Literature DB >> 6135137

Spontaneous diabetes mellitus syndrome in the rat. III. Pancreatic alterations in aglycosuric and untreated diabetic BB Wistar-derived rats.

T A Seemayer, E Colle, G S Tannenbaum, L L Oligny, R D Guttmann, H Goldman.   

Abstract

The pancreatic alterations in aglycosuric and untreated diabetic BB Wistar-derived rats are described. A common finding, often seen in young aglycosuric rats, is that of discrete foci of periductular and/or acinar aggregates of lymphocytes and macrophages. Sites of periductular mononuclear cell infiltrates usually lack endocrine cells. In contrast, foci of acinar infiltrates, although distinct from the predominant endocrine cell mass in the islets of Langerhans, often contain small numbers of alpha and/or beta cells. It is suggested that these clusters of endocrine cells may in some way be antigenically different from those resident in the principal islets and thus serve as an additional target for the immune system in rats bearing the BB genome. The development of overt diabetes requires a massive destruction of beta cells within the islets of Langerhans. Two forms of diabetes mellitus emerge in untreated animals. The more common, designated unstable diabetes, is severe and lethal unless treated with insulin. Less commonly, a stable type of diabetes mellitus ensues for which insulin therapy is not mandatory. In each, the concentration of pancreatic immunoreactive insulin is profoundly decreased, although relatively greater amounts are present in the stable form. Unstable diabetic rats demonstrate a reduction in the concentration of pancreatic immunoreactive glucagon and somatostatin, suggesting that alpha and delta cells also sustain injury in this model of insulin-dependent diabetes mellitus.

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Year:  1983        PMID: 6135137     DOI: 10.1016/s0026-0495(83)80007-9

Source DB:  PubMed          Journal:  Metabolism        ISSN: 0026-0495            Impact factor:   8.694


  7 in total

1.  In vivo prevention of thyroid and pancreatic autoimmunity in the BB rat by antibody to class II major histocompatibility complex gene products.

Authors:  C Boitard; S Michie; P Serrurier; G W Butcher; A P Larkins; H O McDevitt
Journal:  Proc Natl Acad Sci U S A       Date:  1985-10       Impact factor: 11.205

2.  Diet and insulin-dependent diabetes in the BB rat.

Authors:  F W Scott; R Mongeau; W A Behrens
Journal:  Diabetologia       Date:  1985-01       Impact factor: 10.122

3.  Lipid abnormalities in pancreatic tissue of streptozotocin-induced diabetic rats.

Authors:  E Levy; C C Roy; G Lepage; M Bendayan
Journal:  Lipids       Date:  1988-08       Impact factor: 1.880

4.  Pre-diabetes in the spontaneously diabetic BB/E rat: lymphocyte subpopulations in the pancreatic infiltrate and expression of rat MHC class II molecules in endocrine cells.

Authors:  B M Dean; R Walker; A J Bone; J D Baird; A Cooke
Journal:  Diabetologia       Date:  1985-07       Impact factor: 10.122

5.  Obliterative segmental sclerosis of pancreatic islets. A possible consequence of hypotensive shock in young BB rats.

Authors:  T A Seemayer; J F Yale; J P de Chadarévian; M Grose; E B Marliss
Journal:  Am J Pathol       Date:  1986-11       Impact factor: 4.307

6.  Major histocompatibility complex gene product expression on pancreatic beta cells in acutely diabetic BB rats.

Authors:  B Issa-Chergui; J F Yale; C Vigeant; T A Seemayer
Journal:  Am J Pathol       Date:  1988-01       Impact factor: 4.307

7.  Macrophage infiltration precedes and is a prerequisite for lymphocytic insulitis in pancreatic islets of pre-diabetic BB rats.

Authors:  H Hanenberg; V Kolb-Bachofen; G Kantwerk-Funke; H Kolb
Journal:  Diabetologia       Date:  1989-02       Impact factor: 10.122

  7 in total

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