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At least 19 recordsLinked to original sources
PubMed1991

Leukocytosis at the onset of diabetes in crosses of inbred BB rats.

Inbred lymphopenic, diabetes-prone (DP) and non-lymphopenic, diabetes-resistant (DR) BB rats in a specific pathogen-free (SPF) colony were subjected to a cross-intercross breeding experiment which showed diabetes to segregate as a recessive trait. All DP rats, but none of the DR and F1 rats, developed diabetes. In contrast, about 25% of the F2 rats developed diabetes which made it possible to study these rats without maternal influence of diabetes. All rats were bled at regular intervals between 30 and 150 days of age, and the samples analyzed for numbers of leukocytes, lymphocytes, neutrophils, monocytes and eosinophils. Leukocyte numbers tended to increase with age until about 100 days, and to decline thereafter. Males had more leukocytes than females. Coinciding with the time of onset of overt diabetes, there was a large increase in eosinophils, along with smaller increases in neutrophils, monocytes and lymphocytes. These data in SPF DP and DR BB rats and their cross-intercross offspring demonstrate that the overt onset of diabetes is associated with a significant leukocytosis.

Aging↗
PubMed1991

Diabetes segregates as a single locus in crosses between inbred BB rats prone or resistant to diabetes.

Diabetes-prone (DP) BB rats spontaneously develop insulin-dependent diabetes resembling type 1 diabetes mellitus in man. They also exhibit lifelong T cell deficiency. The segregation of both diabetes and lymphopenia was studied in crosses between this inbred line of rats and the related but nondiabetic and nonlymphopenic inbred diabetes-resistant (DR) BB rat line. Diabetes segregated as a single, autosomal recessive trait and was always accompanied by lymphopenia. Among the limited number of differences in the genomic DNA sequences of the two lines, DP and DR BB, one may account for the development of diabetes and lymphopenia in the DP BB rats. It may be possible to screen the genomic DNA for such differences to detect a marker for the phenotypes.

Aging↗
PubMed1995

Recombinant haplotype bearing the lymphopenia gene of the BB rat.

The development of insulin-dependent diabetes mellitus in the BB rat requires the presence of the class II major histocompatibility complex alleles of the RT1u haplotype and a T cell lymphopenia. The lymphopenia gene (lyp) behaves as an autosomal recessive trait that co-segregates with markers of rat chromosome 4. The current study examines two congenic and four recombinant inbred rat strains derived from BB and Buffalo rat strains using markers for simple-sequence length polymorphisms to confirm the linkage of the lymphopenia gene to chromosome 4. In two of these lines the lymphopenia associates with a recombinant haplotype that is BB-like at the D4Mit6 marker and Buffalo-like at D4Mit7 (neuropeptide Y locus) thus placing the lyp locus between these two closely linked markers.

Animals↗
PubMed1989

The effect of islet-activating protein (IAP) of pertussis toxin on the spontaneous diabetic syndrome in the rat.

The administration of the Islet-Activating Protein (IAP) of pertussis toxin results in an increased insulin response to oral glucose in a dose- dependent manner. This response can be detected for up to 12 days after a single injection. In addition, IAP increases the number of peripheral blood leucocytes and lymphocytes. Inbred strains of rats differ in the magnitude of the leucocyte but not the insulin responses to IAP. Multiple injections of 1,000 ng of IAP to diabetes-prone BB rats at 50, 64 and 78 days of age caused an increased release in response to glucose challenge and a slight increase in peripheral blood leucocytes when compared to animals receiving saline injections. The prevalence of insulin-dependent diabetes in BB rats was increased in the IAP group as compared to controls. Histolgic examination of the pancreas at the time of detection of diabetes revealed a widespread intense insulitis. We speculate that the increased expression of disease observed in the BB rats receiving IAP may be secondary to the chronic increase in insulin release and/or to an effect on the cells of the immune system.

Animals↗
PubMed1986

Large increase of cytotoxic/suppressor T-lymphoblasts and eosinophils around manifestation of diabetes in BB rats.

In order to gain more insight into the pathogenetic mechanism leading to beta cell destruction in BB rats we searched for specific changes in the immune system at the time of diabetes development. We performed a density gradient fractionation of all major leukocyte types in the peripheral blood and the spleen of acutely diabetic or non-diabetic BB rats as well as of normal Wistar rats in order to identify proliferating low density blasts. Acutely diabetic BB rats showed a 4-6 times higher percentage of lymphoblasts among spleen cells than non-diabetic BB or Wistar rats. The majority of blasts was of the T-cytotoxic/suppressor (Ox8+) phenotype (61%) in acutely diabetic BB rats, but of the T-helper (W3/25+) phenotype (51%) in non-diabetic BB or Wistar rats. Plasma cell and monocyte numbers were not increased in acutely diabetic BB rats. At the time of diabetes manifestation BB rats develop a pronounced eosinophilia. These observations indicate a state of enhanced cellular immunity involving cytotoxic/suppressor T cells during diabetes development in BB rats.

Animals↗
PubMed1987

The BB rat.

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Animals↗
PubMed1988

Prevention of lymphocytic thyroiditis and insulitis in diabetes-prone BB rats by the depletion of macrophages.

Diabetes-prone biobreeding (BB) rats often develop lymphocytic thyroiditis. Intraperitoneal administration of silica to young BB rats (40-days-old) nearly completely prevented the development of lymphocytic thyroiditis as well as insulitis. Since silica is known to be toxic to macrophages, these data suggest that the presentation of autoantigen(s) on the specific target cells such as thyroid and pancreatic B cells by antigen-presenting cells (e.g., macrophages) would be the initial step in the development of organ-specific autoimmune diseases in diabetes-prone BB rats.

Animals↗
PubMed1995

Cytotoxicity towards neonatal versus adult BB rat pancreatic islet cells.

Cell-mediated autoimmunity is believed to influence the development of diabetes in BB rats. It has been suggested that the autoimmune destruction is due to lack of tolerance induction in early neonatal life caused by delayed maturation of the pancreatic beta cells. The present experiment has been initiated to investigate if there is any difference in in vitro cytotoxicity, and therefore antigenicity, to islet cells from neonatal, young and adult diabetes prone BB rats, and to establish the possible developmental difference in these rats compared to non diabetes prone Wistar Furth rats. Islets from rats of different ages were isolated, dispersed and 51C-labeled. In vitro cytotoxicity mediated by mononuclear spleen cells from newly diabetic BB rats was measured by counting gamma-ray emission from the culture supernatant after 16 h coincubation. We found that full adult-like islet cell maturation in BB rats--as evidenced by sensitivity to cytotoxicity--is not seen before the age of 8 to 21 days after birth. In contrast adult-like cytotoxicity to neonatal islets cells from Wistar Furth rats is seen already at the age of 8 days. Thus delayed islet cell maturation is a fact observed in BB rats.

Aging↗
PubMed1988

[Hepatic microsomal delta 9 desaturation of stearic acid in the spontaneously diabetic female BB rat].

delta 9 desaturation of stearic (1-14C) acid has been estimated from incubation of liver microsomes of adult female spontaneously diabetic BB rat, an animal model resembling the spontaneous juvenile diabetes in humans, comparatively to adult female control Wistar rat. The animals were sacrificed, when hyperglycemic, 24 hours after the last insulin injection to the BB rats. Stearic acid delta 9 desaturase activity is drastically depressed in the BB rats when fatty acid composition of liver phospholipids and microsomal total liver lipids are changed in spite of the daily injection of insulin necessary for the BB rats survival.

Animals↗
PubMed1988

Neonatal development of lymphoid organs and specific immune responses in situ in diabetes-prone BB rats.

Rats of the BB strain develop diabetes mellitus in a high percentage and display a severe T-cell lymphopenia. In order to investigate the role of micro-environmental factors in the T-cell maturation in BB rats the postnatal development of macrophage subpopulations and T-lymphocyte subsets, in addition to the specific immune response in situ, were studied in thymus, spleen and lymph nodes of BB rats. Wistar rats were used as controls. From the day of birth on, a severe reduction was noticed in the macrophage subpopulations in the thymic cortex of BB rats, but not in spleen and lymph nodes, as compared to Wistar rats. The population of T-suppressor/cytotoxic cells (OX8-positive cells) did not increase any longer from Day 10 after birth in the thymic cortex and from Day 14 in spleen and lymph nodes. This is indicative for an intrathymic maturational defect of the OX8-positive cells in BB rats. No deviations could be observed in the development of the T-helper (ER2-positive) cell population. Young adult BB rats were as capable as Wistars of developing a specific immune response to thymus-independent (TI) antigens, but the response to a thymus-dependent (TD) antigen was delayed and decreased. Also the distribution pattern of the specific antibody-containing cells in a TD response in BB rats differed from that in Wistar rats. The ER2-positive cells, although present in normal numbers, may function insufficiently as T-helper cells in BB rats.

Animals↗
PubMed1994

Nitric oxide produced by macrophages mediates suppression of ConA-induced proliferative responses of splenic leukocytes in the diabetes-prone BB rat.

Splenic cells from the diabetes-prone BB rat show reduced proliferative responses to concanavalin A (ConA) and other mitogens. This study was undertaken to test whether this reduced lymphoproliferation in the BB rat is mediated by an increased production of nitric oxide (NO) by macrophages. Splenic leukocytes from diabetes-prone BB rats and five strains of control rats (BB-R, Wistar-Furth, Sprague-Dawley, Wistar, and Lewis) were cultured in RPMI-1640 media containing ConA. The leukocytes from BB rats showed reduced [3H]thymidine uptake and increased release of NO compared with the control rats. Partial depletion of macrophages from the culture or incubation with -NG-monomethylarginine (NGMMA), a specific NO synthase inhibitor, markedly augmented ConA-induced proliferation of the splenic leukocytes from BB but not the control rats. Enrichment of BB rat macrophages suppressed the proliferation of BB-R rat spleen cells. Excess L-arginine added to the culture reversed the NGMMA effect. These results suggest that increased production of NO by macrophages is partly responsible for the reduced proliferative responses of splenic leukocytes in the BB rat.

Analysis of Variance↗
PubMed1987

Genetic studies of IDDM in BB rats: the incidence of diabetes in F2 and first backcross hybrids allows rejection of the recessive hypothesis.

The BB rat spontaneously develops an IDDM with many analogies to human IDDM, i.e. the genetic basis is a puzzle, since more than one mode of inheritance of IDDM in BB rats has been proposed. These different proposals reflect the heterogeneity of BB rats used for genetic studies. This prompted us to investigate the inheritance of IDDM in two subpopulations of BB rats (BB/OK and BB/PhiK) by crossing studies with the production of (diabetic BB x LEW 1.A) F1, F2 generations and of first backcross hybrids onto BB (B1BB) and LEW.1A (B1A) rats respectively. Both BB rat subpopulations were different in origin, degree of inbreeding, incidence and age at onset of diabetes and in certain immunologic, metabolic and hematologic traits. All hybrids were serotyped and checked for diabetes by determination of urine and plasma glucose twice weekly up to an age of 200 days. None of the F1 and B1A hybrids developed diabetes. Some cases were observed in the F2 hybrids with a different incidence in the two subpopulations (2.3% in BB/OK, 11.0% in BB/PhiK). The percentage of diabetes in the B1BB hybrids was 13.8% (BB/OK) and 24.0% (BB/PhiK) respectively. All diabetic hybrids were characterized by at least one RT1uv haplotype which was derived from the original BB animals. These results demonstrated clearly (1) that the mode of inheritance depends on the genotype of the animals observed and (2) simple autosomal-recessive genetics cannot be accepted for BB rat diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗