Nerve conduction velocity and evoked potential latencies in streptozotocin‐diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor

Manschot, S.M.; Gispen, Willem Hendrik; Kappelle, L. Jaap; Biessels, Geert Jan

doi:10.1002/dmrr.401

Cited by 36 publications

(17 citation statements)

References 50 publications

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“…Malik, et al (1998) demonstrated that the angiotensin converting enzyme inhibitor trandolapril improved peripheral neuropathy in normotensive patients with diabetes. In studies with diabetic rats we and others have shown that inhibition of angiotensin converting enzyme can improve diabetic peripheral neuropathy (Aggarwal et al, 2001; Cameron et al, 1993; Coppey et al, 2006; Manschot et al, 2003). α-Lipoic acid, also known as thioctic acid, is an organosulfur compound derived from octanoic acid.…”

Section: Discussionmentioning

confidence: 92%

Early vs. late intervention of high fat/low dose streptozotocin treated C57Bl/6J mice with enalapril, α-lipoic acid, menhaden oil or their combination: Effect on diabetic neuropathy related endpoints

et al. 2017

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We have previously demonstrated that enalapril, α-lipoic acid and menhaden (fish) oil has potential as a treatment for diabetic peripheral neuropathy. In this study we sought to determine the efficacy of these treatments individually or in combination on multiple neuropathic endpoints in a high fat fed low dose streptozotocin treated mouse, a model of type 2 diabetes, following early or late intervention. Four or twelve weeks after the onset of hyperglycemia, diabetic mice were treated with enalapril, α-lipoic acid, menhaden oil or their combination for 12 weeks. Afterwards, endpoints including glucose tolerance, motor and sensory nerve conduction velocity, thermal nociception, and intraepidermal and cornea nerve fiber density was determined. Glucose clearance was impaired in diabetic mice and significantly improved only with combination treatment and early intervention. Diabetes caused steatosis, slowing of motor and sensory nerve conduction velocity, thermal hypoalgesia and reduction in intraepidermal and cornea nerve fiber density. Treating diabetic mice with enalapril, α-lipoic acid or menhaden oil partially protected diabetic mice from these deficits, whereas the combination of these three treatments was more efficacious following early or late intervention. These studies suggest that a combination therapy may be more effective for treating neural complications of type 2 diabetes.

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Section: Discussionmentioning

confidence: 92%

Early vs. late intervention of high fat/low dose streptozotocin treated C57Bl/6J mice with enalapril, α-lipoic acid, menhaden oil or their combination: Effect on diabetic neuropathy related endpoints

et al. 2017

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“…In addition, angiotensin-converting enzyme inhibitors have shown an improvement of nerve conduction velocity in distal symmetrical polyneuropathy. 92) Thus, the pathophysiological process of autonomic neuropathy is closely related with vascular function in subjects with diabetes.…”

Section: Disclosure Statementmentioning

confidence: 99%

The Relationship between Vascular Function and the Autonomic Nervous System

Amiya

Watanabe

Komuro

2014

Annals of Vascular Diseases

105

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Endothelial dysfunction and autonomic nervous system dysfunction are both risk factors for atherosclerosis. There is evidence demonstrating that there is a close interrelationship between these two systems. In hypertension, endothelial dysfunction affects the pathologic process through autonomic nervous pathways, and the pathophysiological process of autonomic neuropathy in diabetes mellitus is closely related with vascular function. However, detailed mechanisms of this interrelationship have not been clearly explained. In this review, we summarize fi ndings concerning the interrelationship between vascular function and the autonomic nervous system from both experimental and clinical studies. The clarifi cation of this interrelationship may provide more comprehensive risk stratifi cation and a new effective therapeutic strategy against atherosclerosis.

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“…neurological and cognitive complications, and dysfunctions of the visual system (Manschot et al 2003, Gregori et al 2006. Therefore, we planned to evaluate the following parameters: 1) Brain cortex flash-visual evoked potentials (VEPs) and rapid oscillatory potentials (OPs), because in stable type 2 diabetes and in diabetes models both color-VEP and VEP latency are consistently slower vs controls.…”

Section: Diabetes-related Stress Mechanismsmentioning

confidence: 99%

Enhanced brain performance in mice following postnatal stress

Loizzo

Spampinato

Campana

et al. 2012

Journal of Endocrinology

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The double postnatal stress model (brief maternal separation plus sham injection daily applied from birth to weaning) induces metabolic alterations similar to type 2 diabetes in young-adult male mice. We verify whether 1) the stress also induces brain metabolic-functional alterations connected to diabetes and 2) different alterations are modulated selectively by two stress-damaged endogenous systems (opioid-and/or ACTH-corticosteroid-linked). Here, diabetes-like metabolic plus neurophysiologicneurometabolic parameters are studied in adult mice following postnatal stress and drug treatment. Surprisingly, together with 'classic' diabetes-like alterations, the stress model induces in young-adult mice significantly enhanced brain neurometabolic-neurophysiologic performances, consisting of decreased latency to flash-visual evoked potentials (Kw8%); increased level (Cw40%) and reduced latency (Kw30%) of NAD(P)H autofluorescence postsynaptic signals following electric stimuli; enhanced passive avoidance learning (Cw135% latency); and enhanced brain-derived neurotrophic factor level (Cw70%). Postnatal treatment with the opioid receptor antagonist naloxone prevents some alterations, moreover the treatment with antisense (AS; AS vs proopiomelanocortin mRNA) draws all parameters to control levels, thus showing that some alterations are bound to endogenous opioid-system hyper-functioning, while others depend on ACTHcorticosterone system hyper-functioning. Our stress model induces diabetes-like metabolic alterations coupled to enhanced brain neurometabolic-neurophysiologic performances. Taken all together, these findings are compatible with an 'enduring acute-stress' reaction, which puts mice in favorable survival situations vs controls. However, prolonged hormonal-metabolic imbalances are expected to also produce diabetes-like complications at later ages in stressed mice.

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Nerve conduction velocity and evoked potential latencies in streptozotocin‐diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor

Abstract: Enalapril partially prevents the development of neurophysiological alterations in the peripheral and central nervous system and partially reverses deficits in brain stem auditory evoked potential latencies in STZ-diabetic rats.

Cited by 36 publications

References 50 publications

Early vs. late intervention of high fat/low dose streptozotocin treated C57Bl/6J mice with enalapril, α-lipoic acid, menhaden oil or their combination: Effect on diabetic neuropathy related endpoints

Early vs. late intervention of high fat/low dose streptozotocin treated C57Bl/6J mice with enalapril, α-lipoic acid, menhaden oil or their combination: Effect on diabetic neuropathy related endpoints

The Relationship between Vascular Function and the Autonomic Nervous System

Enhanced brain performance in mice following postnatal stress

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