Zur Virusgenese des Diabetes mellitus bei der weißen Maus

Müntefering, Horst; Schmidt, Werner; Körber, W

doi:10.1055/s-0028-1108315

Cited by 26 publications

(8 citation statements)

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“…It is remarkable that both changes are already evident during the first and second day after infection even though the first morphological alterations at the light or electron microscopic level become visible in the pancreas only after the end of the second day. A biphasie blood sugar curve, with the first peak occurring during days 1 and 2, has also been observed by MLintefering et al [6], whereas Craighead and coworkers [3--5] recorded no blood glucose values before the fourth day after infection. The cause for this initial episode of hyperglycaemia and for the concomitant decrease of pancreatic insulin concentration during days 1 and 2 of the experiment is not readily apparent.…”

Section: Discussionsupporting

confidence: 61%

“…Damage to the islets of Langerhans is often severe enough to induce a diabetes mellitus-likc syndrome [3,4]. Virologic, physiologic and morphologic changes that characterize this syndrome have recently been recorded by Craighcad and Steinke [5] as well as by M/intefcring and coworkers [6]. The present communication supplements and extends these observations, especially at the ultrastruetural level.…”

Section: Jfeinstruktur Der Langerhansschen Inseln Der Maus Nach Infeksupporting

confidence: 66%

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Fine structure of pancreatic islets of mice infected with the M variant of the encephalomyocarditis virus

et al. 1972

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Seventy-seven male, 12 to 16 week old CD-1 mice were injected subcutaneously with the M variant of the encephalomyoearditis (EMC) virus. Thirteen saline-injected mice served as controls. The 45 surviving virus-injected mice were sacrificed at intervals ranging from 24 h to 15 days following injection. Blood glucose values were distinctly elevated during the first 2 days and again between the seventh and fifteenth day of the experiment. Immunoassay of pancreatic tissue revealed a lowering of the mean insulin concentration to one half of that of the control mice. Pancreas suspensions assayed for the presence of virus 2~ to 9~ days after infection yielded significant titers as determined by cytopathie effect. No morphologic changes were detected during the first 2 days after virus injection. Thereafter, disruption of islet cell architecture, B cell necrosis, B cell degranulation, and mononuclear cell infiltrates were noted by light microscopy. Ultrastrueturally, disruption of nuclear material, dilatation of the perinuclear space, and the appearance of cytoplasmic vesicles filled with fine granular substance were seen in B cells during the early phase of the experiment. Histiocytic response and removal of damaged B cells was prompt. Crystalline viral arrays were not identified. Poor granulation and dilatation of the units of the endoplasmic reticulum were noted in many surviving B cells. Damage to exocrine aeinar cells was of limited extent. No salivary gland lesions were identified.

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Section: Discussionsupporting

confidence: 61%

Section: Jfeinstruktur Der Langerhansschen Inseln Der Maus Nach Infeksupporting

confidence: 66%

Fine structure of pancreatic islets of mice infected with the M variant of the encephalomyocarditis virus

et al. 1972

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“…First, infectious virus can be recovered from the pancreas during the acute phase of the infection. Second, the infection results in diminution in the number and size of the islets of Langerhans and marked degranulation of beta cells (10,11,15). Third, decreased levels of IRI in the pancreas of infected mice have been reported, but the effect of EMC infection on the IRI levels in the blood has been difficult to evaluate because of wide variation in the data and small numbers of animals (11).…”

Section: Discussionmentioning

confidence: 99%

Virus-Induced Diabetes Mellitus

Boucher

Notkins

1973

The Journal of Experimental Medicine

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Infection of DBA/2N male mice with encephalomyocarditis virus resulted in a diabeteslike syndrome characterized by hyperglycemia, glycosuria, hypoinsulinemia, polydipsia, and polyphagia. Blood glucose levels were elevated within 4 days after infection and reached a maximum mean level of 320 mg/100 ml within 12 days. Approximately 60–80% of the animals developed a transient hyperglycemia while 10–15% of the animals remained hyperglycemic for well over 6 mo. The remaining animals failed to become hyperglycemic but many had abnormal glucose tolerance curves. Hyperglycemia was most pronounced when animals were allowed free access to food, and the incidence of byperglycemia was related both to the strain and sex of the animals, with few females developing hyperglycemia. The amount of immunoreactive insulin in the plasma of infected hyperglycemic mice was significantly lower than in appropriate controls, and injection of exogenous insulin resulted in a rapid drop in the blood glucose levels. Despite the fact that certain animals were hyperglycemic for many months, virus could not be recovered from the pancreas after the first 10 days of the infection.

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“…EMC, a picornavirus biologically similar to the group B coxsackie viruses, produces a disease in mice which exhibits many features of human juvenile-type diabetes (9)(10)(11)(12)(13). Accordingly, it seemed appropriate to employ this model using inbred strains of mice in an effort to define the role of genetic factors which might affect the occurrence of the disease in animals.…”

Section: Discussionmentioning

confidence: 99%

“…I t was found that the onset of the metabolic abnormalities was associated with virus replication in the pancreas and damage to beta cells in the islets of Langerhans. Detailed virologic, biochemical, and pathologic studies of this animal model have been reported in several recent publications (10)(11)(12)(13).…”

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confidence: 99%

Genetic Influences Affecting the Occurrence of a Diabetes Mellitus-Like Disease in Mice Infected With the Encephalomyocarditis Virus

Craighead

Higgins

1974

The Journal of Experimental Medicine

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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 F1 (DBA/2 x C3H) progeny exhibit the disease, whereas the prevalence in backcrosses (F1 x DBA/2, F1 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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Zur Virusgenese des Diabetes mellitus bei der weißen Maus

Cited by 26 publications

References 0 publications

Fine structure of pancreatic islets of mice infected with the M variant of the encephalomyocarditis virus

Fine structure of pancreatic islets of mice infected with the M variant of the encephalomyocarditis virus

Virus-Induced Diabetes Mellitus

Genetic Influences Affecting the Occurrence of a Diabetes Mellitus-Like Disease in Mice Infected With the Encephalomyocarditis Virus

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