Neurologic Disorders of Diabetes Mellitus: Part II of a Two-part Review

Colby, A. O.

doi:10.2337/diab.14.8.516

Cited by 13 publications

(4 citation statements)

References 32 publications

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“…This assessment of clinical data is striking in the absence of any relationship between these variables and the elevation of perceptual threshold in the diabetic. Although past reports suggest the contributions or interactions of these factors in states of diabetic sensory disorders (Martin, 1953;Sullivan, 1958;Colby, 1965), our data fail to confirm these assumptions. Our clinical-perceptual correlative studies rather suggest the following: 1.…”

Section: Resultscontrasting

confidence: 99%

Cutaneous sensory function in diabetes mellitus.

Conomy¹,

Barnes²,

Conomy³

1979

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Resultscontrasting

confidence: 99%

Cutaneous sensory function in diabetes mellitus.

Conomy¹,

Barnes²,

Conomy³

1979

Journal of Neurology, Neurosurgery & Psychiatry

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“…Chronic hyperglycemic state and impaired insulin signaling induce neurological disorders including peripheral nerve system [ 91 , 92 ]. It has been reported that the effects of GLP-1 and GIP on the peripheral nervous system could be of significance in diabetic neuropathy.…”

Section: The Effects Of Incretin-based Therapeutic Agents On Diabmentioning

confidence: 99%

Incretin-Based Therapy for Prevention of Diabetic Vascular Complications

Mima

2016

Journal of Diabetes Research

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Diabetic vascular complications are the most common cause of mortality and morbidity worldwide, with numbers of affected individuals steadily increasing. Diabetic vascular complications can be divided into two categories: macrovascular andmicrovascular complications. Macrovascular complications include coronary artery diseaseand cerebrovascular disease, while microvascular complications include retinopathy and chronic kidney disease. These complications result from metabolic abnormalities, including hyperglycemia, elevated levels of free fatty acids, and insulin resistance. Multiple mechanisms have been proposed to mediate the adverse effects of these metabolic disorders on vascular tissues, including stimulation of protein kinase C signaling and activation of the polyol pathway by oxidative stress and inflammation. Additionally, the loss of tissue-specific insulin signaling induced by hyperglycemia and toxic metabolites can induce cellular dysfunction and both macro- and microvascular complications characteristic of diabetes. Despite these insights, few therapeutic methods are available for the management of diabetic complications. Recently, incretin-based therapeutic agents, such as glucagon-like peptide-1 and dipeptidyl peptidase-4 inhibitors, have been reported to elicit vasotropic actions, suggesting a potential for effecting an actual reduction in diabetic vascular complications. The present review will summarize the relationship between multiple adverse biological mechanisms in diabetes and putative incretin-based therapeutic interventions intended to prevent diabetic vascular complications.

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“…It is well documented that neuropathy due to diabetes mellitus causes neuronal degeneration in both motor and sensory nerves (Colby, 1965). Several studies have correlated the presence of urinary bladder dysfunction with signs of peripheral autonomic neuropathy (Bartley et al, 1966;Bradley, 1980).…”

Section: Introductionmentioning

confidence: 99%

Effect of Diabetes on the Cholinergic Enzyme Activities of the Urinary Bladder and the Seminal Vesicles of the Rat

Wahba

Soliman²,

Kolta³

2009

Exp Clin Endocrinol Diabetes

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Choline acetyltransferase (ChAT) and acetyl-cholinesterase (AChE) activities were determined in the seminal vesicles and in two regions of the urinary bladder, the detrusor muscle and sphincter-trigon in control and streptozotocin(STZ)-induced diabetic male Sprague-Dawley rats. In this study, STZ was administered (65 mg/kg, i.p.) to induce diabetes 14 days prior to sacrifice and enzyme analysis. Diabetic rats exhibited significant increase in both ChAT and AChE activities in the detrusor compared to the control animals. Significant increases in ChAT activity, however, were observed only in the seminal vesicles of diabetic animals compared to the control group. AChE activity in the seminal vesicles and sphincter-trigon region of the diabetic rats was not altered significantly. These findings suggest that urogenital complications associated with diabetes may be related to the dysfunction of the peripheral cholinergic system.

show abstract

Neurologic Disorders of Diabetes Mellitus: Part II of a Two-part Review

Cited by 13 publications

References 32 publications

Cutaneous sensory function in diabetes mellitus.

Cutaneous sensory function in diabetes mellitus.

Incretin-Based Therapy for Prevention of Diabetic Vascular Complications

Effect of Diabetes on the Cholinergic Enzyme Activities of the Urinary Bladder and the Seminal Vesicles of the Rat

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