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Insulin Resistance Induced Elevations in Cardiac Glycogen are not Attenuated by Regular Exercise
Author(s) -
Chan Carol WY,
Ross Karen D,
Carley Andrew N,
Carroll Rogayah,
Severson David L,
Shearer Jane
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a393-a
Subject(s) - glycogen , medicine , endocrinology , insulin resistance , glycogen synthase , insulin , diabetes mellitus , chemistry
Glycogen is a central mediator of cellular homeostasis, insulin signaling and substrate utilization. Insulin resistance results in a doubling of cardiac glycogen stores, however, the mechanisms governing this increase are unknown. Elevated glycogen occurs by either the formation of new granules (proglycogen) or the expansion of existing glycogen stores (macroglycogen). Aims were to i) determine the nature of augmented glycogen stores in insulin resistance and ii) examine whether regular exercise attenuated this increase. Employing the db/db mouse model of type 2 diabetes, hearts were removed following 6wk of sedentary or regular treadmill exercise (EX) (1h/d, 5d/wk) in both control ( db/+) and db/db littermates. On the day of the study, mice were rested for 48h before cardiac muscle was collected and assessed for pro‐, macro‐ and total glycogen concentration (umol/g dw). In the sedentary groups, glycogen was elevated in db/db mice compared to db/+ (272±25 vs. 134±17). Macroglycogen contributed the largest proportion of this increase indicating the majority of diabetes‐induced cardiac glycogen was due to larger granule size rather than number. Unexpectedly, EX resulted in further increases rather than the normalization of glycogen stores in db/db but not db/+ (432±43 vs. 149±17). Additional glycogen in db/db from EX was equally distributed between pro‐ and macroglycogen. Data indicate insulin resistance results in an increase in cardiac glycogen stores that is not corrected by regular exercise. Rather, it appears that the mechanisms by which insulin resistance and exercise augment cardiac glycogen stores are distinct and additive. Supported by CIHR (DS) & Genome Alberta (JS).