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

The influence of Coxsackie B4 and AI3 viruses on the pancreas of mice (resistant and susceptible to diabetes) was studied. Glucose intolerance and changes in the synthesis of immunoreactive insulin were detected in all the treated groups of animals. Biochemical changes were more prominent in male DBA/2 mice, infected with Coxsackie B4 virus, in FI (CBA X C57Bl/6) hybrids and in female DBA/2 mice infected with Coxsackie AI3 virus and alloxan.
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PMID:[Experimental diabetes in mice infected with Coxsackie viruses]. 302 28

The non-obese diabetic (NOD) mouse is an animal model of insulin-dependent diabetes mellitus (IDDM), in which 80% of the females become diabetic after the age of 12 weeks. Using an in vitro assay we investigated the capacity of spleen lymphocytes from NOD mice to inhibit the insulin secretion of normal islet cells after stimulation by theophylline plus arginine. Spleen cells from diabetic NOD mice inhibited the insulin release of DBA/2 islet cells. Depletion experiments using monoclonal antibodies demonstrated that inhibitory cells belonged to the Lyt2 positive T lymphocyte subset. The phenomenon was not restricted by the MHC class I K region, shared by NOD and DBA/2 mice, since lymphocytes from diabetic NOD mice also inhibited the insulin secretion of normal Wistar rat islet cells. Inhibitory T cells were detected in overtly diabetic mice but also in non-diabetic females aged 5-11 weeks indicating that they are not secondary to metabolic disturbances and might contribute to their onset. Conversely they were not found in male NOD mice although some of these mice show insulitis. The presence of these inhibitory T cells might thus represent an early and sensitive marker of anti-islet cell-mediated autoimmunity.
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PMID:Cell-mediated immunity to pancreatic islet cells in the non-obese diabetic (NOD) mouse: in vitro characterization and time course study. 305 43

To determine genetic factors involved in diabetes susceptibility in inbred strains of mice, we initially evaluated differences in fed plasma glucose and insulin concentrations among six strains (AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J). There was considerable variation in fed plasma glucose concentration, with C3H/HeJ mice the most glucose tolerant (174 +/- 7 mg/dl) and C57BL/6J mice the least glucose tolerant (252 +/- 7 mg/dl, P less than .0001 vs. C3H/HeJ mice). Glycosylated hemoglobin of C57BL/6J mice (4.0 +/- 0.06%) was also higher than that of C3H/HeJ mice (3.52 +/- 0.06%, P less than .0001). The fed plasma insulin concentration did not differ between these two strains. Glucose tolerance was further evaluated in overnight-fasted C3H/HeJ and C57BL/6J mice by an intraperitoneal glucose tolerance test (IPGTT). Although fasting plasma glucose did not differ, the most remarkable difference in plasma glucose during IPGTT between C57BL/6J and C3H/HeJ mice was noted at 30 min (489 +/- 29 vs. 227 +/- 20 mg/dl, P less than .001). To determine the number of genes involved in the phenotypic difference in glucose tolerance, C57BL/6J males were crossed with C3H/HeJ females (F1, C3H/HeJ X C57BL/6J), and the F1 hybrid females were backcrossed with C57BL/6J males (backcrossed, F1 X C57BL/6J). Plasma glucose after 30 min on IPGTT was 219 +/- 8 (n = 21), 456 +/- 18 (n = 23), and 292 +/- 13 (n = 23) mg/dl for C3H/HeJ, C57BL/6J, and F1 mice, respectively (P less than .001 for all comparisons).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1988 Jun
PMID:Genetic analysis of glucose tolerance in inbred mouse strains. Evidence for polygenic control. 328 91

The chronogram of hyperglycaemia in alloxan-induced diabetic DBA/2 mice (living under conditions standardized for light-synchronized periodicity and fed ad libitum) presented an ultradian rhythm (during spring) different from the circadian blood glucose chronogram of normal control mice. Simultaneously, the [3H]thymidine ([3H]TdR) incorporation chronogram of diabetic mouse splenocytes, stimulated or unstimulated with Concanavalin-A (Con-A), was changed and unbalanced, compared to that of normal control mice. Previous experiments showed that the [3H]TdR incorporation chronogram of stimulated or non-stimulated splenocytes of normal DBA/2 mice presented seasonal variations. They were characterized generally by an ultradian rhythm. Yet, during spring, they exhibited a circadian rhythm because one phase was advanced and superimposed on the other, the latter being typically unvarying. It seems probable that the unbalanced rhythm of [3H]TdR incorporated in diabetic mouse splenocytes, stimulated or not, was responsible for a dysfunction of that population in diabetes.
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PMID:Effect of diabetes on the rhythm of [3H]thymidine incorporation in Con-A-stimulated mice splenocytes. 395 32

The M variant of encephalomyocarditis virus produces a diabetes mellitus-like disease in DBA/2 mice but not in animals of the C3H strain. Fewer than one-third of infected F(1) (DBA/2 x C3H) progeny exhibit the disease, whereas the prevalence in backcrosses (F(1) x DBA/2, F(1) x C3H) is comparable to the parental inbred strain. Thus, the mode of inheritance of the diabetic predisposition appears to be polygenic. DBA/2 animals develop striking inflammatory and necrotizing lesions of the islets of Langerhans; in contrast, alterations of the insular tissue in the C3H mice are minimal. Although metabolic abnormalities appear to be consequent to lesions of beta cells, the factors influencing the severity of these insular changes are incompletely understood.
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PMID:Genetic influences affecting the occurrence of a diabetes mellitus-like disease in mice infected with the encephalomyocarditis virus. 435

Infection of DBA 2 male mice with the M variant of encephalomyocarditis virus resulted in a diabetes-like syndrome. Histologic examination of the pancreas revealed damage to the beta cells with little involvement of the acinar cells. The severity of the hyperglycemia correlated closely with the degree of beta cell damage. By immunofluorescence, viral antigens could be detected in the beta cells during the first 10 days of the infection. In contrast to the response found in male DBA 2 mice, infection of DBA 2 female mice and male mice of several other strains resulted in little if any elevation of blood glucose concentration. Histologic examination of the pancreas of these animals revealed only minimal damage to the beta cells. It is concluded that differences in the severity of the hyperglycemia between DBA 2 males and females and among the different strains of male mice tested are directly related to the degree of beta cell damage produced by the viral infection.
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PMID:Virus-induced diabetes mellitus. II. Relationship between beta cell damage and hyperglycemia in mice infected with encephalomyocarditis virus. 436 78

A diabetes mellitus-like disease occurs in male DBA/2 mice infected with the M variant of the encephalomyocarditis virus. Female mice of this strain sustain systemic infection, but rarely exhibit hyperglycaemia. The diabetogenic effects of the virus were studied in 3 groups of adult DBA/2 males-castrates, castrates treated with testosterone, and sham-operated controls. After infection, pancreatic insulin concentrations decreased precipitously to approximately 10% of control values in intact males and castrates treated with testosterone; hyperglycaemia occurred concomitantly in both groups. In contrast, untreated castrates failed to develop hyperglycaemia and the effect on the insulin content of the pancreas was less striking.
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PMID:Testosterone effect on experimental diabetes mellitus in encephalomyocarditis (EMC) virus infected mice. 624 84

The diabetogenic potential of the human isolate, Coxsackievirus B4 (CB4) (Edwards) was studied in three inbred mice strains, SWR/J, DBA/2, and C57BL/6. The mice were infected with this agent and evaluated for mortality, pancreatic histopathology, and glucose tolerance. Results showed that the mortality induced by CB4 in these inbred strains differed considerably. There was no evidence of a correlation between virus-induced mortality and virus-induced pancreopathy. Although CB4 (Edwards) was most lethal to C57BL/6 mice, based on the infecting 50 per cent lethal dose (LD50), this mouse strain developed no pancreatic pathology. The most severe pancreopathy, i.e., acinar necrosis with acute interstitial inflammation and islet atrophy, was observed in SWR/J mice, which had an intermediate susceptibility to virus-induced mortality. DBA/2 mice, which displayed the lowest susceptibility to virus-induced lethality, showed less pancreatic pathology (i.e., acute and chronic interstitial inflammation) than SWR/J mice. IN SWR/J mice, virus-mediated alteration in glucose homeostasis was expressed by an increase in glucose tolerance 7 and 21 days after infection. In contrast, C57BL/6 mice showed a tendency toward chemical diabetes at 21 days postinfection. This study suggests that CB4-induced mortality and pancreatic pathology are independent parameters and do not necessarily determine the glucose tolerance of a given host genotype.
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PMID:Host factors in Coxsackievirus B4-induced pancreopathy. 627 60

Quantitative estimations were made of insulin receptors on liver cell membrane of DBA/2 mice infected with M variant of encephalomyocarditis virus. The virus produced an impairment of glucose metabolism on day 3 of infection, which lasted for 5 months. The fasting plasma insulin concentration was markedly decreased on day 14. The specific binding of 125-I insulin to the membrane receptor was significantly decreased on day 3 of infection. The binding inhibitions were stronger in male mice than in females. The number of insulin receptors began to decrease on day 1, was decreased remarkably by day 3, and returned on day 7 to the level before infection. A decrease of receptor affinity was also observed in infected animals. These results seem to show that changes in insulin receptors are one cause of the impairment of glucose metabolism in the initial phase of virus-induced diabetes.
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PMID:Insulin receptors in virus-induced diabetes mellitus in mice. 629 50

Intracisternal Type A particles (IAPs) are retroviruslike structures identified by a core protein antigen (p73) and found in mouse embryos, in many mouse tumor cells, and in pancreatic B cells of some strains of genetically diabetic mice. Using both peroxidase-antiperoxidase and protein A-gold immunocytochemical techniques to localize p73, the authors have observed differences in intracellular antigen distribution between MOPC-104E, a mouse tumor cell line rich in IAP, and B cells from genetically diabetic (db/db) mice of the CBA/LtJ and C57BL/KsJ strain. In MOPC-104E cells studied by electron microscopy, localization of protein A-gold complex label was almost exclusively limited to IAP and their sites of assembly on the rough endoplasmic reticulum. In contrast, p73 appeared widely distributed throughout the cytoplasm of B cells from hyperglycemic db/db mice but not normal littermate controls. In addition to distribution over budding IAP, label was also found dispersed through other cytoplasmic organelles involved in secretion, including Golgi complexes and secretory granules. Patch labeling of B cell surfaces was sometimes observed. An ultrastructural survey of islets isolated from normal mice of 7 inbred genetic backgrounds on which the "diabetes" (db) gene has been studied showed that constitutive ability to produce IAP was associated with strain susceptibility to severe diabetes (eg, C57BL/KsJ, DBA/2J, CBA/LtJ, and C3HeB/FeJ). Strains whose B cells failed to show constitutive expression in situ or glucose-inducible expression in cell culture were resistant to the diabetogenic action of db genes. The possibility is discussed that p73 may represent a "neoantigen" which sensitizes the diabetic mouse to reject, by autoimmune mechanisms, the B cells expressing it.
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PMID:Intracisternal Type A particles in murine pancreatic B cells. Immunocytochemical demonstration of increased antigen (p73) in genetically diabetic mice. 636 24


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