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

The so-called M-variant (especially subtype D) of encephalomyocarditis virus (EMCV) induces a diabetes-like syndrome in certain mouse strains which may serve as a model of insulin-dependent diabetes mellitus (IDDM) in man. The development and course of diabetes was influenced by a number of virus and host factors, among these being virus strain, virus dose, mouse strain, age, sex, and the host's immunological status. In a D-variant stock of EMCV, we found a virus plaque variant (PV 2) diabetogenic for DBA/2 mice, and at least one variant (PV 7) that did not affect carbohydrate metabolism. Although the diabetogenicity of PV 2 proved to be a genetically stable characteristic after further passages in vivo and in vitro, the incidence of diabetes varied somewhat (mean value 65% in 10-week-old DBA/2 mice infected with 10(5) p.f.u.). Both lower (10(1) or 10(3) p.f.u.) and higher (10(7) or 10(8) p.f.u.) virus doses led to a diminished incidence and severity of diabetes. In younger animals (5 weeks) transient hyperglycaemia often appeared, whereas in older animals (20 weeks) there was a higher rate of mortality. Histological examination of the islets of Langerhans in diabetes-susceptible (DBA/2) and resistant (C57BL/6) mice revealed that EMCV-induced hyperglycaemia appeared to develop in parallel to islet cell damage. Even in diabetic animals, some unaffected islets were regularly found. This study demonstrates that EMCV mutants may have completely different biological effects and produce diabetes only in special circumstances. Host factors play a significant role in the development of diabetes.
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PMID:Encephalomyocarditis virus and diabetes mellitus: studies on virus mutants in susceptible and non-susceptible mice. 298 15

During the fall of 1979, 22/250 Swedish UN soldiers serving in Egypt were hospitalized with fever and gastroenteritis associated with aseptic meningitis. One of the 22 developed insulin dependent diabetes mellitus (IDDM) 10 weeks following the infection. The majority of the 22 patients showed significant titer rise for coxsackievirus B by plaque reduction neutralization test. The serology results indicate that coxsackievirus B4 most likely caused the outbreak. All 22 were also tested for islet cell cytoplasmic antibodies and islet cell surface antibodies and found negative. The individual developing diabetes mellitus had the HLA-DR phenotype 3,4, which is associated with IDDM.
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PMID:An outbreak of coxsackievirus B infection followed by one case of diabetes mellitus. 298 80

DBA/2 and Balb/cBY mice were infected with approximately 30 plaque-forming units of the M-variant of encephalomyocarditis (EMC-M) virus. Seven days after inoculation the majority of the animals of both strains were hyperglycemic. A significant correlation between increased concentrations of virus in the pancreas and hyperglycemia was found among individual DBA/2 animals, but not among Balb/cBY mice. T-lymphocyte depletion of DBA/2 mice before infection failed to alter the incidence or severity of hyperglycemia in comparison to intact animals. Conversely, hyperglycemia in T-lymphocyte-depleted Balb/cBY mice was reduced substantially in comparison to infected immunocompetent animals. There appears to be at least two genetically influenced pathogenic mechanisms of diabetes in EMC-M virus-infected mice. In some strains of animals, hyperglycemia results exclusively from viral infection and the consequent injury to the beta cells, whereas in other animals, viral damage to the islets is compounded by immunologic events.
Diabetes 1985 Nov
PMID:Genetic influences on the immunologic pathogenesis of encephalomyocarditis (EMC) virus-induced diabetes mellitus. 299 82

Experiments were performed to determine whether genetic predisposition to diabetes mellitus (DM) or clinical DM or both exert an influence on the production of neutralization antibodies to coxsackievirus B4 (CB4). The homozygous diabetic mutant mouse db+/db+, on the inbred C57BL/KsJ genetic background, develops a diabetes-like disease when maintained on ad libitum diet but restriction of excess food intake prevents overt disease. The doubly heterozygote db+/+m or the homozygote +m/+m misty coat color mutant, on the C57BL/KsJ genetic background, do not develop DM and served as controls. Animals infected with one-half a previously determined LD50 of CB4 were bled prior to infection and at 3, 5, 7, 14, 21 days and at 1, 2, 3, 4 and 5 months after infection. Serum neutralization antibody (NA) levels were determined from the percent CB4 plaque reduction. Until 2 months following infection, NA levels were not significant in either of the homozygous diabetic mutant groups, db+/db+. In the diabetic mutant group db+/db+, without overt disease, neutralization of CB4 when observed, was low, short-lived, and apparently not specific. However, in the homozygous diabetic mutants with spontaneous diabetes, CB4 NA became evident at 2 months after infection. By 3 months post-infection, serum NA levels were sufficient to cause 90% virus plaque reduction. These observations demonstrate that hereditary DM as characterized by the mutation diabetes, db, in the C57BL/KsJ mouse, is associated with a marked impaired humoral immune response to a diabetogenic human CB4. Specifically, there is an inability to develop an adequate level of anti-CB4 antibodies. The type and degree of immunological impairment are apparently different prior to and after onset of diabetes mellitus.
Diabetes Res Clin Pract 1986 May
PMID:Genetic predisposition to diabetes mellitus is associated with impaired humoral immunity to coxsackievirus B4. 301 55

Patients with diabetes mellitus are more prone to stroke than non-diabetic patients. Using Duplex ultrasound imaging of the carotid bifurcation, we have found it possible to classify atherosclerotic plaques into four groups which appear to reflect the plaque pathology. Using this classification we have found that diabetics and non-diabetics have similar ultrasound plaque type distributions in symptomatic patients. Further subdivision of the diabetic patients on the basis of their mode of diabetic control has shown that insulin treated diabetics tend to show little evidence of intraplaque haemorrhage and ulceration. These features suggest that factors other than atherosclerosis at the carotid bifurcation may be responsible for the increased stroke risk in diabetic patients. Diabetic microangiopathy and reduced vessel compliance due to medial calcification have been suggested as possible factors. Insulin treatment of diabetics may protect against the development of occlusive atherosclerosis.
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PMID:Carotid artery disease: the influence of diabetes mellitus. 306 9

This study was designed to evaluate the relationship of inflammatory periodontal disease to the diabetic status of the insulin-dependent diabetes mellitus (IDDM) patient. 52 IDDM patients, ages 11-22 years, were evaluated. These patients were closely monitored at regular intervals in the University of Kentucky pediatric diabetic clinic. A periodontal examination was carried out for each patient. The patients were then assigned to a periodontitis or non-periodontitis group. Moderate to advanced periodontitis was found in 5.8% of the subjects. The gingival index and sulcular bleeding index were significantly higher in the periodontitis group (P less than 0.05). There was no significant difference between groups for plaque index, age of diabetic onset, duration of diabetes, present age, insulin dosage/weight, or serum glucose (P greater than 0.05). There was a greater % of ketoacidosis, retinopathy and neuropathy in the periodontitis group. IDDM patients with neurological complications or a history of chronic infections had a significantly higher gingival index score than those without the complication (P less than 0.05).
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PMID:The relationship of inflammatory periodontal disease to diabetic status in insulin-dependent diabetes mellitus patients. 314 83

The subgingival microflora and serum antibody response was examined in periodontitis patients with noninsulin-dependent diabetes mellitus (NIDDM), impaired glucose tolerance (IGT), and normal glucose tolerance (NGT). The predominant cultivable microflora was determined for subgingival plaque sampled from two deep periodontal pockets in each of eight adult periodontitis patients with NIDDM. Indirect immunofluorescence for Bacteroides intermedius, Bacteroides gingivalis, and Haemophilus actinomycetemcomitans was used to examine these same samples as well as 186 additional subgingival plaque samples from 47 patients with moderate to severe generalized periodontitis including 25 subjects with NIDDM, six subjects with IGT, and 16 subjects with NGT. Serum antibody levels to 13 microorganisms including seven oral bacterial species and one nonoral control species were measured by enzyme-linked immunosorbent assays (ELISA) in 377 subjects including 84 normal subjects without periodontal disease, 112 normal subjects with periodontitis, 19 periodontally normal subjects with IGT, 65 periodontitis patients with IGT, 15 periodontally normal subjects with NIDDM, and 82 periodontitis patients with NIDDM. Three hundred eighty-two bacterial isolates were recovered from the eight patients. B. intermedius was the most frequently isolated microorganism constituting 16% of the total isolates followed by Wolinella recta and B. gingivalis, which each accounted for 13% of the total. Streptococcus sanguis was the most prevalent microorganism, which was found in 75% of the sites. Subgingival plaque samples examined by immunofluorescence demonstrate a high prevalence of black-pigmented Bacteroides and suggest that the proportion of B. gingivalis but not B. intermedius is higher in NIDDM with periodontitis than in other groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microbiological and immunological studies of adult periodontitis in patients with noninsulin-dependent diabetes mellitus. 327 68

Theories of intimal injury leading to plaque formation include platelet adhesion and production of growth factors, hypercholesterolemia, smooth muscle cell proliferation, macrophage activity, defective utilization of low-density lipoproteins via deficient receptors, and deficiency in cellular lysosomal enzymes. High levels of low-density lipoproteins and intermediate-density lipoproteins, as well as their apoproteins, are strong risk factors for cardiovascular disease. The lowering of the cholesterol level has been shown to produce significant regression of atherosclerotic lesions. Data also suggest an interaction between lipids and platelets, although the role of coagulation disorders as an independent risk factor for atherosclerosis is difficult to assess. Although much of the data are controversial, there is evidence that platelet survival time is a strong predictor of severe vessel damage. In addition, some studies have reported decreased activity of antithrombin III with coronary artery disease, and there appears to be a direct correlation between fibrinogen and cholesterol levels. Finally, diabetes mellitus (both types I and II) is a significant independent risk factor for atherosclerosis. The risk is not related to the severity or duration of diabetes, and it appears to be greater in women than in men.
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PMID:Lipids, clotting factors, and diabetes: endogenous risk factors for cardiovascular disease. 328 30

A morphometric study was performed on histological sections of the extramural coronary arteries from 10 Type 2 (non-insulin-dependent) diabetic patients and 10 non-diabetic subjects, matched for age and sex. Standardised samples were taken from the two coronary arteries and the fractional contents of Periodic Acid-Schiff-positive material, acid mucopolysaccharides and connective tissue was determined in the arterial tunica media from the two groups using a point-counting technique. The thickness of tunica intima and tunica media was obtained by micrometric measurements. There was no difference in the thickness of tunica intima with and without atherosclerotic plaque between the vessels from diabetic and nondiabetic hearts. However, the thickness of tunica media was significantly reduced in arteries from the diabetic patients (2p less than 0.01). In tunica media of the diabetic patients there was a significant increase (50%) in the amount of Periodic Acid-Schiff-positive material (2p less than 0.01), whereas the content of acid mucopolysaccharides (alcian-blue positive) was significantly reduced (2p less than 0.02). These changes in tunica media were similar in areas below and outside the intimal atherosclerotic plaques. The content of connective tissue was found to be significantly increased in the arteries from the diabetic patients, but only in areas outside atherosclerotic plaques (2p less than 0.025). There was no correlation between the observed changes in tunica media and the known duration of diabetes. The results obtained in the present study may be ascribed to the presence of a non-atherosclerotic diabetic macroangiopathy.
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PMID:Diabetic macroangiopathy. Quantitative histopathological studies of the extramural coronary arteries from type 2 (non-insulin-dependent) diabetic patients. 344 55

The periodontal pocket probing depths of mandibular incisors of plaque-susceptible (Sus) rats, which spontaneously exhibit gingivitis with accumulation of plaque, were increased 20 days after injection of streptozotocin (70 mg/kg, i.v.). The accumulated plaque weights were also increased in Sus rats with streptozotocin diabetes, and a positive correlation was found between the plaque weights and the pocket depths. Histological findings showed that this inflammatory reaction in gingival tissue was higher and more extensive in diabetic Sus rats than in control Sus rats. These findings suggest that the accumulated plaque is the important factor for the severe breakdown of gingival tissue in this experimental model.
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PMID:Effect of streptozotocin diabetes on gingivitis in plaque-susceptible rats. 345 98


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