Date of Award
5-2026
Culminating Project Type
Thesis
Styleguide
apa
Degree Name
Biological Sciences - Cell and Molecular: M.S.
Department
Biology
College
College of Science and Engineering
First Advisor
Marina Cetkovic-Cvrlje
Second Advisor
Gengyun Le-Chan
Third Advisor
Kyle Reason
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Keywords and Subject Headings
T1D, hyperglycemia, glycemia, Voluntary exercise, NOD mice, C57BL/6J mice (B6), autoimmune disease
Abstract
Type 1 diabetes (T1D) is caused by the progressive destruction of insulin-producing β cells of the pancreas by the body’s own T cells resulting in hyperglycemia. A growing body of evidence suggests that exercise offers protective benefits against the development of various metabolic illnesses such as obesity and type 2 diabetes (T2D). However, the exercise impact on T1D demands more rigorous investigation. The objective of this study was to evaluate whether voluntary exercise impact the onset and severity of T1D in non-obese diabetic (NOD) and chemically induced streptozotocin (STZ) C57BL/6J (B6) mice by acting on immune system. All experimental procedures were approved by St. Cloud State University’s Institutional Animal Care and Use Committee. There were four studies, investigating two groups of 5-9-week-old NOD female mice during the late and early (prediabetic) periods of T1D development, and two groups of 7-9-week-old B6 males, STZ-exposed (STZ-B6) and healthy mice, randomly assigned to either sedentary or exercise groups. Exercise mice had 24h/day access to running wheels, while sedentary mice remained in cages without wheels for 10 weeks. Late time point NOD mice were monitored for glycemia levels and body mass during and after the exercise intervention until T1D onset or by 24 weeks of age. STZ-B6 mice received intraperitoneal injections of low-dose STZ for five consecutive days in the sixth week of intervention period and were monitored biweekly for T1D development up to 34 days following the first STZ injection. Daily running distance, and weekly food and water consumption, in parallel with glycemia and body mass, were recorded during the 10-week intervention period in all four studies. Immune system parameters were studied in the spleens of all groups of mice, immediately after the intervention period in the early time point prediabetic NODs, STZ-B6 and healthy B6, and at late time point in NOD mice. Spleen mass, splenocyte counts, flow cytometric analysis of T helper (Th), cytotoxic (Tc), regulatory T cells (Treg), and B cells, and cytokines levels were assessed. Results were analyzed using survival analysis (diabetes incidence), two-way repeated measures ANOVA (food, water glycemia levels and body mass) and unpaired Student's t-test (flow cytometry data and cytokine analysis) and reported as means ± SD. Results demonstrated that exercise delayed disease onset, reduced T1D incidence, and glycemia levels in both NOD and STZ-B6 mice. Exercise did not affect body mass but increased food consumption across all groups Water consumption decreased in late time point NOD and STZ-B6 mice. Despite these metabolic changes, exercise did not alter any of studied immunological splenic parameters. In conclusion, our findings show that voluntary exercise delays disease onset and reduces disease severity in experimental T1D models without altering systemic immune parameters. The underlying mechanism may involve localized pancreatic immune modulation. Future studies should investigate the effects of voluntary exercise on β cell mass preservation and insulin metabolism.
Recommended Citation
Addo, Hans, "Study on Effects of Voluntary Exercise Training on Onset of Type 1 Diabetes (T1D) in Mouse Models" (2026). Culminating Projects in Biology. 92.
https://repository.stcloudstate.edu/biol_etds/92
