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M C Venturino

Publications and source records attributed to M C Venturino.

6 recordsLinked to original sources

Increase in insulin secretion induced by plasma from mice injected with allogeneic lymphocytes.

Plasma from BALB/c mice bled 90 minutes after allogeneic lymphocyte injection significantly rises glucose induced insulin secretion. This rise is observed in pancreas either from non-treated or from allogeneized mice. This rise is time and dose-dependent. An 1/40 dilution is enough to bring about a significant increase on insulin secretion. This effect is seen when mice are bled between 60 and 180 minutes after injection with a maximum effect at 90-120 minutes. Plasma from BALB/c mice injected with C57BL/6 J lymphocytes rises insulin secretion from BALB/c, C57BL/6 J, C3h and C57BL/KsJ mice pancreas. Plasma from streptozotocin diabetic BALB/c mice and from genetically diabetic C57BL/KsJ mdb-mdb mice injected with allogeneic lymphocytes stimulates glucose induced insulin secretion but to a lesser extent than plasma from normal non-diabetic mice does.

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Insulin secretion stimulated by allogeneic lymphocytes in an inbred strain of mice.

Effects of intraperitoneal injection of allogeneic lymphocytes on insulin secretion were studied in incubated pancreas slices from BALB/c mice. Injection of allogeneic lymphocytes from C57BL/6J (H2b) mice increased insulin secretion, both in basal and 11-mM glucose-stimulated conditions. This effect was only present when at least 5 X 10(6) or 1 X 10(6) cells were injected (in basal and stimulated conditions, respectively). Glucose-induced insulin secretion (3.3-27.5 mM) was significantly increased in pancreata from mice injected with allogeneic lymphocytes. No effect was observed when glucose was not included in the incubation medium. Intraperitoneal injection of Dextran 70 produced no change in glucose-elicited insulin secretion. There were no differences in glucagon and somatostatin (SRIF) secretion obtained from pancreas of mice injected with allogeneic or syngeneic lymphocytes. Injection of allogeneic cells increases insulin secretion (basal and both phases of 11 mM glucose-stimulated secretion). Puromycin significantly inhibited the second phase of insulin secretion. These results suggest that: Injection of allogeneic lymphocytes raises both basal and glucose-stimulated insulin secretion. This effect seems to be connected with the major histocompatibility complex, and to be related to the number of allogeneic cells injected. Injection of allogeneic lymphocytes seems to sensitize the beta cell response to glucose stimulus. Neither glucagon nor SRIF secretion are altered by alloantigen injection. The stimulatory effect of allogeneic lymphocytes is related, at least in part, to insulin synthesis.

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Insulin secretion induced by allogeneic lymphocytes in genetically diabetic mice C57BL/KsJ mdb.

Insulin and somatostatin (SRIF) secretion induced by alloantigen were studied in genetically diabetic mice from the C57BL/KsJ mdb-mdb strain. Diabetic (db) mice injected with allogeneic lymphocytes (A.L.) did not show any increase in their second phase of 27.5 mM glucose stimulated secretion and slightly increased their first phase. Normal A.L. injected mice showed a significant increase in both phases of 27.5 mM glucose stimulated secretion. SRIF secretion of A.L. injected normal and diabetic mice did not significantly differ from that obtained when injected with syngeneic lymphocytes. Lymphocytes from db mice injected into allogeneic mice caused an insulin secretion similar to that produced by allogeneic lymphocytes from non-diabetic mice. Lymphocytes from db mice injected into normal syngeneic mice caused an insulin secretion which was not significantly different from the one caused by syngeneic lymphocytes from non-diabetic mice, and is smaller than the secretion caused by A.L. injection. In summary, db mice showed an impaired hormone response to alloantigenic stimulus, while their lymphocytes maintained their alloantigenic action.

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Insulin secretion induced by alloantigens. Mechanisms of action.

Basal insulin secretion stimulated by allogeneic lymphocyte injection was inhibited by SRIF, diazoxide and verapamil but was not affected by theophylline or imidazole. Glucose stimulated insulin secretion induced by alloantigens was inhibited by imidazole. Maximum insulin secretion was achieved with 2.1 mg/ml theophylline in allogeneized mouse pancreata and with 4.2 mg/ml in control pancreata. Propranolol also blocked allogen-induced glucose-stimulated insulin secretion. Phentolamine enhanced insulin secretion from both experimental groups, but phentolamine plus epinephrine only stimulated insulin secretion in control pancreata. Verapamil, diazoxide and SRIF diminished insulin secretion in both experimental groups. These results suggest that: a) basal insulin secretion induced by alloantigens may be mediated by an increase in calcium translocation, and b) glucose-stimulated insulin secretion induced by alloantigen may be mediated by a rise in B-cell cAMP.

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