Authors
Grace A Reese, Laura E Kusumo, Madilyn Johnson, Sarah Burley, Kaylea Gawf, Elisabeth G Vichaya
Published in
Physiology & behavior. Pages 115489. Aug 30, 2026. Epub Aug 30, 2026.
Abstract
Diabetes is a chronic disease characterized by hyperglycemia. It is associated with a variety of co-morbidities, including depression. This link is likely mediated in part by hyperglycemia-induced increases in inflammation. Given that exercise can benefit diabetes, inflammation, and depression, the aim of this study was to investigate if exercise may treat hyperglycemia-induced neuroinflammation and depressive-like behavior. We used the STZ model of hyperglycemia in male C57BL/6J mice and voluntary wheel running as exercise. To circumvent possible STZ-induced issues with wheel running, we provided mice with wheels for 10 days prior to STZ. Unexpectedly, we observed that 10 days of wheel access was sufficient to blunt development of STZ-induced hyperglycemia as well as most STZ-induced behavioral and inflammatory effects. Mice continued to show mild hyperglycemia, impaired glucose tolerance, and intermediate levels of insulin. No significant behavioral differences were observed. Increases in liver Tnf mRNA expression, but not TNF protein, were noted without changes in Il6 or Il1b. There were no changes in hippocampal Tnf or Il1b. We observed an interesting interaction for Bdnf, such that exercise increased expression in VEH but not STZ mice. This may indicate a neural response to mild hyperglycemia, though additional studies are required to confirm this effect. Overall, these data suggest that 10 days of voluntary exercise is sufficient to blunt STZ-induced hyperglycemia. This model may be useful in investigating the chronic effects of pre-diabetic blood glucose levels on brain health.
PMID:
42669391
Bibliographic data and abstract were imported from PubMed on 31 Aug 2026.
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