Nerve conduction velocity, laser Doppler flow, and axonal caliber in galactose and streptozotocin diabetes

Kalichman, Michael W.; Dines, K. C.; Bobik, Marketta; Mizisin, Andrew P.

doi:10.1016/s0006-8993(98)00898-1

Cited by 33 publications

(24 citation statements)

References 40 publications

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“…It is also important to note that despite dramatically improved glycemia in the recovered mice, mean plasma glucose persisted somewhat above control values. Although STZ-induced diabetic rat models similarly develop significant slowing of motor and sensory conduction velocity (20,21), they do not later exhibit the loss of M waves or nerve action potentials or the myelin thinning that are observed in humans.…”

Section: Discussionmentioning

confidence: 92%

Experimental Diabetic Neuropathy With Spontaneous Recovery

2005

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Progressive diabetic neuropathy has hitherto been irreversible in humans. New approaches raise the question of whether islet cell reconstitution rendering euglycemia can reverse specific features of neuropathy. We evaluated physiological and structural features of experimental neuropathy in a long-term murine model of diabetes induced by streptozotocin. By serendipity, a subset of these diabetic mice spontaneously regained islet function and attained near-euglycemia. Our hypotheses were that this model might better reflect axon loss observed in human disease and that spontaneous recovery from diabetes might identify the features of neuropathy that are reversible. In this model, experimental neuropathy closely modeled that in humans in most critical aspects: declines in motor conduction velocities, attenuation of compound muscle (M waves) and nerve action potentials, axon atrophy, myelin thinning, loss of epidermal axons, and loss of sweat gland innervation. Overt sensory neuron loss in dorsal root ganglia was a feature of this model. In mice with recovery, there was robust electrophysiological improvement, less myelin thinning, and remarkable epidermal and sweat gland reinnervation. There was, however, no recovery of populations of lost sensory neurons. Our findings identify a robust model of human diabetic neuropathy and indicate that overt, irretrievable loss of sensory neurons is one of its features, despite collateral reinnervation of target organs. Sensory neurons deserve unique protective strategies irrespective of islet cell reconstitution. Diabetes 54: 830 -837, 2005

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Section: Discussionmentioning

confidence: 92%

Experimental Diabetic Neuropathy With Spontaneous Recovery

2005

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“…[3][4][5] Similarly, the onset and progression of these vascular lesions in animals with either DM or galactosemia are also reduced by the tight control of hyperglycemia or the reduction of galactosemia, respectively. [6][7][8] In addition to hyperglycemia, the establishment of tight glycemic control is also associated with deleterious effects because the administration of insulin or hyperglycemic drugs often results in acute glucose fluctuations and hypoglycemia.…”

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confidence: 99%

Response of Rat Retinal Capillary Pericytes and Endothelial Cells to Glucose

Makita

Hosoya

Zhang

et al. 2011

Journal of Ocular Pharmacology and Therapeutics

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Aim: The purpose of this study was to investigate the effects of hyperglycemia, its fluctuations, and glucose starvation on the expression of glucose-regulated protein 78/binding immunoglobulin protein (GRP78/BiP), one of the most commonly used markers of endoplasmic reticulum stress, in rat capillary pericytes and endothelial cells cultured separately and together. Methods: Conditionally immortalized rat retinal pericyte and endothelial cell lines were cultured in dishes coated with collagen type I in Dulbecco's modified Eagle's medium containing 5.5 mM glucose. For cocultures, pericytes and endothelial cells were seeded together on rat tail collagen type I-coated cell culture plates. After 24 h of initial culture, the medium was replaced with serum-free medium containing 0-100 mM glucose for periods of up to 72 h. GRP78/BiP, caspase-3, and nuclear factor-kB expression were investigated using western blots. Results: No significant increase in GRP78/BiP expression was observed when pericytes, endothelial cells, or cocultures were exposed to either 25, 50, or 100 mM glucose for 48 h compared with the control level of 5.5 mM glucose. Similarly, no change in expression of GRP78/BiP was observed when media glucose levels were reduced from either 5.5 or 25 to 1 mM. GRP78/BiP expression significantly increased when cells were cultured for 24 h in glucose-deprived medium. This was accompanied by a time-dependent increase in the expression of caspase-3 and nuclear factor-kB. Conclusion: In diabetic retinopathy, hyperglycemia has been reported to induce apoptosis in retinal capillary vascular cells, but these studies suggest that the apoptosis is not linked to the expression of GRP78/BiP, one of the most commonly used markers of endoplasmic reticulum stress. However, GRP78/BiP-linked apoptosis may play a role in vascular changes associated with retinal ischemia/reperfusion.

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“…Furthermore, because MNCV was lower in rats with ITED, these data support previous observations that diabetesrelated nerve dysfunction can occur independent of reductions in NBF. [8][9][10][11][12] These data imply that in the absence of microangiopathy, basal NBF may be elevated in humans with combined poorly controlled type 1 diabetes and hypertension who are at risk of DPN.…”

Section: Perspectivesmentioning

confidence: 89%

“…Also, such issues do not alter the overall conclusion that the relationship between MAP and NBV remains intact in rats with ITED and reductions in NBF do not always precede diabetes-induced nerve dysfunction. [8][9][10][11][12] …”

Section: Limitationsmentioning

confidence: 99%

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The relationship between blood pressure and sciatic nerve blood flow velocity in rats with insulin-treated experimental diabetes

Olver

Grisé

McDonald

et al. 2014

Diabetes and Vascular Disease Research

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Peripheral nerve blood flow (NBF) does not autoregulate but, instead, responds passively to changes in mean arterial pressure (MAP). How this relationship is impacted by insulin-treated experimental diabetes (ITED) is unknown. We tested the hypothesis that ITED will reduce NBF across a range of MAP in Sprague Dawley rats. Following 10 weeks of control or ITED conditions, conscious MAP (tail-cuff) was measured, and under anaesthesia, the MAP (carotid artery catheter, pressure transducer) and NBF (Doppler ultrasound, 40 MHz) responses to sodium nitroprusside (60 µg/kg) and phenylephrine (12 µg/kg) infusion were recorded (regression equations for MAP vs NBF were created for each rodent). Thereafter, motor nerve conduction velocity (MNCV) and nerve vascularization (haematoxylin and eosin stain) were determined. Conscious MAP was higher and MNCV was lower in the ITED group (p < 0.01). In response to drug infusions, the ΔMAP and ΔNBF were similar between groups (p ≥ 0.18). Estimated conscious NBF (based on substituting conscious MAP values into each individual regression equation) was greater in the ITED group (p < 0.01). Sciatic nerve vascularization was similar between groups (p ≥ 0.50). In contrast to the hypothesis, NBF was not reduced across a range of MAP. In spite of increased estimated conscious NBF values, MNCV was reduced in rats with ITED.

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Nerve conduction velocity, laser Doppler flow, and axonal caliber in galactose and streptozotocin diabetes

Cited by 33 publications

References 40 publications

Experimental Diabetic Neuropathy With Spontaneous Recovery

Experimental Diabetic Neuropathy With Spontaneous Recovery

Response of Rat Retinal Capillary Pericytes and Endothelial Cells to Glucose

The relationship between blood pressure and sciatic nerve blood flow velocity in rats with insulin-treated experimental diabetes

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