Soleus myosin heavy chain isoform expression in diabetic neuropathy and in aging: A comparison.

摘要

Diabetes mellitus is a condition of disordered glucose metabolism that is associated with the complication of peripheral neuropathy. When motor nerves are involved in this neuropathy, skeletal muscle may subsequently exhibit changes. Relatively little investigation, however, has focused on experimental diabetic skeletal muscle apart from its metabolic functions. Aging is a process that also is associated with neurological alterations that affect skeletal muscle. There is overlap between diabetic complications and aging in terms of peripheral nerve effects and their proposed etiologies. It was the goal of the present research to document motor peripheral neuropathy in the streptozotocin-diabetic rat, and to examine myosin heavy chain (MHC) isoform expression in soleus muscle of both diabetic and aged rats. Particular attention was paid to immunohistochemical manifestations of neurological changes affecting these muscles. Results of electrophysiological testing confirmed the presence of peripheral neuropathy in the diabetic rats, including those given insulin. Results also showed that soleus muscle in diabetes exhibited increased fast MHC isoform expression, as did aged muscle. The form of this expression differed between the models, however. While diabetics showed an increased percentage of fibers expressing solely the fast MHC, the aged animals showed an increase in the percentage of fibers coexpressing slow and fast MHC isoforms. Immature MHC isoform expression was increased in both diabetic and aged muscle, but was greater in aged muscle. Muscle fiber atrophy presented in both models, but was absent in the diabetics if small doses of insulin were given. Histological characteristics of muscle denervation and reinnervation were evident in both diabetic and aged rats. It was concluded that neuropathic processes appear to influence MHC isoform expression in both diabetic and aged skeletal muscle, and that active muscle regeneration is present in the midst of the denervating processes. It was also concluded that insulin appears to influence fiber size and reinnervation patterns in diabetic muscle.