Metabolic Impacts of Diabetes on Oocyte Quality
Summary
Diabetes alters the metabolic landscape of the ovarian follicle, compromising oocyte competence through hyperglycaemia‐induced oxidative stress, mitochondrial dysfunction and disrupted energy homeostasis. Elevated blood glucose and insulin resistance perturb cumulus–oocyte communication, impairing substrate exchange and leading to aberrant reactive oxygen species accumulation. In turn, mitochondrial membrane potential declines, ATP synthesis falters and the balance of key metabolites is upset, compromising meiotic spindle assembly and chromosome alignment. Concomitant changes in histone modification and epigenetic regulators further erode oocyte developmental potential, manifesting as reduced maturation rates, delayed embryo cleavage and poorer pregnancy outcomes. Research has also highlighted alterations in key signalling pathways—such as AMPK, SIRT3 and pyruvate dehydrogenase complex regulation—underscoring how diabetes disrupts enzymatic control of energy flux. Together, these metabolic derangements have global significance for fertility, driving efforts to develop targeted interventions that restore redox balance, enhance mitochondrial resilience and optimise epigenetic integrity in diabetic oocytes.
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Metabolic Impacts of Diabetes on Oocyte Quality publication trend
The graph below shows the total number of articles in metabolic impacts of diabetes on oocyte quality across all publications each year (not limited to Nature Index journals).
Technical terms
Nicotinamide mononucleotide (NMN): A key precursor of NAD+, essential for mitochondrial energy metabolism and redox regulation.
Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen that, in excess, induce oxidative damage to cellular structures.
Meiotic spindle: A microtubule‐based structure responsible for accurate chromosome segregation during oocyte meiosis.
SIRT3: A mitochondrial deacetylase enzyme that regulates metabolic enzymes and maintains mitochondrial function under stress.
Pyruvate dehydrogenase kinase 1 (PDK1): An enzyme that phosphorylates and inactivates the pyruvate dehydrogenase complex, modulating the entry of glycolytic products into the tricarboxylic acid cycle.
References
- Nicotinamide Mononucleotide improves oocyte maturation of mice with type 1 diabetes. Nutrition & Diabetes (2024).
- Involvement of SIRT3‐GSK3β deacetylation pathway in the effects of maternal diabetes on oocyte meiosis. Cell Proliferation (2020).
- Loss of PDK1 Induces Meiotic Defects in Oocytes From Diabetic Mice. Frontiers in Cell and Developmental Biology (2021).
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