Genetic control of non obese diabetic mice susceptibility to high-dose streptozotocin-induced diabetes

González, Cristina; Cuvellier, Sylvain; Hue-Beauvais, Catherine; Lévi‐Strauss, Matthieu

doi:10.1007/s00125-003-1168-7

Cited by 19 publications

(16 citation statements)

References 28 publications

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“…This drug is a potent alkylating agent which directly damages DNA. In addition, the metabolism of STZ generates free radicals and nitric oxide (NO) which could aggravate the situation [14] , as confirmed by the recent report that STZ can directly exert its detrimental effects in the absence of pancreatic toxicity [20] . STZ has also been shown to impair cardiac contractile function in the absence of hyperglycemia and hypoinsulinemia [20] .…”

Section: Discussionmentioning

confidence: 73%

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Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Vignaud¹,

Ramond²,

Hourdé³

et al. 2007

Pathobiology

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It is of common knowledge that diabetes decreases skeletal muscle contractility and induces atrophy. However, how hyperglycemia and insulin deficiency modify muscle mass and neuromuscular recovery after muscle injury is not well known. We have analyzed two models of diabetes: streptozotocin (STZ)-treated Swiss mice and Akita mice that spontaneously develop diabetes. A fast muscle, the tibialis anterior, was injured following injection of a myotoxic agent (cardiotoxin). Neuromuscular function was evaluated by examining in situ isometric contractile properties of regenerating muscles in response to nerve stimulation 14, 28 and 56 days after myotoxic injury. We found that STZ-induced diabetes reduces muscle weight and absolute maximal tetanic force in both regenerating and uninjured muscles (p = 0.0001). Moreover, it increases specific maximal tetanic force and tetanic fusion in regenerating and uninjured muscles (p = 0.04). In the Akita mice, diabetes decreases muscle weight and absolute maximal tetanic force, and increases tetanic fusion in both regenerating and uninjured muscles (p ≤ 0.003). Interestingly, STZ-induced diabetes exerts more marked effects than diabetes of genetic origin, in particular on muscle weight. This reduction in muscle mass was not due to an increased expression of the atrogenes MuRF1 and atrogin-1 during STZ-induced diabetes. The present study in mice demonstrates that both models of diabetes impair regenerating muscles as well as uninjured muscles. Regenerating fast muscles are weaker, lighter and slower in diabetic compared with nondiabetic mice.

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Section: Discussionmentioning

confidence: 73%

“…In the present study, two procedures were used to generate diabetes. Diabetes was induced by streptozotocin (STZ, a pancreatic ␤ -cell toxin) administration [14] . We also used Akita mice that spontaneously develop diabetes [15] , a genetic model of diabetes without the potential toxic side effects of chemical administration.…”

Section: Introductionmentioning

confidence: 99%

Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Vignaud¹,

Ramond²,

Hourdé³

et al. 2007

Pathobiology

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“…That possibility is supported by the previous finding that islets from C57BL/6J and C57BL/KsJ mice differ markedly in their glucose-stimulated islet cell replication both in vivo and in vitro (13). In addition, the genetic background is important for the phenotypic outcome of several models of genetically induced diabetes such as the Lep ob and Lepr db mutations (14), mice double heterozygous for knockout of the insulin receptor and insulin receptor substrate-1 (15), as well as chemically induced diabetes (16). Another possibility is that the observed differences in, e.g., the ␤-cell mass, reflect compensatory effects due to genetically determined differences in processes important for the need for insulin, such as insulin sensitivity or gluconeogenesis.…”

Section: Discussionmentioning

confidence: 99%

Genetic Background Determines the Size and Structure of the Endocrine Pancreas

2005

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Key parameters of the endocrine pancreas, such as islet number, islet mass, ␤-cell mass, and ␣-cell mass, were studied in different strains of inbred mice to investigate the impact of genetic background on the size and structure of the endocrine pancreas. Six mice from each of seven different strains of inbred mice were included in the study. For all parameters investigated, there was a pronounced interstrain variation. ANCOVA showed that only mouse strain was statistically significant as an explanatory parameter for the number of islets. Mouse strain, body weight, and pancreas mass reached statistical significance as explanatory parameters for the islet mass, with mouse strain as the most significant predictor. These data show that genetic background is the most important predictor of both the number of islets and total islet volume. We also conclude that inbred mice could be a valuable resource to identify the genes responsible for the size and structure of the endocrine pancreas. Diabetes 54:133-137, 2005

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“…Mice were randomly assigned into healthy and diabetic groups. The diabetic group received a single peritoneal injection of streptozotocin (STZ, Sigma-Aldrich, France, 180 mg/kg) dissolved in sodium citrate buffer solution (0.1 mol/l, pH 4.5) to induce experimental type 1 diabetes (21). The other group received a sham injection of an equal vol of the buffer.…”

Section: Animals and Experimental Setupmentioning

confidence: 99%

Effects of experimental type 1 diabetes and exercise training on angiogenic gene expression and capillarization in skeletal muscle

et al. 2006

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Diabetes alters microvascular structure and function and is a major risk factor for cardiovascular diseases. In diabetic skeletal muscle, impaired angiogenesis and reduced VEGF-A expression have been observed, whereas in healthy muscle exercise is known to have opposite effects. We studied the effects of type 1 diabetes and combined exercise training on angiogenic mRNA expression and capillarization in mouse skeletal muscle. Microarray and real-time PCR analyses showed that diabetes altered the expression of several genes involved in angiogenesis. For example, levels of proangiogenic VEGF-A, VEGF-B, neuropilin-1, VEGFR-1, and VEGFR-2 were reduced and the levels of antiangiogenic thrombospondin-1 and retinoblastoma like-2 were increased. Exercise training alleviated some of these changes, but could not completely restore them. VEGF-A protein content was also reduced in diabetic muscles. In line with the reduced levels of VEGF-A and other angiogenic factors, and increased levels of angiogenesis inhibitors, capillary-to-muscle fiber ratio was lower in diabetic mice compared to healthy controls. Exercise training could not restore capillarization in diabetic mice. In conclusion, these data illustrate that type 1 diabetes is associated with reduced skeletal muscle capillarization and the dysregulation of complex angiogenesis pathways.

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Genetic control of non obese diabetic mice susceptibility to high-dose streptozotocin-induced diabetes

Cited by 19 publications

References 28 publications

Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Genetic Background Determines the Size and Structure of the Endocrine Pancreas

Effects of experimental type 1 diabetes and exercise training on angiogenic gene expression and capillarization in skeletal muscle

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