Distal axonopathy in streptozotocin diabetes in rats

Chokroverty, Sudhansu; Seiden, David L.; Navidad, P.; Cody, R. J.

doi:10.1007/bf01940542

Cited by 12 publications

(8 citation statements)

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“…Although most of the previous studies have described alterations of distal muscles (Feczko and Klueber, 1988;Chokroverty et al, 1988;Cotter et al, 1989;Klueber et al, 19891, our results suggest that experimental diabetes also produces structural alterations in proximal skeletal muscle. In addition to the existence of type I1 myofiber atrophy, the appearance of type IIC fibers without degenerative changes in the diabetic rectus femoris suggests a possible muscle denervation (Sunderland, 1985).…”

Section: Discussioncontrasting

confidence: 70%

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

et al. 1991

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The response of rat quadriceps muscle fibers to chronic streptozotocin (STZ) diabetes was studied. Transverse sections of rectus femoris muscle from diabetic and weight-matched control rats were assayed for myofibrilar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR). A quantitative analysis was carried out by an automatic interactive analysis system focused on the fiber type size and distribution. STZ-induced diabetes caused important effects in this muscle, with changes in the distribution of oxidative enzyme reactions, type I fiber hypertrophy, and type II fiber atrophy, which was greater in type IIB than in type IIA. It is concluded that hypoinsulinism produces morphological alterations in proximal skeletal muscle fibers that are similar to those of neurogenic myopathy. Thus the pathological changes in these mammalian muscle fibers could explain the clinical syndrome seen in diabetic patients called "diabetic symmetrical proximal motor neuropathy," perhaps the least understood of the major neuropathic complications of diabetes.

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Section: Discussioncontrasting

confidence: 70%

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

et al. 1991

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“…Metabolic changes in nerve vasculature, with resulting decrease in nerve blood flow and endoneurial hypoxia, have a key role in nerve conduction slowing in short-term diabetes [4, 15±20]. Metabolic imbalances in the neural tissues, closely associated with impaired neurotrophism [13, 25±27, 33] and neurotransmission [34±36], contribute to Schwann cell injury [37,38] and axonopathy [39,40]. These abnormalities which develop gradually and become manifest in long-standing diabetes [38,39] exacerbate nerve functional deficits acquired in the initial phase of diabetic neuropathy.…”

mentioning

confidence: 99%

“…Metabolic imbalances in the neural tissues, closely associated with impaired neurotrophism [13, 25±27, 33] and neurotransmission [34±36], contribute to Schwann cell injury [37,38] and axonopathy [39,40]. These abnormalities which develop gradually and become manifest in long-standing diabetes [38,39] exacerbate nerve functional deficits acquired in the initial phase of diabetic neuropathy. The importance of sorbitol pathway-linked metabolic imbalances in neural structures is illustrated by findings [41] of a large increase in neuroaxonal dystrophy with SDH inhibition by the dose of SDI not affecting nerve blood flow in the diabetic model of lesser duration [4].…”

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confidence: 99%

Evaluation of a sorbitol dehydrogenase inhibitor on diabetic peripheral nerve metabolism: a prevention study

Obrosova

Fathallah

Lang³

et al. 1999

Diabetologia

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Numerous studies in experimental models of diabetes [1±5] as well as a few clinical trials [6±9] have shown a reduction of peripheral nerve conduction deficit and morphological abnormalities by structurally different aldose reductase inhibitors thus implicating increased activity of the sorbitol pathway in the pathogenesis of diabetic neuropathy. The mechanisms leading from increased sorbitol pathway activity to complex functional, metabolic and morphological changes in the peripheral nervous system in diabetes are not com- Diabetologia (1999) AbstractAims/hypothesis. Studies of the role of sorbitol dehydrogenase in nerve functional deficits induced by diabetes reported contradictory results. We evaluated whether sorbitol dehydrogenase inhibition reduces metabolic abnormalities and enhances oxidative stress characteristic of experimental diabetic neuropathy. Methods. Control and streptozotocin-diabetic rats were treated with or without sorbitol dehydrogenase inhibitor (SDI)-157 (100 mg × kg ±1 × day ±1 , in the drinking water, for 3 weeks). Sciatic nerve free mitochondrial (cristae and matrix) and cytosolic NAD + : NADH ratios were calculated from the b-hydroxybutyrate, glutamate and lactate dehydrogenase systems. Concentrations of metabolites, e. g. sorbitol pathway intermediates and variables of energy state were measured in individual nerves spectrofluorometrically by enzymatic procedures. Results. The flux through sorbitol dehydrogenase (manifested by nerve fructose concentrations) was inhibited by 53 % and 74 % in control and diabetic rats treated with SDI compared with untreated control and diabetic groups. Free NAD + :NADH ratios in mitochondrial cristae, matrix and cytosol were decreased in diabetic rats compared with controls and reduction in either of the three variables was not prevented by sorbitol dehydrogenase inhibitor. Phosphocreatine concentrations and phosphocreatine:creatine ratios were decreased in diabetic rats compared with controls and were further reduced by the inhibitor. Malondialdehyde plus 4-hydroxyalkenals concentration was increased and reduced gluthathione concentration was reduced in diabetic rats compared with the control group, and changes in both variables were further exacerbated by sorbitol dehydrogenase inhibitor. Neither NAD-redox and energy states nor lipid aldehyde and reduced gluthathione concentrations were affected by treatment with the inhibitor in control rats. Conclusion/interpretation. Inhibition of sorbitol dehydrogenase does not offer an effective approach for prevention of oxidation and metabolic imbalances in the peripheral nerve that is induced by diabetes and is adverse rather than beneficial. [Diabetologia (1999

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“…Britland et al (1985) and Bhoyrul et al (1988) showed a reduction of the myelinated axonal area in the sciatic and tibial nerves of SZT-diabetic rats while Sharma et al (1985), McCallum et al (1986) 58 axonal caliber in the tibial and sural nerves of STZ-diabetic rats. The investigation of distal (plantar) nerves confirmed the axonal atrophy (Brown et al, 1980;Sharma et al, 1981;Chokroverty et al, 1988;Thomas et al, 1990) present in this experimental model of diabetic neuropathy. These findings added the information of a "dying back" neuropathy with breakdown of myelinated fibers in the most distal nerves with preservation of the fibers in more proximal ones (Brown et al).…”

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confidence: 68%

Diabetic Peripheral Neuropathies: A Morphometric Overview

et al. 2010

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FAZAN, S. V. P.; DE VASCONCELOS, C. C. A.; VALENÇA, M. M.; NESSLER, R. & MOORE, K. C. Diabetic peripheral neuropathies: a morphometric overview. Int. J. Morphol., 28(1):51-64, 2010. SUMMARY: Diabetes is now considered one of the main threats to human health in the 21st century and many researchers are dedicated to investigate the physiopathology of the disease, with further insights on the managements of its major complications. Since understanding the pathophysiology of the major complications of diabetes and their underlying processes is mandatory, experimental models of the disease may be useful as they allow the recognition of the early mechanisms involved in the long-term complications of diabetes. Peripheral nerve involvement is highly frequent in diabetes mellitus and it has been documented that one third of diabetic patients have peripheral neuropathy. The true prevalence is not known and reports vary from 10% to 90% in diabetic patients, depending on the criteria and methods used to define neuropathy. In this review, the most common experimental models of diabetes are presented and the pathological findings on major peripheral nerves are discussed. Also, the insights brought by morphometry to the diabetic neuropathy research are highlighted.

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Distal axonopathy in streptozotocin diabetes in rats

Cited by 12 publications

References 11 publications

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

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

Evaluation of a sorbitol dehydrogenase inhibitor on diabetic peripheral nerve metabolism: a prevention study

Diabetic Peripheral Neuropathies: A Morphometric Overview

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