Effect of Endurance Exercise on Myosin Heavy Chain Isoform Expression in Diabetic Rats with Peripheral Neuropathy

Snow, LeAnn M.; Sánchez, Otto A.; McLoon, Linda K.; Serfass, R. C.; Thompson, LaDora V.

doi:10.1097/01.phm.0000176350.61935.d6

Cited by 17 publications

(16 citation statements)

References 33 publications

(49 reference statements)

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“…General muscle fiber typing was performed by immunolabeling for myosin heavychain isoforms (MHC). Mouse monoclonal immunoglobulin G antibodies to fast and slow MHCs (Novocastra, Newcastle upon Tyne, UK) were used in dilutions of 1: 20 (slow MHC) and 1: 10 (fast MHC) [16,17] . Controls were included in which the primary antibody incubation step was omitted.…”

Section: Tissue Staining and Analysismentioning

confidence: 99%

Advanced Glycation End Product in Diabetic Rat Skeletal Muscle in vivo

et al. 2006

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Background: Advanced glycation end products (AGEs) are implicated in the etiology of diabetic complications in the kidney, nerve and eye. Skeletal muscle contractile parameters have also been found to be altered in diabetes. Glycation has not been extensively studied in skeletal muscle, but AGE-modified proteins may influence contractility. Objective and Methods: The aim of this study was to use immunohistochemistry to identify distribution patterns of the AGE NΕ-(carboxymethyl)-lysine in plantaris muscle of diabetic rats. Results: Results revealed the presence of NΕ-(carboxymethyl)-lysine intracellularly and also at sites along the myofiber periphery. The number of myofibers immunolabeling for AGE in animals with diabetes was more than 4-fold greater than in control animals. Additionally, there was a greater proportion of slow + fast myosin heavy chain coexpression in the AGE-positive cells from diabetic animals than in AGE-positive fibers from control animals. No significant difference was present between cross-sectional areas of AGE-positive fibers and AGE-negative fibers within the respective experimental groups. Conclusions: AGE accumulation is greater in skeletal muscle in vivo from diabetic animals than in control animals. This AGE accumulation appears to be associated with fiber-type transformation rather than with myofiber size. Further study is needed to determine the identity of these AGE-modified proteins and to determine how they influence skeletal muscle function in diabetes.

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Section: Tissue Staining and Analysismentioning

confidence: 99%

Advanced Glycation End Product in Diabetic Rat Skeletal Muscle in vivo

et al. 2006

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“…[2] DPN consists of demyelization and axonal degeneration of peripheral nerves, [16], leading to slowing of nerve conduction velocity and reduction of the amplitude of the compound muscle and sensory nerve action potentials. [16,23] These features of diabetic polyneuropathy are observed in human diabetes [16,24] and in experimentally induced diabetic animals. [17][18][19][20][21][22][23] DPN is one of the main complications of diabetes, which may impair the peripheral nerve regeneration.…”

Section: Introductionmentioning

confidence: 96%

“…[16,23] These features of diabetic polyneuropathy are observed in human diabetes [16,24] and in experimentally induced diabetic animals. [17][18][19][20][21][22][23] DPN is one of the main complications of diabetes, which may impair the peripheral nerve regeneration. Though the causes for failed regeneration in diabetic peripheral nerves are not completely elucidated, possible etiopathologies have been reported, such as structural changes in peripheral blood vessels and reductions in blood flow, [25,54] delays in recruitment of macrophages to clean degrading myelin in injured peripheral nerve fibers, [26,54] and reductions in neurotrophic supports for nerve tissue regeneration.…”

Section: Introductionmentioning

confidence: 96%

An Update On Rodent Model Studies In Diabetic Neuropathy: A Brief Communication

Lima¹,

Vasconcelos²,

Júnior³

et al. 2016

Int Arch Med

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The diseases of the peripheral nerves are quite common and diversified, are directly related to several factors, ranging from the imbalance related to good nutrition and adequate needs of nutrients, going to the injuries caused by drugs or mechanisms external to the human organism. Diabetes is a complex syndrome that affects and kills millions of people worldwide. We demonstrated through the experimental model of diabetes using STZ@ in single intraperitoneal dose of 60 mg / kg, that both a purely motor nerve can be directly affected as well as a special afferent nerve (cranial nerve), this comparison showed us that there is a possibility of having a new type of mixed type neuropathy, this may be related to the amount of the dose involved, such as the time of disease progression, but more studies need to be done for definitive confirmation. We can extrapolate the original results to understand the mechanisms of diabetes in humans, although it does not yet have an experimental model of type II diabetes, more related to eating disorders, the STZ application simulates the effects of type I or insulin dependent diabetes, with more serious and deleterious effects mainly the more distal portions of the nerves. Prevention and food control are very important, especially those related to the mechanisms that involve carbohydrate metabolism and its peripheral resistance. The original results commented here are relevant for the continuous study of this serious but old illness, but quite current in the medical and therapeutic clinic.

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Section: Introductionmentioning

confidence: 99%

“…It consists of demyelization and axonal degeneration of peripheral nerves 1 , leading to slowing of nerve conduction velocity and reduction of the amplitude of the compound muscle and sensory nerve action potentials [1][2][3][4][5][6][7][8] . These features of diabetic polyneuropathy are observed in humans diabetes 1,9 and experimentally induced diabetes in animals [2][3][4][5][6][7][8] . Along with the sciatic, fibular, tibial, sural, saphenous, and facial nerves 3,6,10,11 , the caudal nerve has often been used for electrophysiological studies in rats 2,4,5,12 , because the long tail allows accurate measurement of distances and the small diameter of the tail facilitates the placement of the stimulating and recording electrodes close to the nerve 12,13 .…”

Section: Introductionmentioning

confidence: 99%

Sensory nerve conduction in the caudal nerves of rats with diabetes

Carvalho¹,

Maia²,

Lins³

et al. 2011

Acta Cir. Bras.

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PURPOSE: To investigate sensory nerve conduction of the caudal nerve in normal and diabetic rats. METHODS: Diabetes was induced in twenty 8-weeks old Wistar male rats. Twenty normal rats served as controls. Caudal nerve conduction studies were made before diabetes induction and the end of each week for six consecutive weeks. The caudal nerve was stimulated distally and nerve potentials were recorded proximally on the animal's tail using common "alligator" clips as surface electrodes. RESULTS: After induction, nerve conduction velocities (NCV) increased slower in the diabetic than in the control group. Sensory nerve action potentials (SNAP) conduction velocities increased slower in the diabetic than in the control group (slope of regression line: 0.5 vs 1.3m/s per week; NCV in the 15th week = 39±3m/s vs 44±4m/s). Tukey's tests showed differences between groups at the 11th, 13th and 15th weeks old. From the 10th week on, SNAP amplitudes increased faster in the diabetic than in the control group (slopes of the regression line: 10 vs 8µV per week; SNAP amplitudes in the 15th week: 107±23µV vs 85±13µV). Differences at the 12th, 13th and 15th weeks were significant. CONCLUSION: In diabetic rats nerve conduction velocities were slower whereas amplitudes were larger than in normal rats.

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Effect of Endurance Exercise on Myosin Heavy Chain Isoform Expression in Diabetic Rats with Peripheral Neuropathy

Cited by 17 publications

References 33 publications

Advanced Glycation End Product in Diabetic Rat Skeletal Muscle in vivo

Advanced Glycation End Product in Diabetic Rat Skeletal Muscle in vivo

An Update On Rodent Model Studies In Diabetic Neuropathy: A Brief Communication

Sensory nerve conduction in the caudal nerves of rats with diabetes

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