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This Article Full Text Full Text (PDF) All Versions of this Article: 294/2/E271    most recent 00476.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Király, M. A. Articles by Vranic, M. Search for Related Content PubMed PubMed Citation Articles by Király, M. A. Articles by Vranic, M.

Swim training prevents hyperglycemia in ZDF rats: mechanisms involved in the partial maintenance of β-cell function

Departments of ¹Physiology, ²Obstetrics and Gynecology, ³Medicine, ⁴Molecular and Medical Genetics, University of Toronto, Toronto, Ontario; ⁵Cell Biology Program, Hospital for Sick Children, Toronto, Ontario; and ⁶School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada

Submitted 20 July 2007 ; accepted in final form 12 November 2007

Exercise improves glucose tolerance in obese rodent models and humans; however, effects with respect to mechanisms of β-cell compensation remain unexplained. We examined exercise's effects during the progression of hyperglycemia in male Zucker diabetic fatty (ZDF) rats until 19 wk of age. At 6 wk old, rats were assigned to 1) basal-euthanized for baseline values; 2) exercise-swam individually for 1 h/day, 5 days/wk; and 3) controls (n = 8–10/group). Exercise (13 wk) resulted in maintenance of fasted hyperinsulinemia and prevented increases in fed and fasted glucose (P < 0.05) compared with sham-exercised and sedentary controls (P < 0.05). β-Cell function calculations indicate prolonged β-cell adaptation in exercised animals alone. During an intraperitoneal glucose tolerance test (IPGTT), exercised rats had lower 2-h glucose (P < 0.05) vs. controls. Area-under-the-curve analyses from baseline for IPGTT glucose and insulin indicate improved glucose tolerance with exercise was associated with increased insulin production and/or secretion. β-Cell mass increased in exercised vs. basal animals; however, mass expansion was absent at 19 wk in controls (P < 0.05). Hypertrophy and replication contributed to expansion of β-cell mass; exercised animals had increased β-cell size and bromodeoxyuridine incorporation rates vs. controls (P < 0.05). The relative area of GLUT2 and protein kinase B was significantly elevated in exercised vs. sedentary controls (P < 0.05). Last, we show formation of ubiquitinated protein aggregates, a response to cellular/oxidative stress, occurred in nonexercised 19 wk-old ZDF rats but not in lean, 6 wk-old basal, or exercised rats. In conclusion, improved β-cell compensation through increased β-cell function and mass occurs in exercised but not sedentary ZDF rats and may be in part responsible for improved glucoregulation.

Zucker diabetic fatty; exercise; diabetes; glycemia; insulin; C-peptide; β-cell mass; β-cell function; glucose transporter 2; protein kinase B; apoptosis; proliferation; islet morphology