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

The susceptibility to competitive ganglionic blocking agents such as hexamethonium (C6), tetraethylammonium bromide (TEAB), mecamylamine and d-tubocurarine (d-TC), of the superior cervical ganglion in cats with pancreatectomy and spontaneous diabetes or in animals treated with contrainsular drugs such as cortisone or dihydrochlorothiazide, was found to be decreased as compared to the reactivity of normal controls. The increased tolerance to ganglioplegics was not correlated with the elevation of the blood sugar level, and proved to be resistant to an acute administration of insulin. The results could not be explained by a decrease in the specific cholinesterase activity of the ganglionic tissue due to diabetes. Alteration of the peripheral autonomic synaptic transmission may be an early sign of diabetic neuropathy.
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PMID:Diabetes-induced alterations of autonomic nerve function in the cat. 3 32

Accumulation of acetylcholinesterase (AChE) and choline acetylase (ChAc) activities proximal to a tie placed on the sciatic nerve was measured in control, untreated diabetic, and insulin-treated diabetic rats. In the diabetic animals AChE accumulation was reduced by about 20% and ChAc accumulation by about 40%. Insulin treatment eliminated the impairment. It remains an open question whether these reversible functional changes in rat have any counterpart in the diabetic neuropathy of man.
Diabetes 1975 Dec
PMID:Fast and slow axoplasmic flow in sciatic nerve of diabetic rats. 5 67

The author discusses abnormalities in gastric emptying due to diabetes mellitus, and in particular, diabetic gastroparesis, on the basis of his own experience and the relevant literature. Diabetic gastroparesis is a result of a diabetic neuropathy of the vagus. Even in the presence of mild abdominal symptoms, particularly with repeated hypoglycaemic episodes, this condition should be considered and the stomach should be examined readiologically. A diabetic phytobezoar may develop. It may be presumed that these changes are more common than had previously been realized. The author has observed six cases. The gastric atony associated with diabetic coma has to be differentiated from the condition under discussion. Conservative treatment is recommended.
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PMID:[Disturbance of gastric emptying in diabetes mellitus (author's transl)]. 12 11

In a morphometric study of isolated fibres of the common peroneal nerve in short-term diabetic rats reduced fibre calibre was observed. No segmental demyelination or remyelination was found, but the nodes of Ranvier were slightly widened and paronodal bulbi were swollen relative to fibre calibre. It is suggested that axonal dwindling is the primary event in experimental diabetes. The reduction of the myelin sheath may be a consequence of the abnormal nerve cell offshoot. The results obtained suggest that streptozotocin diabetes in the rat is a useful model for the elucidation of diabetic neuropathy.
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PMID:Axonal dwindling in early experimental diabetes. II. A study of isolated nerve fibres. 13 58

The female patient initially showed the acquired type of total lipoatrophy at about 8 years of age. At 12 years of age, the onset of diabetes mellitus was speculated from advanced pyodermia and dedentition. At 29 years of age, glucosuria was found, and she developed proteinuria, ascites, and pretibial edema. The physical examination revealed: hepatosplenomegaly, complete absence of subcutanous fat, cutaneous xanthomas, and emaciated facies with pronounced zygomatic arches. Diabetic retinopathy was revealed in the ophthalmological examination, and nephropathy was evident in renal biopsy specimens. She also had peripheral diabetic neuropathy. No adipose tissue was found in the mesenterium under peritoneoscopy. The hepatic biopsy specimen revealed advanced portal liver cirrhosis. Laboratory findings included: hyperlipidemia, elevation of BMR without evidence of hyperthyroidism, impaired renal function, and undetected anti-insulin antibodies and anti-insulin antibodies. Endocrinological examinations revealed normal value, except for an impaired hGH response in the arginine test. C-peptide immunoreactivity was high. Her condition was fairly well controlled by 140 units of insulin injection daily.
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PMID:Lipoatrophic diabetes. Report of a case. 15 92

Serum pyridoxal (vitamin B6) concentrations were measured in 50 patients with significant diabetic neuropathy. There were 24 males and 26 females with a mean age of 58.2 years and a mean duration of diabetes of 9.8 years. The level of pyridoxal was significantly lower in these patients when compared with randomly selected diabetic patients matched for age and sex without clinical evidence of neuropathy. There was no significant difference in the duration of the diabetes between the two groups. The results indicate an association between pyridoxal deficiency and neuropathy in diabetic patients.
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PMID:Serum pyridoxal concentrations in patients with diabetic neuropathy. 21 98

Diabetes, with only mild ketosis, was induced in male rats by a single injection of streptozotocin. After 12 weeks the specific activities of enzymes concerned with the metabolism of inositol and of inositol lipids were measured in various tissues. Inositol 1-phosphate synthase (EC 5.5.1.4) was most active in testis and the activity was significantly less in diabetic rats than in controls on a similar diet. Inositol oxygenase (EC 1.13.99.1), which converts myo-inositol into glucuronic acid, was also less active in kidney from diabetic animals. CDP-diacylglycerol-inositol phosphatidyltransferase (EC 2.7.8.11) and phosphatidylinositol 4-phosphate kinase (EC 2.7.1.68) showed decreased specific activities in brain and sciatic nerve of diabetic rats. By contrast the diabetic state did not affect the specific activities of phosphatidylinositol kinase (EC 2.7.1.67) or phosphatidylinositol 4,5-bisphosphate phosphatase (EC 3.1.3.36) in these tissues. The results are discussed in relation to diabetic neuropathy.
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PMID:Enzymes of myo-inositol and inositol lipid metabolism in rats with streptozotocin-induced diabetes. 22 62

The role of metabolic abnormalities in the development of diabetic neuropathy is controversial. To investigate the influence of hyperglycemia on nerve conduction, we studied 20 untreated maturity-onset diabetic patients and 23 normal control subjects of similar age. Nerve conduction velocity of motor (median, peroneal, and tibial) and sensory (median and sural) nerves in diabetic patients was significantly slowed and H-reflex latency time prolonged. Levels of fasting plasma glucose in diabetic subjects were correlated with slowed motor conduction velocity of the median, peroneal, and tibial nerves but not with sensory nerve conduction velocities. Levels of glycosylated hemoglobin, an index of long-term glycemia, were correlated with slowing of peroneal motor conduction velocity in diabetic patients. These associations could not be explained by patient age or duration of diabetes. These findings suggest that the degree of hyperglycemia of untreated maturity-onset diabetes contributes to the motor nerve conduction abnormalities in this disease.
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PMID:Nerve conduction abnormalities in untreated maturity-onset diabetes: relation to levels of fasting plasma glucose and glycosylated hemoglobin. 42 98

To study endoneurial lipid composition in human diabetic neuropathy, we biopsied sural nerves from 3 middleaged men with adult-onset diabetes mellitus. Magnitude of electrophysiological abnormalities and myelinated fiber loss paralleled the clinical severity of neuropathy in all cases. Cholesterol ester concentration was elevated to about 800% of normal in diabetic nerves. Reduction in total endoneurial lipid concentration correlated best with decrease in myelin volume as calculated from measured fiber diameters. Cholesterol, cerebroside, and most phospholipids were reduced in keeping with the severity of fiber loss in each nerve. The phosphatidylinositol-phosphatidylserine fraction was most reduced in the least affected nerves. Cerebroside nonhydroxy fatty acids in diabetic nerves were of shorter chain length and more saturated than normal. It is not yet clear whether the abnormalities of phosphatidylinositol-phosphatidylserine and cerebroside fatty acids are of pathogenetic importance or whether these changes may be the nonspecific consequence of axonal degeneration.
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PMID:Nerve lipid abnormalities in human diabetic neuropathy: a correlative study. 44 57

The clinical details of six patients who developed spontaneous dislocations in the foot or ankle are presented. All were shown to have diabetic neuropathy. This previously unreported condition can occur with a short history of diabetes. Some cases can be managed without operation, though arthrodesis probably offers the best chance of obtaining a stable foot of satisfactory shape.
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PMID:Spontaneous dislocation in diabetic neuropathy. A report of six cases. 50 Jul 61


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