ArticleFrontiers in cell and developmental biology2021
Loss of PDK1 Induces Meiotic Defects in Oocytes From Diabetic Mice.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- The roles of centrosome amplification in diabetes-associated diseases.Frontiers in cell and developmental biology · 2026Article
- Nicotinamide riboside supplementation protects against maternal diabetes-associated decline in oocyte quality.Reproduction (Cambridge, England) · 2025Article
- β-hydroxybutyrate impairs bovine oocyte maturation via pyruvate dehydrogenase (PDH) associated energy metabolism abnormality.Frontiers in pharmacology · 2023Article
- Pleiotropic Effects of IGF1 on the Oocyte.Cells · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
Maternal diabetes has been shown to impair oocyte quality; however, the underlying mechanisms remain unclear. Here, using a streptozotocin (STZ)-induced diabetic mouse model, we first detected and reduced expression of pyruvate dehydrogenase kinase 1 (PDK1) in diabetic oocytes, accompanying with the lowered phosphorylation of serine residue 232 on α subunit of the pyruvate dehydrogenase (PDH) complex (Ser232-PDHE1α). Importantly, forced expression of PDK1 not only elevated the phosphorylation level of Ser232-PDHE1α, but also partly prevented the spindle disorganization and chromosome misalignment in oocytes from diabetic mice, with no beneficial effects on metabolic dysfunction. Moreover, a phospho-mimetic S232D-PDHE1α mutant is also capable of ameliorating the maternal diabetes-associated meiotic defects. In sum, our data indicate that PDK1-controlled Ser232-PDHE1α phosphorylation pathway mediates the effects of diabetic environment on oocyte competence.
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