ArticleProceedings of the National Academy of Sciences of the United States of America2018
Chronic social stress-induced hyperglycemia in mice couples individual stress susceptibility to impaired spatial memory.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 92 citations in OpenAlex.
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- Association between hemoglobin glycation index and cognitive function: Evidence in the elderly.PloS one · 2026Article
- High glucose induces hippocampal neuron impairment through the SKP1/COX7C pathway: A potential mechanism for perimenopausal depression.Acta pharmaceutica Sinica. B · 2025Article
- Stress-induced dysfunction of neurovascular astrocytes in the prefrontal cortex contributes to sex-dependent deficits in cognition and behavior.Molecular psychiatry · 2025Article
- Diminished Social Memory and Hippocampal Correlates of Social Interactions in Chronic Social Defeat Stress Susceptibility.Biological psychiatry global open science · 2025Article
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- Transient impact of chronic social stress on effort-based reward motivation in non-food restricted mice: Involvement of corticosterone.Neurobiology of stress · 2024Article
- Inhibition of Glycolysis Alleviates Chronic Unpredictable Mild Stress Induced Neuroinflammation and Depression-like Behavior.Brain sciences · 2024Article
- Adaptations in hepatic glucose metabolism after chronic social defeat stress in mice.Scientific reports · 2024Article
- Article
- Stress-induced dysfunction of neurovascular astrocytes contributes to sex-specific behavioral deficits.bioRxiv : the preprint server for biology · 2024Article
- GLUT1-mediated microglial proinflammatory activation contributes to the development of stress-induced spatial learning and memory dysfunction in mice.Cell & bioscience · 2024Article
- Article
- A lone spike in blood glucose can enhance the thrombo-inflammatory response in cortical venules.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Therapeutic ketogenic diet as treatment for anorexia nervosa.Frontiers in nutrition · 2024Review
- Review
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stringent glucose demands render the brain susceptible to disturbances in the supply of this main source of energy, and chronic stress may constitute such a disruption. However, whether stress-associated cognitive impairments may arise from disturbed glucose regulation remains unclear. Here we show that chronic social defeat (CSD) stress in adult male mice induces hyperglycemia and directly affects spatial memory performance. Stressed mice developed hyperglycemia and impaired glucose metabolism peripherally as well as in the brain (demonstrated by PET and induced metabolic bioluminescence imaging), which was accompanied by hippocampus-related spatial memory impairments. Importantly, the cognitive and metabolic phenotype pertained to a subset of stressed mice and could be linked to early hyperglycemia 2 days post-CSD. Based on this criterion, ∼40% of the stressed mice had a high-glucose (glucose >150 mg/dL), stress-susceptible phenotype. The relevance of this biomarker emerges from the effects of the glucose-lowering sodium glucose cotransporter 2 inhibitor empagliflozin, because upon dietary treatment, mice identified as having high glucose demonstrated restored spatial memory and normalized glucose metabolism. Conversely, reducing glucose levels by empagliflozin in mice that did not display stress-induced hyperglycemia (resilient mice) impaired their default-intact spatial memory performance. We conclude that hyperglycemia developing early after chronic stress threatens long-term glucose homeostasis and causes spatial memory dysfunction. Our findings may explain the comorbidity between stress-related and metabolic disorders, such as depression and diabetes, and suggest that cognitive impairments in both types of disorders could originate from excessive cerebral glucose accumulation.
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