No abstract

Pancreatic glands of 22-day-old rat foetuses or 0-12 day old rats were incubated in a Krebs-Ringer phosphate-buffered salt solution, and the insulin secretion measured at a lower (0.6 mg/ml) or a higher (3 mg/ml) glucose concentration in the medium. Stimulation of the insulin release by glucose could not be detected until the second postnatal day, when there was a marked increase in the amount of hormone secreted into the medium. Since the presence of insulin has been demonstrated in the B-cells of rat foetuses, the data suggest that in this species the cellular mechanism for insulin synthesis becomes manifest considerably earlier than that for glucose-regulated insulin release. Stimulation par le glucose de la sgcrdtiOn d'insuline par le 29ancrgas isold de rats foetaux et nouveau-ntis l?dsumg. Les glandes pancr6atiques de foetus de rats ~gds de 22 jours ou de rats ~gds de 0-12 jours ont dtd incubdes dans une solution tampon au phosphate de Krebs Ringer, et la s6crdtion d'insuline a dtd mesurde pour une faible concentration de glucose (0.6 mg/ml) ou pour une concentration de glucose plus dlev6e (3 mg/ml) dans le milieu. La stimulation de la lib6ration d'insuline par le glucose ne pouvait pas 6tre ddcel6e jusqu'au deuxi&me jour postnatal, o~t il y avait une nette augmentation de la quantitd d'hormone sdcrdtde dans le milieu. Puisque la prdsence d'insuline a 6t6 d6montrde dans les cellules B de foetus de rats, les donndes suggbrent que dans cette esp~ce le mdcanisme cellulaire de la synthbse de l'insuline devient manifeste beaucoup plus t6t que celui de la lib6ration d'insuline r6gul6e par le glucose. Stimulation der Insulinsekretion mit Glucose aus dem isolierten Pankreas yon foetaten und neugeborenen l?atten Zusammenfassung. Das Pankreas yon 22 Tage alten Rattenfoeteu oder 0-12 Tage alten Ratten wurde in einer Krebs-Ringer-Phosphat-Puffer-LSsung inkubiert, und die Insulin-Sekretion bet ether niedrigeren (0.6 mg/ml) oder hSheren (3 mg/ml) Glucosekonzentration der L6sung gemessen. Stimulation der Insulinfreisetzung durch Glucose konnte bis zum 2. postnatalen Tag nicht festgestellt werden, an dem ein bemerkenswerter Anstieg des in die L6sung sezernierten Hormons eintrat. Da die Gegenwart yon Insulin in den B-ZeUen yon Rattenfoeten gezeigt wurde, lassen die Werte vermuten, da2 sich bet dieser Spezies der Zellmechanismus fiir Insulin-Synthese be-tr~chtlich friiher manifestiert als die glucoseregulierte Insulinfreisetzung.

IgE antibodies have potent immunoregulatory effects in vivo, and mice immunized with IgE–antigen (IgE/Ag) complexes exhibit a several hundred‐fold higher humoral Ag‐specific response than mice immunized with non‐complexed Ag. In vitro studies indicate that this is a result of efficient endocytosis of the IgE/Ag complexes via the low‐affinity receptor for IgE (CD23) on B cells, leading to efficient antigen presentation to T cells. Previous studies of IgE‐induced Ab responses in vivo have only measured serum responses. The authors have now studied the up‐regulated response as the number of IgG‐, IgA‐, IgE‐ and IgM‐secreting single B cells in spleen, lymph nodes and bone marrow of mice immunized with IgE‐anti‐TNP + BSA‐TNP (2,4,6‐trinitrophenylated bovine serum albumin). IgE and Ag induced a greater than 500‐fold increase of specific IgG‐secreting spleen cells with the peak of the response 6 days after primary immunization. The response of other Ab isotypes and the response in other lymphoid organs was marginal. The rapid increase in the number of IgG‐secreting cells in the spleen suggests that IgE/Ag complexes induce a secondary type of antibody response without requirement for conventional priming.

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Hellman, B., S. Larsson and S. Westman. Mast cell content and fatty acid metabolism in the epididymal fat pad of obese mice. Acta physiol. scand. 1963. 58. 255–262. — The changes in the mast cell content of the epididymal and subcutaneous adipose tissues were studied in two different types of obesity in mice. Both with the obesity induced by goldthioglucose and that associated with the American variety of the obese‐hyperglycemic syndrome there was a considerable accumulation of mast cells in the fat depots. While the relative number of mast cells was calculated as 3 per 100 epididymal fat cells in the lean controls, it was more than 50 for the obese‐hyperglycemic animals. This finding stresses the importance of expressing metabolic data on lipogenesis directly in terms of the fat cells and not per tissue weight, nitrogen or DNA, when comparing the adipose tissue in normal and obese individuals. The greatly increased mast cell content of the adipose tissue in obesity would be consistent with previous work on the rat, in which it was suggested that the lipase activity of the adipose tissue is concerned with accumulation of fat in depots. However, in so far as heparin did not influence the release of free fatty acids or clearing factor lipase from the isolated epididymal adipose tissue, no in vitro effect of heparin was demonstrated.