Muscle contractility decrement and correlated morphology during the pathogenesis of streptozotocin-diabetic mice

Fahim, Mohamed A.; El‐Sabban, Farouk; Davidson, Nicholas O.

doi:10.1002/(sici)1097-0185(199806)251:2<240::aid-ar13>3.0.co;2-o

Cited by 41 publications

(40 citation statements)

References 26 publications

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“…The age chosen for induction of diabetes is consistent with most previous studies of this model (10,12,23,33,39,40,41,51,55,56). Animals were studied 4 wk after streptozotocin or buffer injection, as this amount of time postinjection is in the middle of the range used in previous studies (10,12,19,23,31,33,39,40,41,51,55,56,63). Furthermore, 4 wk is in line with the two previous diabetic heart gene expression array studies, which examined animals 2 wk post-streptozotocin (31) or 3 days, 4 wk, and 6 wk poststreptozotocin (19).…”

Section: Discussionmentioning

confidence: 81%

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Oxidoreductase, morphogenesis, extracellular matrix, and calcium ion-binding gene expression in streptozotocin-induced diabetic rat heart

Lunteren

Moyer

2007

American Journal of Physiology-Endocrinology and Metabolism

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 92%

Oxidoreductase, morphogenesis, extracellular matrix, and calcium ion-binding gene expression in streptozotocin-induced diabetic rat heart

Lunteren

Moyer

2007

American Journal of Physiology-Endocrinology and Metabolism

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“…Down-regulation of nNOS in muscle cells and at the neuromuscular junction could thus be responsible for the long-term impairment in muscle contractile properties in the pathogenesis of diabetic neuromyopathy. Supporting this hypothesis is the recent finding that long-term diabetes impairs contractile function by affecting presynaptic control at the neuromuscular junction as well as at the muscle cells [19]. There is also evidence that diabetes can directly impair the contractile/regulatory system of a subpopulation of fast-twitch fibres [18,39].…”

Section: Discussionmentioning

confidence: 93%

“…A lack of NOS activity in diabetic muscle could explain the reported defect in NO vascular bioactivity and contribute to the impaired insulin-stimulated glucose uptake in diabetes. An abnormal NO synthesis at the neuromuscular junctions as well as in muscle cells could also be involved in the development of contractile dysfunction (neuromyopathy) in diabetes [18,19]. The goal of our study was therefore to test the hypothesis that muscle NOS activity is reduced in insulin-deficient diabetes and if the case, to determine the mechanism of NOS dysregulation in this disorder.…”

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confidence: 99%

Mechanism of impaired nitric oxide synthase activity in skeletal muscle of streptozotocin-induced diabetic rats

2000

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Type I (insulin-dependent) diabetes mellitus is characterised by pronounced insulin resistance for glucose disposal in skeletal muscle [1,2]. This metabolic impairment is at least in part related to a post-insulin signalling defect in the expression and translocation of GLUT4 glucose transporters to the muscle cell surface [3±5]. The lack of insulin action on glucose metabolism in muscle of people with Type I diabetes could also be explained by an impaired vasodilatory effect of insulin on the muscle vasculature [2], although this impairment has not been confirmed in a more recent study [1]. Several studies have shown that endothelium-dependent relaxation is altered in Abstract Aims/hypothesis. The aims of our study were to investigate whether nitric oxide synthase (NOS) activity is impaired in skeletal muscle of insulin-deficient [Type I (insulin-dependent)] diabetic rats and if the case, to determine the mechanism of NOS dysregulation in this disorder. Methods. Rats were rendered diabetic by streptozotocin injection (65 mg/kg, i. v.) and NOS activity and expression in gastrocnemius muscles were studied 1, 2, 3 or 4 weeks after diabetes induction. Results. The diabetic state was associated with a progressive reduction (down to 42 % of control values after 4 weeks) in muscle NOS activity compared with control rats. Using reverse transcriptase-polymerase chain reaction, we could not detect statistically significant changes in the expression of either neuronal NOS (nNOS) or endothelial NOS (eNOS) mRNAs in diabetic muscle. The contents of nNOS and eNOS protein were, however, progressively reduced in muscle homogenates of diabetic rats and these alterations were prevented by insulin treatment. Subcellular fractionation of skeletal muscle showed that both nNOS and eNOS proteins are mainly localised to the plasma membrane with lower abundance in T-tubules and not detectable in sarcoplasmic reticulum-enriched fractions. After 1 week of diabetes, eNOS protein content was decreased only in the plasma membrane whereas nNOS protein abundance was not affected at this time. Neither the expression nor the interaction of caveolin-1 and caveolin-3 with NOS enzymes was found to be altered in muscle of diabetic rats. Conclusion/interpretation. These results show that skeletal muscle NOS activity is impaired during the progression of insulin-deficient diabetes and reduced NOS activity is associated with a decreased abundance of both nNOS and eNOS proteins, which appears to involve post-transcriptional mechanisms.

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“…[32,33] Its mechanism of action is based on the destruction of pancreatic beta cells, and the great advantage of its use is that it has a high affinity for these cells. [34] STZ-induced DM is obtained by a single intravenous or intraperitoneal injection. When STZ is administered at doses of 50-60 mg/Kg, insulin levels decrease by 30% of the normal, leading to hyperglycemia, polyuria, polydipsia, and weight loss.…”

Section: Discussionmentioning

confidence: 99%

Superoxide Dismutase Ameliorates the Bowel Alterations Induced by Diabetes Mellitus – An Experimental Study

Fillmann

Tieppo

Filho

et al. 2011

Free Radicals and Antioxidants

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Introduction: The gastrointestinal system is frequently affected in patients with diabetes mellitus (DM). Some of these alterations are due to oxidative stress and the production of free radicals. The present study was designed to evaluate whether treatment with superoxide dismutase (SOD) exerts protection on established bowel alterations in experimental diabetes mellitus induced by streptozotocin. We measured the lipid peroxidation, the superoxide dismutase activity and the DNA damage. Materials and Methods: We used the anorectal pressure to evaluate the nitrosative stress and used an inflammatory score to measure the macroscopic and microscopic bowel alterations. Results: The oxidative stress and the DNA damage was elevated in DM group and reduced with the SOD administration. The use of SOD also ameliorates the inflammatory bowel alterations and the anorectal pressure. Conclusion: SOD administration showed beneficial effects in all parameters of large bowel alterations in DM rats. IntroductIonDiabetes mellitus is a metabolic endocrine disorder that affects many systems. The complications may arise in several organs in different moments and situations, the gastrointestinal often being among the affected systems. Diabetes mellitus is one of the most common metabolic diseases, affecting about 2.5-3% of the world's population and 7% or more in some countries.[1] A considerable amount of evidence suggests that oxidative stress may play an important role in the pathogenesis and complications of diabetes. Different mechanisms can contribute to the enhanced oxidative stress in diabetic patients, in particular in subjects with poor glycaemic control and hypertriglyceridaemia.[2] Diabetic patients may have reduced antioxidant defenses, such as diminished activity of glutathione peroxidase, catalase and superoxide dismutase, as well as decreased levels of non-enzymatic antioxidants. In consequence, they may suffer from an increased risk of oxidative stress-related diseases, Hospital Clínic. University of Barcelona, Spain including atherosclerosis, the most common reason for premature death. [3] The accumulation of oxidative stress products can cause damage to biological molecules: proteins, lipids and DNA. The production of reactive oxidative species (ROS) is elevated in diabetes, particularly among those who have poor glycaemic control. It has been hypothesized that increased ROS generation in longstanding diabetes may result in oxidative damage to DNA. Studies with comet assay have shown increased levels of DNA breakage in peripheral blood cells of type I diabetic patients with poor glycaemic control, but not in patients with normal glycaemia. [4,5] Dinçer et al. found increased strain breakage and formamidopyrimidine DNA glycosylase (Fpg)-sensitive sites by the comet assay in DNA from leukocytes of patients with type I diabetes. [6] Lipid peroxidation of cellular structures, a consequence of free radical activity, is thought to play an important role in late complications of diabetes mellitus. [2,7]

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Muscle contractility decrement and correlated morphology during the pathogenesis of streptozotocin-diabetic mice

Cited by 41 publications

References 26 publications

Oxidoreductase, morphogenesis, extracellular matrix, and calcium ion-binding gene expression in streptozotocin-induced diabetic rat heart

Oxidoreductase, morphogenesis, extracellular matrix, and calcium ion-binding gene expression in streptozotocin-induced diabetic rat heart

Mechanism of impaired nitric oxide synthase activity in skeletal muscle of streptozotocin-induced diabetic rats

Superoxide Dismutase Ameliorates the Bowel Alterations Induced by Diabetes Mellitus – An Experimental Study

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