Neuropathy and myopathy in the diaphragm of rats after 12 months of streptozotocin-induced diabetes mellitus

Proximal skeletal muscle alterations in streptozotocin‐diabetic rats: A histochemical and morphometric analysis

“…Nevertheless, metabolic and vascular implications should not be excluded, because they also produce differential effects in the fiber type as well as mitochondria1 alterations (Carpenter and Karpati, 1984). Perhaps the changes seen can be ascribed to a combination of these three factors, as has been suggested by Bestetti et al (1981) and Feczko and Klueber (1988) …”

“…Armstrong et al (1975) in gastrocnemius from STZ-diabetic rats found different abnormalities depending on the fiber type, with more atrophy in type I1 fibers (glycolytic fibers). Bestetti et al (1981) studied the diaphragm in STZ-diabetic rats and reported shrinkage of white fibers (type 11). More recently, Klueber et al (1989) found wasting of fast muscle, particularly of the fast glycolytic (type IIB) fibers, and impairment of oxidative capacity in the EDL muscle from C57BLKs db/ db mice.…”

Streptozotocin induced diabetes as a model of phrenic nerve neuropathy in rats

“…Interestingly, the fascicular area was not different between groups indicating that, although diabetic rats did not gain weight as the other two groups, the nerve fascicles were able to grow satisfactorily. Bestetti et al (1981) studied the distal (intra-diaphragm) phrenic nerve myelinated fibers in rats after 12 months of STZ induced diabetes. These authors showed a significant reduction of the whole fiber cross-section, resulting from a decrease in thickness of axon and myelin sheath.…”

“…To mimic the human situation in an experimental animal model, the diabetes should be treated with insulin and marked short-term fluctuations of blood sugar level should be avoided (Mohseni and Hildebrand, 1998). Phrenic neuropathies are increasingly recognized in peripheral neuropathies and, in rats, the phrenic nerve-diaphragm muscle preparations are of particular interest for studies involving changes in functionally related muscles and nerves (Bestetti et al, 1981). Despite this, reports on experimental models of the phrenic nerves diabetic neuropathy are scanty.…”

Polyol pathway‐related skeletal muscle contractile and morphological abnormalities in diabetic rats

“…Thus, there have been reports of contraction prolongation in slow muscles and preferential atrophy and reduced tetanic tension in fast muscles (Grossie, 1982;Paulus & Grossie, 1983;Cotter, Cameron, Lean & Robertson, 1989). Histochemical and ultrastructural changes include a general dedifferentiation of fast twitch fibres (Bestetti, Zemp, Probst & Rossi, 1981) reduction in staining for mitochondrial enzymes , loss of mitochondria, disruption of mitochondrial cristae, intracellular lipid accumulation, and disorientation of the T-tubule-sarcoplasmic reticulum system (Chao, lanuzzo, Armstrong, Albright & Anapolle, 1976). At the biochemical level there is depressed protein synthesis and enhanced proteolysis (Pain & Garlick, 1974), falls in amino acid and glucose transport (Manchester, 1970), reduced Na+-K+-ATPase activity and pump density (Moore, Munford & Pillsworth, 1983;Kjeldsen, Braendgaard, Sidenius, Larsen & Norgaard, 1987) changes in sarcoplasmic reticulum Ca2+-ATPase (Ganguly, Pierce, Dhalla & Dhalla, 1983;Eibschutz, Lopaschuk, McNeill & Katz, 1984) and reductions in intracellular ATP concentration (Moore et al 1983).…”