi.2022.109958"xsd:string |
| http://purl.uniprot.org/citations/35472412 | http://purl.uniprot.org/core/author | "Kilarkaje N."xsd:string |
| http://purl.uniprot.org/citations/35472412 | http://purl.uniprot.org/core/author | "Al-Hussaini H."xsd:string |
| http://purl.uniprot.org/citations/35472412 | http://purl.uniprot.org/core/author | "Alfarhan M.W."xsd:string |
| http://purl.uniprot.org/citations/35472412 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35472412 | http://purl.uniprot.org/core/name | "Chem Biol Interact"xsd:string |
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| http://purl.uniprot.org/citations/35472412 | http://purl.uniprot.org/core/title | "Role of PPAR-gamma in diabetes-induced testicular dysfunction, oxidative DNA damage and repair in leptin receptor-deficient obese type 2 diabetic mice."xsd:string |
| http://purl.uniprot.org/citations/35472412 | http://purl.uniprot.org/core/volume | "361"xsd:string |
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