Abstract
Diabetes adversely affects glucose metabolism, resulting in elevated levels of heart glycogen. Exercise training increases glycogen synthesis activity in diabetes; therefore the aim of this study was to examine the effects of exercise on glycogen content in hearts from streptozotocin-induced (insulin-deficient for duration of study) type 1 diabetic mice (T1D) mice compared to CD-1 controls. Mice were exercised by running for 60 min/d, 5 d/wk for 6 wk at low-moderate intensity. Hearts from T1D and control mice at 12 wk of age were subjected to a 60 min working heart perfusion with glucose and palmitate, prior to glycogen measurements (μmol/g dw) as total glycogen (Gt), proglycogen (PG) and macroglycogen (MG). Gt for T1D sedentary (SED) hearts was not significantly different from SED or exercised (EX) non-diabetic, CD1 controls. In T1D SED hearts, PG contributed 60% of total glycogen, which was significantly elevated compared to EX controls but not to SED controls. EX T1D hearts showed a nearly 2-fold increase in Gt compared to SED diabetic hearts (935±86 vs 584±20) with PG and MG contributing 558±21 and 436±80 glucosyl units respectively. There are intriguing aspects of this data: i) there was no difference in Gt between SED T1D and controls implying glycogen synthesis is not impaired in T1D hearts. (ii) Elevated PG levels in T1D hearts reflects a distinct selective process in glycogen formation compared to controls, suggesting T1D hearts form new granules at the expense of MG to maintain Gt. (iii) An exercise-induced improvement in glucose disposal may account for elevated PG and MG levels in EX T1D perfused hearts. Supported by CIHR (DS) and Genome Alberta (JS).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.