<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>39(5)</volume><submitter>Zhao Z</submitter><pubmed_abstract>&lt;h4>Purpose&lt;/h4>To investigate whether fatty acid changes in granulosa cells (GCs) underly the pathogenic mechanisms of diminished ovarian reserve (DOR).&lt;h4>Methods&lt;/h4>GCs were obtained from patients with DOR (n = 70) and normal ovarian reserve (NOR, n = 70). Analysis of fatty acids changes in GCs was then analyzed.&lt;h4>Results&lt;/h4>Patients with DOR had significantly lower levels of antral follicle count and anti-Mullerian hormone and higher levels of follicle-stimulating hormone compared with NOR patients (P &lt; 0.001). The good-quality embryo rate was notably decreased in DOR patients (51.99 vs 39.52%, P &lt; 0.05). A total of 15 significantly decreased fatty acids in GCs from patients with DOR. The ATP levels were markedly lower in DOR patients than in NOR patients (39.07 ± 12.89 vs 23.21 ± 13.69%, P &lt; 0.05). Mitochondrial membrane potential decreased in DOR patients (P &lt; 0.01). In GCs from DOR patients, the β-oxidation genes (HADHA and ACSL) and DNA repair genes (PRKDC and RAD50) were significantly downregulated (P &lt; 0.05). The γH2AX foci/nucleus ratio in DOR patients markedly increased relative to that of NOR patients (0.31 ± 0.03 vs 0.87 ± 0.07, P &lt; 0.001). Meanwhile, the apoptosis rate of GCs was significantly higher in DOR patients (6.43 ± 2.11 vs 48.06 ± 6.72%, P &lt; 0.01).&lt;h4>Conclusion&lt;/h4>GC apoptosis resulting from the decrease of fatty acids, and associated with reduced ATP production and DNA damage, may contribute to the pathogenic mechanisms responsible for DOR.</pubmed_abstract><journal>Journal of assisted reproduction and genetics</journal><pagination>1105-1114</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9107543</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Decreased fatty acids induced granulosa cell apoptosis in patients with diminished ovarian reserve.</pubmed_title><pmcid>PMC9107543</pmcid><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Liang X</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Fan Q</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors><pubmed_authors>Zhu Q</pubmed_authors><pubmed_authors>He R</pubmed_authors><pubmed_authors>Wang J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Decreased fatty acids induced granulosa cell apoptosis in patients with diminished ovarian reserve.</name><description>&lt;h4>Purpose&lt;/h4>To investigate whether fatty acid changes in granulosa cells (GCs) underly the pathogenic mechanisms of diminished ovarian reserve (DOR).&lt;h4>Methods&lt;/h4>GCs were obtained from patients with DOR (n = 70) and normal ovarian reserve (NOR, n = 70). Analysis of fatty acids changes in GCs was then analyzed.&lt;h4>Results&lt;/h4>Patients with DOR had significantly lower levels of antral follicle count and anti-Mullerian hormone and higher levels of follicle-stimulating hormone compared with NOR patients (P &lt; 0.001). The good-quality embryo rate was notably decreased in DOR patients (51.99 vs 39.52%, P &lt; 0.05). A total of 15 significantly decreased fatty acids in GCs from patients with DOR. The ATP levels were markedly lower in DOR patients than in NOR patients (39.07 ± 12.89 vs 23.21 ± 13.69%, P &lt; 0.05). Mitochondrial membrane potential decreased in DOR patients (P &lt; 0.01). In GCs from DOR patients, the β-oxidation genes (HADHA and ACSL) and DNA repair genes (PRKDC and RAD50) were significantly downregulated (P &lt; 0.05). The γH2AX foci/nucleus ratio in DOR patients markedly increased relative to that of NOR patients (0.31 ± 0.03 vs 0.87 ± 0.07, P &lt; 0.001). Meanwhile, the apoptosis rate of GCs was significantly higher in DOR patients (6.43 ± 2.11 vs 48.06 ± 6.72%, P &lt; 0.01).&lt;h4>Conclusion&lt;/h4>GC apoptosis resulting from the decrease of fatty acids, and associated with reduced ATP production and DNA damage, may contribute to the pathogenic mechanisms responsible for DOR.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 May</publication><modification>2025-04-04T09:19:22.467Z</modification><creation>2025-04-04T09:19:22.467Z</creation></dates><accession>S-EPMC9107543</accession><cross_references><pubmed>35347502</pubmed><doi>10.1007/s10815-022-02462-8</doi></cross_references></HashMap>