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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 thymus extract (TFX) on phagocytosis and bactericidal capacity of polymorphonuclear neutrophils (PMN) from patient with insulin-dependent diabetes was studied. In previous observations PMN from these patients revealed the serum-related defect of bacterial killing. The preincubation of cells with standard dose of TFX significantly increased ingestion rate and recovered the bactericidal capacity to normal values. The augmentation of bactericidal capacity due to preincubation with TFX appeared to be dose-dependent and not related to other blood cells participation. The increase of bacterial killing was also evident, when TFX was applied after phagosome formation. The presented studies indicate that, among numerous peptides, thymus extracts contain those exerting their hormone-like activity on polymorphonuclear neutrophils. The observations may be of clinical importance.
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PMID:The influence of thymus extract (TFX) on the phagocytosis and the bactericidal capacity of polymorphonuclear neutrophils from patients with insulin-dependent diabetes mellitus. 406 Feb 15

One week following induction of diabetes in rats by alloxan administration, the thymus and spleen showed marked involution and a highly significant depression of in vivo incorporation of [3H]deoxycytidine into the DNA of these tissues. Adrenalectomy of diabetic rats reduced the decline of lymphatic tissue weight, but uptake of [3H]deoxycytidine into thymic and spleen DNA remained suppressed. These results indicate that in alloxan-induced diabetes, the observed depressed lymphatic tissue weight and cellular proliferation are not simply due to the elevated plasma level of corticosteroids, but are either a result of the insulin deficiency per se or due to other metabolic alterations associated with the diabetic condition.
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PMID:Suppressed proliferation of lymphatic tissue in diabetic and adrenalectomized-diabetic rats. 406 84

The thymus atrophied rapidly in rats rendered diabetic by a single injection of streptozotocin. The weight of the gland was reduced to one-fifth of its original weight within three weeks. Histologically there was a great loss of cortical thymocytes and a marked increase in mast cells lying in the thickened fibrous tissue. These findings may have a bearing on the state of immune deficiency observed in animals with diabetes induced by streptozotocin.
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PMID:Atrophy of the thymus in rats rendered diabetic by streptozotocin. 408 73

Rare carcinoid-like ACTH-active tumour of the thymus in a woman of 40 is described. The tumour was of a solid-trabecular structure with rosette-like figures and consisted of spindle, polyhedral and roundish cells containing electron-dense granules of the neurosecretory type. Hormonal activity of the tumour was manifested in a pronounced hypercorticism with a marked adrenal hyperplasia, atrophy of sex organs and general virilization, skeletal muscle atrophy, osteoporosis, signs of diabetes mellitus, lipid hepatosis and other symptoms of a grave Itsenko-Cushing' syndrome followed by a fever. In spite of the absence of metastasis tumour was characterised by a rapid expansive growth with the compression of neck veins and venous stasis in both mediastinal organs and the tumour itself with the necrosis in its central parts. The cause of death was the thromboembolism of lung arteries from the thrombotic veins of the lower limbs.
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PMID:[Carcinoid-like ACTH-active thymus tumor with adrenal hyperplasia and the Itsenko-Cushing syndrome]. 608 16

Insulin-dependent diabetes induced in susceptible strains of mice by multiple, low-dose streptozotocin treatment has been proposed to entail a thymus-dependent, autoimmune destruction of beta cells. In this study, thymectomized and genetically athymic mice have been tested for susceptibility to streptozotocin. Thymectomy was performed on newborn (day 1) to 3-day-old C57BL/KsJ mice. At 8 wk of age, thymectomized and sham-operated mice of both sexes were tested for susceptibility to diabetes induction by multiple, low-dose streptozotocin treatment (35 mg/kg of body weight per day for 6 consecutive days). Thymectomy failed to block susceptibility of males to induction of severe hyperglycemia. Beta cell necrosis and inflammatory cell infiltrates (insulitis) were consistent histopathological features. In general, females-both thymus-intact and thymectomized-were less susceptible than males to streptozotocin-induced hyperglycemia, and females exhibited an equally severe insulitis by experimental day 14; thus, the detection of an underlying insulitis did not predict the development of a more severe hyperglycemia because most streptozotocin-treated females at experimental day 35 continued to show only a modest hyperglycemia (about 200 mg/dl) compared to males (>400 mg/dl). That streptozotocin-induced hyperglycemia could occur in the absence of an intact thymus was further demonstrated in genetically athymic C57BL/6J NIcrOu nu/nu males and thymus-intact +/? littermate controls. C57BL/6J mice were resistant to streptozotocin-induced insulitis. This study shows that the presence of insulitis does not necessarily presage onset of severe hyperglycemia (e.g., C57BL/KsJ females), and conversely, the presence of severe hyperglycemia after low-dose streptozotocin treatment is not necessarily diagnostic of an underlying insulitis (e.g., C57BL/6J +/? and nu/nu males). These data stress the need for caution in the interpretation of studies of streptozotocin-insulitis sensitivities of nude mice.
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PMID:Multiple low-dose streptozotocin-induced hyperglycemia and insulitis in C57BL mice: influence of inbred background, sex, and thymus. 621 Sep 9

In genetically susceptible strains of mice, repeated injections of a subdiabetogenic dose of streptozotocin induces the development of progressive insulin-dependent hyperglycemia. We showed previously that host T-cell functions play an obligatory etiologic role in this experimental disease by demonstrating that the athymic nude mouse is resistant to diabetes induction unless its T-cell functions are reconstituted by thymus graft (Paik et al., Proc. Natl. Acad. Sci. USA 77:6129-33, 1980). Here we show that lethal irradiation of euthymic (+/nu) mice of BALB/cBOM background causes selective resistance of the mice to the diabetogenic effects of the multiple low doses of streptozotocin without affecting their sensitivity to a high pharmacologic dose of the toxin. We also show that reconstitution of the irradiated mice with splenic lymphocytes causes the restoration of diabetes susceptibility. Lethally irradiated mice thus represent a useful experimental model for analyzing the host functions involved in the development of this disease. These results provide an additional support for the hypothesis that the induction of diabetes in this model system is mediated by an autoimmune amplification mechanism.
Diabetes 1982 Sep
PMID:Diabetes susceptibility of BALB/cBOM mice treated with streptozotocin. Inhibition by lethal irradiation and restoration by splenic lymphocytes. 621 23

The objective of this study was to determine whether mature thymic-derived T-lymphocytes were required for streptozotocin (SZ)-induced insulitis. C57BL/KsJ male mice were immunocrippled by thymectomy at 3 wk of age followed 1 wk later by lethal irradiation (1000 R) and hematopoietic reconstitution with syngeneic bone marrow (pretreated with anti-Thy 1.2 antiserum and complement to eliminate mature T-lymphocytes). As a control for the systemic effects of lethal irradiation itself, thymus-intact males were also irradiated and reconstituted with anti-Thy-1.2-treated marrow cells. This latter treatment resulted in a reconstitution of functional T-lymphocytes. Independent of the presence or absence of functional T-lymphocytes, irradiation extensively damaged the testes and produced at least a 50% reduction in plasma testosterone levels. In such effeminized males, the hyperglycemic response following 6 daily injections of SZ (35 mg/kg) was reduced in comparison to unirradiated males. Pancreatic insulin content was reduced 50% in both thymus-intact and thymectomized groups receiving lethal irradiation and SZ treatment; this correlated with histologic findings of small, beta-cell-depleted islets. Focal leukocytic infiltrates of the exocrine pancreas were induced by the irradiation. Streptozotocin-induced insulitis was also observed regardless of the presence (in thymus-intact mice) or absence (in thymectomized mice) of phytohemagglutinin-responsive T-lymphocytes. Both groups exhibited intact B-lymphocyte function as measured by proliferative responsiveness to lipopolysaccharide. Severe immunosuppression of both T- and B-lymphocyte function was produced by subcutaneous injection of hydrocortisone into thymectomized mice 48 h prior to initiation of SZ treatments. This treatment prevented SZ-induced beta-cell necrosis and eliminated lymphocytic infiltrates in the endocrine and exocrine pancreas. We conclude that functional (mature) T-lymphocytes are not required to mediate the beta cytotoxicity of multiple low doses of SZ in inbred strains in which insulitis accompanies islet destruction. The ability of hydrocortisone to protect beta-cells from the direct cytotoxic action of SZ as well as to eliminate leukocytic infiltration in the pancreas would support the hypothesis that insulitis is a consequence of beta-cell destruction, in this model, rather than its cause. DIABETES 32:148-155, February 1983.
Diabetes 1983 Feb
PMID:The effect of immunosuppression on streptozotocin-induced diabetes in C57BL/KsJ mice. 621 26

The peak plaque-forming-cell (PFC) and serum antibody responses of diabetic mice to type III pneumococcal capsular polysaccharide (S3) were delayed compared with normals. Proliferation of PFC precursors was not inhibited in an insulin-deficient environment. The delay in the PFC response to S3 did not occur in diabetic nude mice but was demonstrable in their thymus-bearing heterozygote littermates. Therefore, T-cells appear to mediate the delay in the response of diabetic mice to S3 probably by delaying their differentiation into PFC. Diabetic mice responded normally to the induction of low-dose tolerance to S3, indicating the presence of active suppressor T-cells (Ts) in these mice. However, inactivation of Ts by anti-lymphocyte serum (ALS) required a higher dose in the diabetic mice. Furthermore, inactivation of Ts by ALS totally abolished the delay in peak PFC response. These findings suggest that the delayed PFC response to S3 in diabetic mice was the result of excessive splenic Ts activity. In peripheral blood, diabetic mice appeared to have more amplifier T-cell activity or less suppressor T-cell activity than normals. This response was normalized by insulin treatment. DIABETES 32:156-164, February 1983.
Diabetes 1983 Feb
PMID:Impairment of T-cell regulation of the humoral immune response to type III pneumococcal polysaccharide in diabetic mice. 621 27

Multiple subdiabetogenic doses of streptozotocin induce an insulin-dependent progressive hyperglycemia in genetically susceptible strains of mice. We have shown previously that T-cell-dependent autoimmune mechanisms play an obligatory role in this model of diabetogenesis by demonstrating that athymic nude mice and lethally irradiated euthymic mice are selectively resistant to diabetes induction and that the susceptibility can be reconstituted by grafting thymus in nude mice or by giving B-cell-depleted splenic lymphocytes to the irradiated mice. In this report we investigate more directly the possible role of host B-cell functions in the induction of hyperglycemia. Mice were rendered selectively deficient in functional B lymphocytes by repeated injections of a polyclonal antiserum against mouse IgM, starting immediately after birth. These B-cell-suppressed mice had no detectable ability to produce antibodies against a test antigen but appeared to have normal levels of T cells. When treated with multiple low doses of streptozotocin, they developed progressive hyperglycemia in a manner indistinguishable from control mice with normal B-cell functions. These results suggest that host B cells, in contrast to host T cells, are not etiologically involved in the development of diabetes induced by multiple subdiabetogenic doses of streptozotocin.
Diabetes 1984 Feb
PMID:Diabetes induction by subdiabetogenic doses of streptozotocin in BALB/cBOM mice. Noninvolvement of host B-lymphocyte functions. 622 38

This article is concerned with the role of thymic immunity in the development of diabetes experimentally induced by multiple injections of subdiabetogenic doses of streptozocin (STZ). Euthymic +/+, +/nu, and athymic nu/nu mice of CD-1 and BALB/cAJcl origin were studied. Daily intraperitoneal (i.p.) injections of 30 mg/kg body wt of STZ for 5 consecutive days in CD-1 +/+ and +/nu mice resulted in hyperglycemia and mononuclear cell infiltrations of islets (insulitis). The CD-1 nu/nu mice developed neither insulitis nor hyperglycemia after the same treatment. In the nu/nu mice, when thymic immunity was restored by thymus grafting, both insulitis and hyperglycemia developed, thus demonstrating that thymic immunity was a prerequisite for the development of insulitis and hyperglycemia. There was a positive correlation among the degrees of thymic immunity, insulitis, and hyperglycemia in CD-1 +/nu, nu/nu with thymus grafts, and nu/nu mice, indicating that thymic immunity may amplify the diabetogenic effect of STZ by eliciting insulitis. In contrast, in BALB/cAJcl mice, a nonsusceptible strain to insulitis, no significant differences in plasma glucose levels were observed between the +/nu and nu/nu or between the nu/nu and thymus-grafted nu/nu mice. Furthermore, no significant difference was found in plasma testosterone levels between the +/nu and nu/nu mice of both CD-1 and BALB/cAJcl origin. In conclusion, our data indicate that thymic immunity enhances the diabetogenic effect of STZ by eliciting insulitis in susceptible mice.
Diabetes 1984 Sep
PMID:The role of thymic immunity and insulitis in the development of streptozocin-induced diabetes in mice. 623 18


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