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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic neuropathy is a degenerative complication of diabetes accompanied by an alteration of nerve conduction velocity (NCV) and Na,K-ATPase activity. The present study in rats was designed first to measure diabetes-induced abnormalities in Na,K-ATPase activity, isoenzyme expression, fatty acid content in sciatic nerve membranes, and NCV and second to assess the preventive ability of a fish oil-rich diet (rich in n-3 fatty acids) on these abnormalities. Diabetes was induced by intravenous streptozotocin injection. Diabetic animals (D) and nondiabetic control animals (C) were fed the standard rat chow either without supplementation or supplemented with either fish oil (DM, CM) or olive oil (DO, CO) at a daily dose of 0.5 g/kg by gavage during 8 weeks. Analysis of the fatty acid composition of purified sciatic nerve membranes from diabetic animals showed a decreased incorporation of C16:1(n-7) fatty acids and arachidonic acids. Fish oil supplementation changed the fatty acid content of sciatic nerve membranes, decreasing C18:2(n-6) fatty acids and preventing the decreases of arachidonic acids and C18:1(n-9) fatty acids. Protein expression of Na,K-ATPase alpha subunits, Na,K-ATPase activity, and ouabain affinity were assayed in purified sciatic nerve membranes from CO, DO, and DM. Na,K-ATPase activity was significantly lower in sciatic nerve membranes of diabetic rats and significantly restored in diabetic animals that received fish oil supplementation. Diabetes induced a specific decrease of alpha1- and alpha3-isoform activity and protein expression in sciatic nerve membranes. Fish oil supplementation restored partial activity and expression to varying degrees depending on the isoenzyme. These effects were associated with a significant beneficial effect on NCV. This study indicates that fish oil has beneficial effects on diabetes-induced alterations in sciatic nerve Na,K-ATPase activity and function.
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PMID:Alterations of Na,K-ATPase isoenzymes in the rat diabetic neuropathy: protective effect of dietary supplementation with n-3 fatty acids. 968 64

Diabetic neuropathy is a common complication in diabetes mellitus. Diabetic neuropathy is accompanied by alterations in axonal excitability, which can lead to either "positive" (paresthesia, dysesthesia, pain) and/or "negative" (hypesthesia, anesthesia) symptoms. The mechanisms underlying these alterations in axonal excitability are not well understood. Clinical tests reveal reduced nerve conduction velocity and axonal loss, but fail to explain nerve excitability. Many different factors have been suggested in relation to the pathophysiology of diabetic neuropathy. There are probably as many factors as there are different clinical pictures in diabetic neuropathy. Nevertheless, it seems that hyperglycemic hypoxia is mainly responsible for the electrophysiological changes seen in damaged diabetic nerves. This article summarizes experimental data indicating that a dysfunction of ion conductances, especially voltage-gated ion channels, could contribute to abnormalities in the generation and/or conduction of action potentials in diabetic neuropathy.
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PMID:The role of axonal ion conductances in diabetic neuropathy: a review. 973 52

Diabetic neuropathy, particularly autonomic disorders, is early and frequent. When it affects the heart, it is also called cardiac autonomic neuropathy (CAN) and its clinical manifestations, especially increased heart rate, and subclinical manifestations are reported here, together with the techniques used to study this disease: Ewing's test, "Finapres", Holter ECG. Tachycardia, occurs early, is almost constant during diabetes and has a prognostic value.
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PMID:[Heart rate and diabetes mellitus]. 977 62

Neuropathy is a classical complication of diabetes mellitus, to the same extent as micro- and macroangiopathy. Diabetic neuropathy can be schematically divided into peripheral neuropathy, especially in the lower limbs (distal polyneuropathy), and autonomic neuropathy, present in all systems (cardiovascular, gastrointestinal, urogenital and even pulmonary abnormalities). Detection should be based on an oriented anamnesis and a careful physical examination. Complementary exams may be performed in order to confirm the diagnosis and assess the severity of the neuropathy. While the diagnosis of peripheral neuropathy is essentially based on clinical examination, that of autonomic neuropathy has been markedly facilitated by simple standardised tests for early detection of cardiac autonomic neuropathy. Depending on the terminology, the diagnostic criteria and the characteristics of the population, the prevalence of diabetic neuropathy can range from 15 to 100%. However, all studies agree that prevalence is important in both types of diabetes (Type 1 and Type 2), that it increases with age and disease duration, and that it is inversely related to the quality of glycaemic control. Detection of neuropathy is an essential step in the clinical approach to diabetic patients, mainly because of the prognosis linked to such a diagnosis, at both an early and late stage of the disease. Once neuropathy is diagnosed, the physician should provide specific advice to diabetic patients in order to prevent possible dramatic complications.
Diabetes Metab 1998 Nov
PMID:[Diabetic neuropathy: epidemiologic and predictive data]. 988 Dec 32

Diabetic neuropathy has been associated with a decrease in nerve conduction velocity, Na,K-ATPase activity and characteristic histological damage of the sciatic nerve. The aim of this study was to evaluate the potential effect of a dietary supplementation with fish oil [(n-3) fatty acids] on the sciatic nerve of diabetic rats. Diabetes was induced by intravenous streptozotocin injection. Diabetic animals (n = 20) were fed a nonpurified diet supplemented with either olive oil (DO) or fish oil (DM), and control animals (n = 10) were fed a nonpurified diet supplemented with olive oil at a daily dose of 0.5 g/kg by gavage for 8 wk. Nerves were characterized by their conduction velocity, morphometric analysis and membrane Na, K-ATPase activity. Nerve conduction velocity, as well as Na,K-ATPase activity, was improved by fish oil treatment. A correlation was found between these two variables (R = 0.999, P < 0.05). Moreover, a preventive effect of fish oil was observed on nerve histological damage [endoneurial edema, axonal degeneration (by 10-15%) with demyelination]. Moreover, the normal bimodal distribution of the internal diameter of myelinated fibers was absent in the DO group and was restored in the DM group. These data suggest that fish oil therapy may be effective in the prevention of diabetic neuropathy.
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PMID:Fish oil supplementation prevents diabetes-induced nerve conduction velocity and neuroanatomical changes in rats. 991 1

Estimates of the prevalence of diabetic neuropathy range from 10% to 90% of the diabetic population, depending on the criteria used to define neuropathy. Diabetic neuropathy encompasses a wide range of abnormalities affecting both the peripheral and autonomic nervous systems and causes considerable injury and death. Neurologic complications occur equally in type 1 and type 2 diabetes mellitus, as well as various forms of acquired diabetes. In this overview, we present and discuss the most recent approaches to the treatment of the common forms of diabetic neuropathy, including distal symmetric, proximal motor, and autonomic neuropathy. We also provide the reader with algorithms for recognition and management of common pain and entrapment syndromes, and a global approach to recognition of syndromes requiring specialized treatments based upon our improved understanding of their causes.
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PMID:Diagnosis and management of diabetic neuropathy. 1033 35

Diabetic neuropathy, which affects 60% to 70% of those with diabetes mellitus, is one of the most troubling complications for persons with diabetes, often leading to foot ulcers and potentially to lower limb amputations, both of which are preventable. The physiologic, structural, and functional changes associated with diabetic neuropathy and foot ulcers are discussed. Advanced practice nurses are in a unique position to implement strategies for the prevention of serious and debilitating complications from diabetic neuropathy, including foot assessment, education, and specialist referrals. Research evidence is given to support the use of the Semmes-Weinstein monofilaments to evaluate decreased plantar sensation, a common precursor to ulceration. Ongoing patient and family education can emphasize the importance of preventive self-care measures. Referrals for specialist care and therapeutic footwear can be made by advanced practice nurses. If begun early, these interventions can prevent foot ulcers from diabetic neuropathy, thereby improving the quality of life and reducing healthcare costs for this chronic disease.
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PMID:Diabetic neuropathy: pathophysiology and prevention of foot ulcers. 1038

Diabetic neuropathy is the most common secondary complication of diabetes mellitus. Several pathogenetic factors have been proposed for diabetic neuropathy. The present investigation was undertaken to study different components of signal transduction from discrete brain regions from streptozotocin-induced diabetic rats. Rats were sacrificed after 1 and 3 months of induction of diabetes, and a control group was also studied in parallel to ascertain the specificity of diabetes-associated changes. Blood glucose level and protein content of discrete brain regions were also estimated. Signal transduction cascade components like protein kinase A, protein kinase C, cAMP, phospholipase C, phospholipase A2, diacylglycerol and inositol phosphate levels were assayed in control and diabetic groups of rats. Significant attenuation in phosphoinositide metabolism along with activation of protein kinase activities were observed. These findings provide evidence to suggest a mechanism linking changes in signal transduction cascade, which is observed in 1- and 3-month diabetic rats, which ultimately leads to development of diabetic neuropathy.
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PMID:Impact of diabetes on CNS: role of signal transduction cascade. 1043 78

Diabetic neuropathy consists of several clinical syndromes affecting motor, sensory and autonomic nerves. Of these the most common is distal symmetric sensory polyneuropathy usually referred to as diabetic neuropathy. Animal studies, mainly in diabetic rodents, have contributed tremendously to our understanding of this disease. From these it is clear that the pathogenesis of diabetic neuropathy is multifactorial involving sequentially occurring and often closely interrelated metabolic aberrations. Major pathogenetic mechanisms include increased activity of the polyol pathway, abnormalities in vasoactive substances, non-enzymatic glycation, increased presence of free radicals, and perturbed neurotrophism. Traditionally the neuropathies accompanying Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus have been regarded as identical. Recent investigations have, however, clearly delineated distinct differences in the functional and structural expressions of the neuropathies in the two types of diabetes. Major future challenges are the identification of the differences in underlying pathogenetic mechanisms in the two types of neuropathy and in gaining a better understanding of the hierarchy of the multifactorial mechanisms underlying the disease. This will be important for designing meaningful therapies which to date have failed miserably in diabetic neuropathy.
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PMID:Experimental diabetic neuropathy: an update. 1044 Jan 18

Diabetic neuropathy is thought to comprise a reversible metabolic and an irreversible structural component of neuronal abnormality. To study whether cardiac sympathetic dysinnervation in poorly controlled longer-term Type 1 Diabetes Mellitus (DM) without myocardial perfusion abnormalities is partially reversible with improved metabolic control, 123-I-metaiodobenzylguanidine (123-I-MIBG) scintigraphy (myocardial uptake score 1-6) was performed in 11 Type 1 DM patients (HbA1c 12.0 +/- 1.8%, duration of diabetes 10 +/- 4 yrs) one year after initial assessment. During follow-up, all patients had been treated with intensive insulin therapy and at one year, HbAlc had fallen to 8.4 +/- 1.4% (p < 0.01). The global myocardial 123-I-MIBG uptake score had improved in 5 patients at one year, remained unchanged in 5 patients, and deteriorated in 1 patient. Cardiac sympathetic dysinnervation (123-I-MIBG myocardial uptake (MU) score >2), initially observed in 10 patients, was detectable in 8 patients at follow-up. Myocardial uptake scores of the anterior, lateral, posterior, septal and apical region had improved in 6, 6, 6, 7 and 6 patients, but the mean changes of these scores did not reach significance. In patients with substantial improvement of metabolic control (HbAlc 7.3 +/- 0.6% at one year, mean HbA1c of months 2-12: 7.8%, n = 6), global myocardial uptake had improved from 4.3 +/- 1.0 to 3.2 +/- 1.0 (p < 0.05). Respectively, myocardial uptake score of the anterior, posterior and septal region had ameliorated: 3.8 +/- 1.3 vs 2.3 +/- 0.8 (p < 0.05), 4.0 +/- 1.7 vs 2.5 +/- 1.0 (p < 0.05), 4.3 +/- 1.2 vs 3.2 +/- 1.5 (p < 0.05). In conclusion, cardiac sympathetic dysinnervation in poorly controlled longer-term Type 1 DM patients is dominated by irreversible neuronal abnormalities. Substantial metabolic improvement, however, partially restores cardiac sympathetic dysinnervation, indicating the presence of a reversible component of cardiac sympathetic dysfunction in longer-term Type 1 DM.
Exp Clin Endocrinol Diabetes 1999
PMID:Scintigraphically assessed cardiac sympathetic dysinnervation in poorly controlled type 1 diabetes mellitus: one-year follow-up with improved metabolic control. 1048 43


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