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Characterizing Diabetic Myopathy: Muscle Contractility and Phenotype of Akita and STZ Diabetic Murine Models
Author(s) -
Krause Matthew Paul,
Imam Abdullah,
Cafarelli Enzo,
Riddell Michael C,
Hawke Thomas J
Publication year - 2008
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.22.1_supplement.961.4
Subject(s) - medicine , skeletal muscle , endocrinology , contractility , diabetes mellitus , stimulation , diabetic cardiomyopathy , gastrocnemius muscle , phenotype , myopathy , streptozotocin , type 1 diabetes , chemistry , heart failure , cardiomyopathy , gene , biochemistry
Steptozotocin (STZ) induced diabetes impairs skeletal muscle function and alters muscle morphology, though recent evidence suggests these changes are a result of the STZ rather than diabetes per se . Thus, the phenotype of diabetic skeletal muscle remains unclear. The Akita mouse is a type 1 diabetes (T1DM) model that displays many similarities to human T1DM including adolescent onset. The purpose of the study was to determine the phenotype and functionality of skeletal muscle in diabetic Akita mice (+/–) vs. non‐diabetic littermates (+/+). Following 10 weeks of overt diabetes in the +/– mice, functional capacity of the gastrocnemius muscle was assessed using in situ electrical stimulation. Body weight (−13 ± 2%), muscle mass (−17 ± 3%), heart mass (−9 ± 2%) and epidydymal fat mass (−81 ± 3%) were less in +/– than +/+ mice. Further, +/– gastrocnemius had more type IIA (+29 ± 6%) and less IIB/D (−24 ± 6%) fibers than +/+. Functionally, peak tetanic force and low frequency stimulation fatigue rates were not different between groups. These data indicate that untreated T1DM attenuates growth and alters skeletal muscle phenotype, but does not appear to alter peak force or low frequency stimulation endurance capacity.