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The dynamics of insulin and chromium release from prelabelled rat pancreatic islet cells were studied by perifusion of cells supported in a column of Bio-Gel P-2 polyacrylamide beads. The column-perifused β cells released insulin in a biphasic pattern in response to 30 mmol/l D-glucose and in a monophasic pattern to 20 mmol/l L-arginine. Rat islet cells, first exposed to a rabbit anti-rat islet c

The influence of sex on pancreatic islet B cell susceptibility to streptozotocin was studied in mice given multiple low doses of streptozotocin. Male C3 D2 F1 mice developed a steadily increasing blood glucose level after a lag period of about 3 weeks, in contrast to females who were resistant. Spleen cells from streptozotocin treated female animals produced hyperglycaemia in total body irradiated

Not only has recombinant DNA added another source of insulin for treatment, but also, and perhaps more important, it has allowed the development of new techniques for studying the structure and function of the B cell at the gene level. We can only hope that this information will bring us closer to the understanding of the disease, so the diabetic patient may benefit from other measures of treatmen

Five daily injections of streptozotocin (40 mg/kg) produced a delayed but progressively increasing level of hyperglycaemia in long term studies with male Naval Medical Research Institute mice and C3D2F1 (DBA 2 J male × C3H/ Tif female) F1 hybrid mice. The development of hyperglycaemia was paralleled by decreased amounts of pancreatic immunoreactive insulin as well as degranulation and necrosis of

Pancreatic islets from A.TH mice were transplanted into the spleen or streptozotocin (SZ)‐diabetic A.TL mice. The two strains of mice are congenic inbred strains, differing only in the I and S subregions of the H‐2 complex. The allogeneic islet grafts decreased blood glucose temporarily, but the islets were rejected after 21 ± 7 days (mean ± SD). The effect of skin presensitization was tested by g

Insulin-dependent diabetic (IDD) patients have a high prevalence of circulating autoantibodies against islet of Langerhans cells at the time of diagnosis1-4. Inflammatory cells within the islets5, leukocyte migration inhibition in response to pancreatic antigens6 and an association with certain HLA-D/DR histocompatibility antigens 7,8, have also been observed. It seems that the autoantibodies may

Islet cell cytoplasmic and cell surface antibodies along with other autogenic tissue antibodies were determined prospectively from the day of diagnosis of insulin-dependent diabetes in a group of children and adolescents. Prior to the initiation of insulin therapy 30 out of 33 were antibody-positive, 67% having islet cytoplasmic antibodies and 67% islet cell surface antibodies. Among 74 age- and s

Diabetic A.TL and A.TH mice, congenic inbred strains differing only in the I and S (non-K, non-D) regions of the major histocompatibility (H-2) complex, received intrasplenic allogeneic and isogeneic pancreatic islet transplants. The isografts were uniformly accepted, while approximately 60% of the recipients receiving allografts rejected the islets, most within 4 weeks of transplantation. With ei

Dispersed rat pancreatic islet cells were mixed into a short column of Bio-Gel P-2 polyacrylamide beads and perifused with an antiserum containing islet cell surface antibodies. The release of radioactive chromium from prelabeled cells, as a measure of cell membrane permeability, was not affected by cell surface antibodies alone, but increased dramatically in the presence of complement. While ther

Streptozotocin (SZ) given in five low doses causes diabetes and an associated lymphocytic infiltration of the pancreatic islets. Using C57BL/KsJ-mice, we demonstrate a reduction in islet number (-38%) and volume (-64%) within 1 day following the last injection of SZ. A substantial fall of insulin secretory capacity (-84%) in the in vitro perfused pancreas matches the reduction in islet cell volume

Genetic susceptibility, environmental factors and immune mechanisms are implicated in the pathogenesis and etiology of insulindependent diabetes mellitus. The onset of the disease is associated with a major loss of beta cells, and inflammatory cells may be seen in and around the islets of Langerhans. Insulin-dependent diabetes is often associated with autoimmune endocrinopathies. Antipancreatic ce

Recent observations have shown the presence of thyrotropin-releasing hormone-like material (TRH-LM) in rat pancreatic islets and in retina. Its immunological and biological properties are identical to those of synthetic thyrotropin-releasing hormone (thyroliberin). This communication deals with the ontogenesis of TRH-LM in rat pancreas and retina as compared to that of rat hypothalamus. Effects of

Dispersed islet cells were prepared from collagenase-isolated lean mouse pancreatic islets by Dispase-II and subsequent mechanical treatment in calcium depleted media. An average yield of 600 cells per islet was obtained, 84% of the cells being β-cells. Cells were incubated with radioactive chromium as a marker of cell viability. Optimal labelling of 1-2 cpm per cell was obtained by incubating 10

Pancreatic islets from rats or ob/ob mice were homogenized and fractionated either by a two-step or one-step sucrose gradient centrifugation. A plasma membrane enriched fraction was obtained at a sucrose density of about 1.10. The distribution of the plasma membrane probe 125I-wheat germ agglutinin was parallel to that of other plasma membrane markers. Hydrolysis of Mg-ATP-gamma-3Pp in rat islet m

Rabbits were immunised with suspensions of viable, insulin-producing islet cells prepared from collagenase-isolated rat or ob/ob mouse pancreatic islets. Antibodies reactive with the surface of dispersed rat islet cells were present in both the rabbit anti-rat and the rabbit anti -ob/ob mouse islet sera as revealed by indirect immunofluorescence or by a radioligandassay using 125 I-Protein A as

There is evidence that the destruction of the pancreatic B cell in insulin-dependent diabetes mellitus is due to autoimmune reactions. Transplantation of islet cell tissue might then provoke 'reimmunization', and this could presumably lead to destruction of the transplanted B cells. The authors have looked for signs of recurrence of autoimmunity following pancreatic transplantation.