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

The development of insulin-dependent diabetes mellitus is thought to be dependent on either the autoimmunity or the interaction of environmental agents with the pancreatic beta cells, or both in a genetically susceptible host. As environmental factors affecting the induction of type I diabetes, diabetogenic chemicals and viruses are likely candidates as primary injurious agents for pancreatic beta cells in man and animal. A number of structurally diverse chemicals including alloxan, streptozotocin, chlorozotocin, vacor, and cyproheptadine are diabetogenic mainly in rodents and sometimes in man. The possible mechanisms for the beta cell destruction by these chemicals include (a) generation of oxygen free radicals and alteration of endogenous scavengers of these reactive species; (b) breakage of DNA and consequent increase in the activity of poly ADP ribose synthetase, and enzyme depleting NAD in beta cells; and (c) inhibition of active calcium transport and calmodulin-activated protein kinase activity. Regarding viruses, a number of different viruses including encephalomyocarditis virus, Mengovirus, Coxsackie B viruses, and Reoviruses can infect and destroy pancreatic beta cells mainly in rodents and sometimes in humans. In the murine model, the development of encephalomyocarditis and Coxsackie B virus-induced diabetes is dependent on the genetic background of the host and the genetic makeup of the virus. Mengo-2T virus has caused diabetes in strains of mice resistant to encephalomyocarditis virus-induced diabetes. In contrast to encephalomyocarditis virus, Coxsackie B viruses, and Mengovirus, reovirus type 1 seems to be somewhat associated with an autoimmune response in the induction of diabetes. In addition to the murine model, cotton rats become diabetic when inoculated with Mengovirus 2T. Furthermore, cumulative environmental insults with Coxsackie B viruses and chemicals result in diabetes in non-human primates. In man, there may be 2 possible roles for viruses in the pathogenesis of insulin-dependent diabetes mellitus. The one is acute cytolytic infection of beta cells (e.g., Coxsackie B viruses), which may sometimes induce diabetes in genetically predisposed individuals, and the other one is slow and persistent infection (e.g., congenital cytomegalovirus and Rubella), which may induce autoimmunity, leading to type I diabetes.
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PMID:Effects of environmental factors on the development of insulin-dependent diabetes mellitus. 331 67

In order to determine if congenital rubella infection is associated with persistent T cell abnormalities, T cell subsets were quantitated in 16 non-institutionalized subjects (ages nine to 21) with the clinical stigmata and history of congenital rubella. Flow cytometric analysis revealed a decreased T4/T8 ratio (mean +/- SEM in subjects with rubella, 1.57 +/- 0.15, p less than 0.01; in normal subjects, 2.3 +/- 0.4; in subjects with type I diabetes, 2.3 +/- 0.3), decreased percent of T4-positive "helper" cells (42.6 +/- 2.3) different from that in both normal subjects (52.6 +/- 2.4, p less than 0.01) and subjects with recent-onset diabetes (51.5 +/- 2.4), and increased percent of T8-positive "suppressor/cytotoxic" T cells (29.9 +/- 1.4, p less than 0.02) relative to that in normal subjects (24.2 +/- 1.5) and subjects with type I diabetes (23.9 +/- 1.4). Five of 16 subjects with congenital rubella had an elevation of la-positive T cells. Approximately 20 percent had antimicrosomal antibodies. One subject had diabetes mellitus and hypothyroidism, one had hypoglobulinemia, and one had previously undiagnosed hyperthyroidism. Glycosylated hemoglobin levels were normal in all except the diabetic subject, and none of the subjects was islet cell antibody-positive. The T cell abnormalities documented may predispose persons with congenital rubella to the development of organ-specific autoimmunity.
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PMID:Congenital rubella. Monoclonal antibody-defined T cell abnormalities in young adults. 349 Jul 85

The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent diabetes mellitus. We have developed an animal model in neonatal golden Syrian hamsters infected with rubella virus passaged in beta-cells that closely parallels the diabetes observed with congenital rubella. The hamsters develop hyperglycemia and hypoinsulinemia, which are sustained throughout the 15-wk study period. A mononuclear infiltration of the islets, isolation of rubella virus from whole pancreas, the presence of viral antigen in beta-cells by immunofluorescent localization, and cytoplasmic islet cell antibodies (40%) are demonstrated. These data suggest that an autoimmune process and diabetes develop after rubella virus infection in neonatal hamsters. This model may uncover the precise mechanism by which rubella virus induces similar disease in humans.
Diabetes 1986 Nov
PMID:Rubella virus-induced diabetes in the hamster. 353 Aug 56

In 1814, George Maton, first recognized that a mild illness characterized by rash, adenopathy, and little or no fever was a discrete entity. Henry Veale, in 1866, named the disease rubella. The illness attracted little attention until 1942, when Norman Gregg noticed that first-trimester maternal rubella caused serious birth defects. The full spectrum and impact of rubella embryopathy remained unclarified until rubella virus was isolated in tissue culture in 1962 by two independent groups: Parkman, Buescher, and Artenstein; and Neva and Weller. Using the new tools of the virus laboratory, many investigators concentrated on the consequences of a severe rubella epidemic in 1964, which affected approximately 1% of pregnancies. Newly recognized transient manifestations of congenital rubella infection (CRI) include neonatal thrombocytopenic purpura, hepatitis, bone lesions, and meningoencephalitis and late-emerging sequelae such as diabetes mellitus and progressive rubella panencephalitis added to the cataract, heart disease, mental retardation, and deafness previously defined as due to CRI. Sharp contrasts were documented between the patterns of virus excretion and immune response of postnatal vs. congenital rubella. Licensure and widespread distribution of attenuated rubella virus vaccines in 1969 have prevented epidemic rubella. Pockets of illness remain, even in the United States. Continued effort will be required to eliminate the rubella problem.
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PMID:The history and medical consequences of rubella. 389 Jan 5

In the practice of diagnosing occupational deafness resulting from noise effects of factors determining workers' hearing, such as living conditions, working conditions, nutritional and other habits, diseases and their therapy, are often neglected. Discussed in the paper are the significance and ototoxic effects of such factors as: aminoglycoside antibiotics, diuretics, salicylic acid derivatives, fenacetin, quinine, fluorine compounds, cytotoxic drugs, chemical compounds other than drugs (carbon monoxide, carbon disulphide, lead, organic solvents), ethyl alcohol, diseases (abdominal typhus, bacillary dysentery, diphtheria, brucellosis, epidemic parotiditis, poliomyelitis, rubella, aural shingles, syphilis, diabetes mellitus, chronic renopathies, hypothyroidism, serologic conflict, pigmentary retinitis). Exposure to intense noise is more and more frequently juxtaposed with the impact of the mentioned factors. If industrial physicians get aware of this association the prevention of deafness and reliability of treatment may be largely promoted.
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PMID:[Ototoxic factors requiring consideration in the diagnosis of occupational hearing loss]. 390 48

This paper contains abstracts from publications of the late Sir Norman McAlister Gregg, published in 1941 and 1944, in which he demonstrated the association between rubella in pregnancy and defects in the baby. Besides cataract and retinopathy with which ophthalmologists are familiar, there occur deafness, deafmutism, cardiac defects, mental retardation, pulmonary and renal abnormalities and diabetes.
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PMID:Congenital cataract following German measles in the mother. Abstracts from the publications of the late Sir Norman McAlister Gregg. 390 70

The manifestations of congenital rubella syndrome (CRS) can be grouped according to time of onset into newborn, extended, and delayed CRS. The delayed manifestations are not present in early life and include the following: endocrinopathies: diabetes, thyroid disease, and growth hormone deficiency; deafness; ocular damage: glaucoma, keratic precipitates, keratoconus, corneal hydrops, and absorption of the cataractous lens; vascular effects: fibromuscular proliferation of the intima, sclerosis of arteries, systemic hypertension secondary to renal disease, and subretinal neovascularization; and progressive rubella panencephalitis. Several mechanisms of pathogenesis of the damage have to be considered for the delayed manifestations, including growth of the virus in tissues, resulting in a reduced growth rate and shortened life-span of the cells; autoimmune responses, initially stimulated by the infection; genetic susceptibility; vascular damage by the viral infection with further stenosis or occlusion of the vessels later; reactive hypervascularization; and chronic persistence of the virus in the tissue with subsequent extension of the infection to other areas.
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PMID:Delayed manifestations of congenital rubella. 400 24

Serological studies were carried out in the time course of insulin-dependent diabetes mellitus in 419 children, among whom paired sera from 66 were studied in the very beginning of diabetes mellitus. By seroconversion in 83% of the children early in the disease, different, frequently mixed virus infections were diagnosed: Coxsackie B2, B3, B4 (46%), rubella (41%), influenza A, B, C (38%), parainfluenza types 1-3 (35%), mumps (23%), adenovirus infection (18%), HB virus infection (4.5%). Acute respiratory diseases preceded or coincided with the onset of diabetes in half of the children with diagnosed acute respiratory and enterovirus infections. No clinical signs of rubella, mumps, or hepatitis immediately before the onset of diabetes or early in the disease were found. A possible role of virus infection diagnosed early in diabetes, in the etiology of chronic insulitis, in provocation of its exacerbation, and manifestation of diabetes mellitus is discussed.
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PMID:[Antibodies to viruses in children with diabetes mellitus]. 631 65

Much clinical and experimental data is in support of a significant role played by viruses in the etiology of diabetes mellitus. This hypothesis is borne out by the association of diabetes mellitus with Coxsackie B, mumps, rubella and herpes simplex virus infections, the presence of high persistent titers of neutralizing antibodies in diabetic patients, the in vitro permissiveness of human beta cells to viruses, and the recovery of viruses from the pancreas of diabetic patients. Viral multiplication is facilitated in HLA B8, B15, B18, Dw3 and Dw4 carriers. Experimental inoculation of EMC and Coxsackie B viruses to mice shows that beta cell involvement is dependent upon viral strains, viral membrane receptors, interferon production, immunological response and less essential factors such as age and sex. The virus is responsible for a specific immunological response and produces autoimmunological phenomena. These result in a decrease in the number and activity of insulin-producing cells through cytotoxic mechanisms. Pathological findings corroborate these physiopathological hypotheses.
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PMID:[Viruses and juvenile diabetes mellitus]. 632 9

Type I diabetes is a heterogeneous disorder and the causes of pancreatic beta-cell destruction are unknown. In 1-2% of all cases, viruses (e.g. coxsackie, rubella, mumps, or beta-cell poisons) have been implicated. Twin studies suggest at most 50% of genetic predisposition. In this review we describe the autoimmune components which, in association with inheritance of HLA-haplotypes in susceptible families, allow the future selection of predisposed sibs for possible preventive therapy to retard loss of insulin secretion. The known association of the endocrine autoimmune organ-specific disorders in 10% of Type I diabetics is the extreme expression of the other main genetic ingredient in the development of insulitis in this disease, irrespective of the triggering environmental components. In this "polyendocrine" subgroup and in the "juvenile-onset" cases there is a prolonged latency period during which pancreatic autoimmunity markers are present before clinical expression of the disease.
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PMID:Etiology of Type I diabetes mellitus: heterogeneity and immunological events leading to clinical onset. 634 51


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