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

Cell-mediated immune reactions, such as allogenic skin-graft rejection and PHA or MLC responses, and antibody synthesis against different antigens (sheep erythrocytes, Brucella antigen, bovine serum albumin) have been evaluated in rats suffering from experimentally-induced diabetes and in age-matched sham-treated controls. Cell-mediated immune reactions are strongly depressed diabetic rats. The cellularity of the thymus and of thymus-dependent areas and the number of peripheral blood lymphocytes is significantly reduced in pancreatectomized rats. Moreover, the immunological recovery from heavy cortisonization is also greatly impaired. Daily treatment with insulin may prevent these immunological alterations. By contrast, antibody responses in diabetic rats are not quantitatively altered in respect to either the number of antibody producing cells in the spleen or the circulating antibody titres. The discrepancy between the abnormality of cell-mediated immune reactions in diabetic rats and their physiological capacity to synthetize antibodies suggests that the sensitivity to an insulin-deprived environment is present only in a definite, although yet undefined, subpopulation of lymphoid cells rather than in the whole lymphoid system.
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PMID:Differential effect of pancreatectomy on humoral and cell-mediated immune responses. 14 53

Following a single injection of 200 mg streptozotocin/kg BW, 25 out of 25 normal mice became diabetic, whereas 12 ( = 20%) out of 50 athymic nude mice did not develop diabetes. In a multiple dosage experiment, where the same total dose was given over a 5 days period, 14 normal and 15 athymic nude mice all became diabetic, but nude mice had significantly lower blood glucose values. These results support our previous suggestion that a thymus dependent immune reaction is, in part, responsible for the diabetogenic effect of streptozotocin.
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PMID:Is the diabetogenic effect of streptozotocin in part thymus-dependent? 15 48

The effect of a known diabetogenic M-strain encephalomyocarditis (EMC)-virus in athymic nude mice (lacking the thymus-dependent lymphocyte system), and in heteroxygous littermates and homozygous normal mice of the background strain (C57/B16) was investigated. While by 3 weeks 4 out of 4 surviving virus-inoculated littermates and 9 out of 9 inoculated normal mice developed diabetes mellitus, none of the 7 surviving virus-inoculated nude mice became diabetic. Virus was isolated from all inoculated animals, including non-diabetic nude mice. It is concluded that it is the response of the thymus-dependent lymphocyte system evoked by the virus rather than the virus itself that leads to damage to the insulin producing cell.
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PMID:The inability of a diabetogenic virus to induce diabetes mellitus in athymic (nude) mice. 18 60

The study describes passive transfer of diabetes mellitus by transplantation of spleen cells from donor mice infected with a diabetogenic encephalomyocarditis virus. Inbred normal C57 mice were used as both donors and recipients, and other recipients were C57 athymic, nude mice. Transplants were made in two series after 12 and 22 days duration of infection of the donors, respectively. All recipients became diabetic. The possibility of virus transfer with the spleen cell transplant is discussed, and found to be highly improbable. The fact that passive cellular transfer can be effected points to a decisive significance of the thymus dependent lymphocyte system in the pathogenesis of the primary diabetes.
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PMID:Passive transfer of virus induced diabetes mellitus with spleen cells. 21 30

The infection of normal DBA2 and BALB/C nu/ + mice with 2 X 10(2,6) TCID50 of the M variant of the EMC virus induced pathological mean glucose values of 426 +/- 99 mg/100 ml in DBA2 mice and 292 +/- 130 mg/100 ml in BALB/C nu/ + mice on day five following infection. As diabetic animals died afterwards, mean glucose values decreased in the surviving animals on day seven and fourteen. The infected immunodeficient BALB/C nu/nu mice with thymus aplasia did not show abnormal mean glucose values or higher standard deviation of the means (114 +/- 37 mg/100 ml) when compared to uninfected controls (117 +/- 23 mg/100 ml). This demonstrates that a complete thymus-dependent immune system seems to be necessary for the development of the acute stage of virus-induced diabetes in the mouse.
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PMID:Virus induced diabetes and the immune system. II -- Evidence for an immune pathogenesis of the acute phase of diabetes. 22 66

This study shows passive transfer of streptozotocin induced diabetes mellitus in mice. Transplants of spleen cells from BALB/c mice, streptozotocin treated for 5 days, induced diabetes in normal BALB/c recipients. Treatment of transplants with anti-theta and complement resulted in a significant decrease in the degree of diabetes. Athymic nude mouse recipients of BALB/c background also developed diabetes after transpant of spleen cells from both syngenic and allogenic (C-7/Bl/6) donors. It is concluded that passive transfer of chemically induced diabetes in mice is practicable, in both syngeneic and allogeneic combinations, and that thymus derived lymphocytes are significant in this process.
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PMID:Passive transfer of streptozotocin induced diabetes mellitus with spleen cells. Studies of synogeneic and allogeneic transfer to normal and athymic nude mice. 30 89

Growth and development of the thymus is dependent on secretions from the anterior pituitary, presumably growth hormone. Diabetes mellitus is known to reduce immunological competence. These studies compare the effects of bovine growth hormone (bGH) and the growth factor produced by plerocercoid larvae of the tapeworm, Spirometra mansonoides, on metabolism of lymphoid tissue, thymus and spleen, in hypophysectomized rats made diabetic with a single intraperitoneal injection of alloxan. Whereas the control diabetic-hypophysectomized rats gradually lost weight throughout the experimental period, both bGH and plerocercoid infection caused significant weight gains during the experimental period. The diabetic-hypophysectomized rats treated with bGH had significantly heavier thymuses and spleens than controls. Plerocercoid infection also caused significant increases in thymus weights. Both bGH and plerocercoids stimulated the metabolic activity of thymocytes isolated from treated rats and tested for their ability to incorporate 3H-thymidine into DNA in vitro. Thus, these growth factors have similar effects on the lymphoid tissue of diabetic-hypophysectomized rats which are apparently independent of normal insulin levels. Whether this anabolic effect is direct or mediated by somatomedin remains to be determined.
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PMID:Comparison of the effects of the growth factor produced by Spirometra mansonoides and growth hormone in diabetic-hypophysectomized rats: lymphoid tissue. 66 Mar 78

There is an increased prevalence (P less than 0.001) of IgA deficiency in children with juvenile-onset insulin-dependent diabetes mellitus (9/366) but not in adults with insulin-dependent diabetes (0/421). The juvenile diabetics with IgA deficiency have other immune-associated diseases, such as thyroiditis and chronic active hepatitis, and have a history of infections. Four of the nine IgA-deficient diabetics we studied have autoantibodies to endocrine organs. Seven of eight have the HLA-B8, a proportion significantly (P less than 0.05) greater than control populations. Based on the clinical findings of IgA deficiency and multiple autoantibodies in patients with ataxia-telangiectasia and chronic mucocutaneous candidiasis, diseases associated with thymus deficiency, we suspect that thymus deficiency and autoimmunity may play a role in the pathogenesis of some types of juvenile-onset diabetes mellitus. In addition, an excess morbidity of the IgA-deficient juvenile diabetic population may explain the lack of IgA deficiency in older insulin-dependent diabetic individuals.
Diabetes 1978 Nov
PMID:Immunopathology of juvenile-onset diabetes mellitus. I. IgA deficiency and juvenile diabetes. 72 Jul 69

In order to investigate the combined effects of diabetes and hypertension on the pathogenesis of cardiovascular disease, adult male and female SHR rats which develop hypertension spontaneously were given a single, 10 mg or 15 mg/100 g body wt. injection of alloxan s.c. to induce moderate or severe diabetes. Insulin was deliberately withheld. Animals were examined by autopsy daily for 7 days post-alloxan and after 4 and 8 weeks. Mortality was high--only 52% of the males survived as against 80% of the females. Most deaths occurred on Day 5 and were associated with adrenal haemorrhage and hyperplasia, thymus galnd involution, fatty liver and marked hypotension despite elevated aldosterone levels. During the first week, corticosterone levels increased significantly in the male; in females they showed little change. After 4 weeks, the severly diabetic animals became emaciated and moribund; corticosterone and aldosterone levels fell to very low levels despite adrenal hyperplasia. The beta cells of the moderately diabetic animals eventually lost their ability to secrete insulin and these animals too became cachetic and moribund with concomitant elevation of lipid, glucose and BUN levels, as well as myocardial infarction, fatty liver, and generalized hyalin arteriolo-, arterio-, and nephrosclerosis. It is suggested that the combined hormonal and metabolic alterations of diabetes and hypertension reinforced one another in these spontaneously hypertensive rats, leading to intense stimulation of the hypothalamic-pituitary-adrenal system, the exacerbation of those cardiovascular degenerative changes known to be associated with uncontrolled diabetes or hypertension, eventual impaired adrenocortical steroidogenesis, hypotension and death.
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PMID:Alloxan diabetes in spontaneously hypertensive rats: gravimetric, metabolic and histopathological alterations. 86 Nov 67

A 26-year-old man having multiple endocrinopathy (pernicious anemia, hypothyroidism, hypoadrenocorticism, gonadal failure, and diabetes mellitus) and chronic candidiasis developed several rapidly growing primary tumors on the oral mucosa. Histologically, the tumors appeared to be very well differentiated squamous cell carcinomas. Yet, in spite of all therapeutic attempts, the tumors rapidly progressed and within eight months resulted in disseminated carcinomatosis and death. At autopsy the patient was found to have had a miniscule dysplastic thymus. It is postulated that in chronic candidiasis and polyendocrinopathy a defect may exist in immunologic cellular surveillance for recognition and destruction of aberrant cells.
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PMID:Candidiasis and multiple endocrinopathy. With oral squamous cell carcinoma complications. 113 Aug 7


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