Ultrastructural alterations in skeletal muscle fibers of streptozotocin-diabetic rats

Chao, Tania; Ianuzzo, C. D.; Armstrong, R. B.; Albright, John T.; Anapolle, Steven E.

doi:10.1007/bf00215880

Cited by 40 publications

(31 citation statements)

References 25 publications

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“…The relaxation deficit shown by HRT measures suggests that SR Ca2" sequestration may also be impaired. Morphological studies provide evidence that SR and T tubules are disrupted in skeletal and cardiac muscle of diabetic rats (Chao et al 1976;Afzal, Ganguly, Dhalla, Pierce, Singal & Dhalla, 1988). In vitro studies of heart (Penparkgul, Fein, Sonnenblick & Scheuer, 1981;Ganguly et al 1983) and skeletal muscle (Eibschutz et al 1984) demonstrated reduced SR Ca2+-ATPase activity, although this has been disputed for skeletal muscle (Ganguly, Mathur, Gupta, Beamish & Dhalla, 1986).…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative capacity was reported to be reduced by diabetes in mixed skeletal muscles (Armstrong et al 1975). A morphological correlate may be decreased mitochondrial density and disruption of their cristae in skeletal and cardiac muscle (Chao et al 1976;Afzal et al 1988). This could explain reduced soleus SDH staining, which may contribute to increased fatiguability if ATP for contraction was limited.…”

Section: Discussionmentioning

confidence: 99%

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

Cameron²,

Robertson³

et al. 1993

Experimental Physiology

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SUMMARYThis study examined the effect of inhibition of aldose reductase, the first enzyme in the polyol pathway, on fast and slow twitch skeletal muscle morphology and function in streptozotocininduced diabetes in rats. There was a preventative investigation with diabetes duration of 4 months, and a reversal investigation where treatment was given for 2 months following an untreated period of 2 months. For slow twitch soleus muscle, contractions were prolonged by diabetes, and this was partially prevented but not reversed by treatment. Relaxation was profoundly slowed, and both prevention and reversal ameliorated the changes. Diabetes had minimal effects on tension production for soleus. However, for fast twitch extensor digitorum longus, although there was little effect on speed-related contractile parameters, tetanic tension production was progressively reduced with diabetes duration. This effect was antagonized by treatment. Soleus fatigue resistance was markedly reduced by diabetes, but restored to normal by treatment. There was a reduction in oxidative enzyme staining (succinic dehydrogenase), and capillary-fibre ratio, both of which were ameliorated by aldose reductase inhibition. Mean soleus fibre area was reduced after 4 months of diabetes, and this was prevented but not reversed by treatment. Fibre area was also reduced in extensor digitorum longus, particularly for fast glycolytic fibres. There was a small amelioration with treatment. It is concluded that enhanced polyol pathway activity makes a contribution to diabetic myopathy, and that aldose reductase inhibitors can prevent this by actions on muscle fibres and their vascular supply.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Cameron²,

Robertson³

et al. 1993

Experimental Physiology

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“…Mitochondrial disruption, including loss of cristae, has been noted in the SO and FOG fibres of rat soleus and plantaris muscle (Chao et al 1976). In the present study, the marked disruption of SDH staining in soleus muscle also implies an impairment of oxidative metabolism.…”

Section: Discussionmentioning

confidence: 99%

Effects of Long‐term Streptozotocin Diabetes on the Contractile and Histochemical Properties of Rat Muscles

et al. 1989

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SUMMARYContractile and histochemical properties of soleus (a slow-twitch muscle) and extensor digitorum longus (EDL, a fast-twitch muscle) were studied in mature rats after 3 months of streptozotocin-induced diabetes. Results were compared with age-and weight-matched controls. Diabetes produced profound wasting of fast muscles and particularly of the fast glycolytic (FG) fibres. Slow muscle fibres, both within the mixed EDL and in soleus, were less atrophied. Strength performance of EDL was reduced by diabetes, but maintained in soleus. Diabetes was without effect on the time to peak tension (TTP) and half-relaxation time (HRT) of EDL. However it produced profound slowing of soleus muscles, particularly of the relaxation phase. Part of the slowing effect of diabetes may be related to a histochemically demonstrable loss of fast oxidative glycolytic (FOG) fibres in soleus. Histochemical staining for the oxidative marker succinic dehydrogenase (SDH) revealed marked disruption of reaction product distribution in soleus, indicating an impairment of oxidative capacity.

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“…Skeletal muscle mitochondria of insulin-deficient rats made diabetic with the b-cell toxin streptozotocin, thereby mimicking type 1 diabetes, showed a loss of cristae and an increase in electron-dense granules along with lipid droplets around the mitochondria (59). Studies using alloxan to damage b cells and induce diabetes in rats revealed a decrease in mitochondrial number in liver and heart, with mitochondrial swelling and damage to mitochondrial membranes and cristae (209).…”

Section: Type 1 and Type 2 Diabetesmentioning

confidence: 99%

Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities

Sivitz

Yorek

2010

Antioxidants & Redox Signaling

630

474

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Given their essential function in aerobic metabolism, mitochondria are intuitively of interest in regard to the pathophysiology of diabetes. Qualitative, quantitative, and functional perturbations in mitochondria have been identified and affect the cause and complications of diabetes. Moreover, as a consequence of fuel oxidation, mitochondria generate considerable reactive oxygen species (ROS). Evidence is accumulating that these radicals per se are important in the pathophysiology of diabetes and its complications. In this review, we first present basic concepts underlying mitochondrial physiology. We then address mitochondrial function and ROS as related to diabetes. We consider different forms of diabetes and address both insulin secretion and insulin sensitivity. We also address the role of mitochondrial uncoupling and coenzyme Q. Finally, we address the potential for targeting mitochondria in the therapy of diabetes. Antioxid. Redox Signal. 12, 537-577.

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Ultrastructural alterations in skeletal muscle fibers of streptozotocin-diabetic rats

Cited by 40 publications

References 25 publications

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

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

Effects of Long‐term Streptozotocin Diabetes on the Contractile and Histochemical Properties of Rat Muscles

Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities

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