Experimental Diabetic Autonomic Neuropathy

Low, Phillip A.

doi:10.1007/978-1-59745-311-0_9

Cited by 6 publications

(13 citation statements)

References 48 publications

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“…The aforementioned tests of sudomotor function are useful in the diagnosis and assessment of severity of distal small fiber neuropathies affecting sudomotor fibers and are particularly sensitive in comparison in detecting early or selectively small fiber neuropathies (Illigens and Gibbons, 2009;Cheshire and Low, 2007;Low et al, 1986). Nerve conduction studies, which preferentially evaluate large myelinated nerve fibers, may be normal in patients with neuropathies that selectively affect small caliber unmyelinated fibers (Low and Hilz, 2008;Low et al, 2006).…”

Section: Small Fiber Neuropathiesmentioning

confidence: 99%

Thermoregulatory disorders and illness related to heat and cold stress

Cheshire

2016

Autonomic Neuroscience

260

184

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Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37°C, which enables normal cellular function. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Hypothermia, defined as a core temperature of <35.0°C, may present with shivering, respiratory depression, cardiac dysrhythmias, impaired mental function, mydriasis, hypotension, and muscle dysfunction, which can progress to cardiac arrest or coma. Management includes warming measures, hydration, and cardiovascular support. Deaths from hypothermia are twice as frequent as deaths from hyperthermia. Hyperthermia, defined as a core temperature of >40.5°C, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. Management requires the immediate reduction of core temperature. Ice water immersion has been shown to be superior to alternative cooling measures. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy.

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Section: Small Fiber Neuropathiesmentioning

confidence: 99%

Thermoregulatory disorders and illness related to heat and cold stress

Cheshire

2016

Autonomic Neuroscience

260

184

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“…Diabetic neuropathy, characterised by nerve fibre atrophy and loss, was recognised early (for reviews, see [130–133]). In T2D animal models, there was early evidence for increased sympathetic activity in STZ-diabetic rats.…”

Section: Purinergic Signalling In Diabetesmentioning

confidence: 99%

Purinergic signalling and diabetes

Burnstock

Novak

2013

Purinergic Signalling

107

127

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The pancreas is an organ with a central role in nutrient breakdown, nutrient sensing and release of hormones regulating whole body nutrient homeostasis. In diabetes mellitus, the balance is broken—cells can be starving in the midst of plenty. There are indications that the incidence of diabetes type 1 and 2, and possibly pancreatogenic diabetes, is rising globally. Events leading to insulin secretion and action are complex, but there is emerging evidence that intracellular nucleotides and nucleotides are not only important as intracellular energy molecules but also as extracellular signalling molecules in purinergic signalling cascades. This signalling takes place at the level of the pancreas, where the close apposition of various cells—endocrine, exocrine, stromal and immune cells—contributes to the integrated function. Following an introduction to diabetes, the pancreas and purinergic signalling, we will focus on the role of purinergic signalling and its changes associated with diabetes in the pancreas and selected tissues/organ systems affected by hyperglycaemia and other stress molecules of diabetes. Since this is the first review of this kind, a comprehensive historical angle is taken, and common and divergent roles of receptors for nucleotides and nucleosides in different organ systems will be given. This integrated picture will aid our understanding of the challenges of the potential and currently used drugs targeted to specific organ/cells or disorders associated with diabetes.

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“…Human diabetic peripheral neuropathy is characterized by nerve fiber loss, axonal degeneration and segmental demyelination with endoneurial microangiopathy [8]. Multifactorial pathogenesis was suggested including accelerated polyol pathway, enhanced advanced glycation product formation and increased oxidative stress [8]. These factors involve directly and indirectly the development of diabetic neuropathy affecting nerve tissues or through vascular tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Its pathogenesis remains to be clarified, but the duration and level of hyperglycemia have a serious impact on the development of neuropathy [8]. Thus, optimum glycemic control is needed to prevent peripheral neuropathy in human patients [1, 10].…”

mentioning

confidence: 99%

“…Human diabetic peripheral neuropathy is characterized by nerve fiber loss, axonal degeneration and segmental demyelination with a slowing of nerve conduction velocity [8]. Rodent models of diabetes develop a slowing of nerve conduction velocity and mild axonal atrophy, but generally lack overt degenerative neuropathy, demyelination and fiber loss in the peripheral nerves.…”

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confidence: 99%

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Insulin-Ameliorated Peripheral Motor Neuropathy in Spontaneously Diabetic WBN/Kob Rats

Ozaki

Yamano

Matsuura

et al. 2013

The Journal of Veterinary Medical Science

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Rodent models of diabetes develop a slowing of nerve conduction velocity and mild axonal atrophy, but generally lack overt degenerative neuropathy. Spontaneously diabetic Wistar Bonn Kobori (WBN/Kob) rats develop severe diabetic peripheral motor neuropathy with a slowing of nerve conduction velocity. We examined the effect of glycemic control, using insulin implant, on neuropathic changes in these rats. Animals were divided into 2 groups: WBN group (spontaneously occurring diabetes rats) and WBN + insulin group (spontaneously occurring diabetes rats treated with insulin implants until 90 weeks of age). Conduction velocity was measured in sciatic–tibial motor nerves. These nerves also underwent qualitative and quantitative histomorphologic analysis. Mild to severe hyperglycemia (>200 mg/dl) and glycosuria (>100 mg/dl) were observed in the WBN group. In contrast, the blood glucose level of the WBN + insulin group fluctuated between normoglycemia (<200 mg/dl) and hyperglycemia. Conduction velocity significantly decreased in WBN group compared with WBN + insulin group. Morphologic analysis of the sciatic and tibial nerves of WBN group showed severe changes, including axonal degeneration, myelin distention, endoneurial fibrosis and microangiopathy. Insulin treatment corrected these changes without microangiopathy. These results suggest that insulin could decrease axonal atrophy and myelin distension of peripheral nerve in diabetic WBN/Kob rats. Observation of WBN/Kob rats revealed changes of axon, myelin and capillary caused by diabetes, thus indicating that this animal is a suitable model for investigating diabetic peripheral neuropathy.

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Experimental Diabetic Autonomic Neuropathy

Cited by 6 publications

References 48 publications

Thermoregulatory disorders and illness related to heat and cold stress

Thermoregulatory disorders and illness related to heat and cold stress

Purinergic signalling and diabetes

Insulin-Ameliorated Peripheral Motor Neuropathy in Spontaneously Diabetic WBN/Kob Rats

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