Peripheral nerve abnormalities in the diabetic mutant mouse

Sharma, Ashutosh; Thomas, P. K.; Gijón-Noguerón, Gabriel; Stolinski, C.; Dockery, P.; Hollins, G. W.

doi:10.2337/diabetes.32.12.1152

Cited by 26 publications

(21 citation statements)

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“…Such neuropathy, both sensory and motor, is characterized by significantly reduced NCV and mean axonal area, by an altered axonal transport of cytoskeletal proteins, norepinephrine, and AChE, and by decreased density of myelin and internodal membrane particles (5)(6)(7)(8)(9)(10)(11)15,19,20). Hence, this serves as an important tool for exploring the potential pathogenetic role of metabolic factors such as Na + -K + -ATPase in structural and functional abnormalities in the diabetic peripheral nerve.…”

Section: Discussionmentioning

confidence: 97%

Sciatic Nerve ATPase Activity Is Unaffected in Diabetic Mutant C57BI/Ks (db/db) Mice

et al. 1987

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We investigated composite (total), Mg2+-(ouabain-resistant), and Na+-K+-(ouabain-inhibited) ATPase in sciatic nerves of diabetic mutant C57Bl/Ks (db/db) and age-related littermate (db/+) control mice at various ages (16, 26, and 40 wk). This is the first report indicating that nerve ATPase activities measured in vitro showed no deficit in mice with spontaneous diabetes. Thus, diabetic neuropathy in the genetically diabetic mouse may occur in the absence of Na+-K+-ATPase abnormalities, which were previously described in association with polyol pathway impairment in experimental diabetic and BB Wistar rats. Control and diabetic groups treated with ganglioside mixture for 30 days before death presented statistically insignificant differences. Therefore, the beneficial effect of gangliosides described in C57Bl/Ks (db/db) mice on electrophysiological and morphometrical parameters must be due to different pharmacological activities rather than to prevention of the decay or better maintenance of ATPase activity.

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Section: Discussionmentioning

confidence: 97%

Sciatic Nerve ATPase Activity Is Unaffected in Diabetic Mutant C57BI/Ks (db/db) Mice

et al. 1987

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“…Human diabetic neuropathy is a worrying complication of DM and it is responsible for severe disability 5,19 . Previous studies have shown that STZ‐induced diabetes can result in a marked reduction in myelinated fiber size in rats 20 . It has also been demonstrated that myelinated fiber area, myelin thickness, and their axons are all significantly reduced in STZ‐induced diabetic rats 21 .…”

Section: Discussionmentioning

confidence: 99%

Contraction and Cation Contents of Skeletal Soleus and EDL Muscles in Age‐Matched Control and Diabetic Rats

Chonkar

Hopkin

Adeghate

et al. 2006

Annals of the New York Academy of Sciences

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Skeletal muscle atrophy and neuropathy are two of the major long-term complications of diabetes mellitus (DM). This article investigates the effect of streptozotocin (STZ)-induced type 1 DM on contraction and cation contents in soleus and EDL muscles compared to age-matched control rats. Adult Wistar rats were humanely killed and the soleus and EDL muscles located and excised rapidly and placed in organ baths. The muscles were electrically stimulated (EFS, 50 V, 1 ms, 1-50 Hz) and isometric contraction monitored using a chart recorder. At the end of the experiments the muscles were blotted, weighed, and dissolved in concentrated nitric acid for the measurements of cation contents. Diabetic rats have significantly (P < 0.05) reduced body and muscle weights and significantly (P < 0.05) elevated blood glucose (29.65 +/- 0.33 mM, n = 10) compared to control (6.06 +/- 0.21 mM, n = 10). EFS evoked frequency dependent contraction in both soleus and EDL muscles of healthy control rats. The response was significantly (P < 0.05, n = 8) increased in EDL compared to soleus. In the diabetic soleus and EDL muscles the force of contraction was significantly (P < 0.05, n = 8) reduced in both muscle types compared to control. The levels of total sodium (Na+), potassium (K+), calcium (Ca2+), magnesium (Mg2+), zinc (Zn2+), copper (Cu2+), and iron (Fe2+) were significantly (P < 0.05) reduced in diabetic soleus and EDL muscles compared to control. The results indicate that STZ-induced skeletal muscle atrophy is associated with marked reductions in both the force of contraction and cation contents in EDL and soleus muscles of the rat.

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“…Structurally this model shows a mild but progressive axonal atrophy but no pronounced fibre loss or paranodal changes [60,62] (Table 1). The fibre atrophy seen in this model was suggested [62] to be due to a maturational defect as reflected by decreased long bone growth.…”

Section: Pathology Of Experimental Diabetic Neuropathymentioning

confidence: 99%

“…The fibre atrophy seen in this model was suggested [62] to be due to a maturational defect as reflected by decreased long bone growth. These data could not, however, be replicated by others [60].…”

Section: Pathology Of Experimental Diabetic Neuropathymentioning

confidence: 99%

Experimental diabetic neuropathy: an update

1999

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Diabetic neuropathy consists of several clinical syndromes affecting motor, sensory and autonomic nerves. Of these the most common is distal symmetric sensory polyneuropathy usually referred to as diabetic neuropathy. Animal studies, mainly in diabetic rodents, have contributed tremendously to our understanding of this disease. From these it is clear that the pathogenesis of diabetic neuropathy is multifactorial involving sequentially occurring and often closely interrelated metabolic aberrations. Major pathogenetic mechanisms include increased activity of the polyol pathway, abnormalities in vasoactive substances, non-enzymatic glycation, increased presence of free radicals, and perturbed neurotrophism. Traditionally the neuropathies accompanying Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus have been regarded as identical. Recent investigations have, however, clearly delineated distinct differences in the functional and structural expressions of the neuropathies in the two types of diabetes. Major future challenges are the identification of the differences in underlying pathogenetic mechanisms in the two types of neuropathy and in gaining a better understanding of the hierarchy of the multifactorial mechanisms underlying the disease. This will be important for designing meaningful therapies which to date have failed miserably in diabetic neuropathy.

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Peripheral nerve abnormalities in the diabetic mutant mouse

Cited by 26 publications

References 0 publications

Sciatic Nerve ATPase Activity Is Unaffected in Diabetic Mutant C57BI/Ks (db/db) Mice

Sciatic Nerve ATPase Activity Is Unaffected in Diabetic Mutant C57BI/Ks (db/db) Mice

Contraction and Cation Contents of Skeletal Soleus and EDL Muscles in Age‐Matched Control and Diabetic Rats

Experimental diabetic neuropathy: an update

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