Effect of low temperatures on glucose-induced insulin secretion and glucose metabolism in isolated pancreatic islets of the rat.

The direct effect of hypothermia on the inhibition of insulin secretion may result from inhibition of the availability of energetic substrates and/or the lack of metabolic signals. In order to verify this hypothesis, the insulin secretion and the main metabolic glucose pathways were measured during the incubation of rat islets. In the presence of 16.7 mmol glucose/l and at 37 degrees C, insulin secretion was 925 +/- 119 microU/2 h per ten islets. With the same experimental conditions, glucose utilization, determined as the formation of 3H2O from [5-3H]glucose was 2225 +/- 184 pmol/2 h per ten islets, glucose oxidation measured as the formation of 14CO2 from [U-14C]glucose was 673 +/- 51 pmol/2 h per ten islets, pentose cycle determined as the formation of 14CO2 from either [1-14C]glucose or [6-14C]glucose was 37 +/- 5 pmol/2 h per ten islets; glucose oxidation by the tricarboxilic acid cycle, calculated to be the difference between glucose oxidation and pentose cycle values, was 636 pmol/2 h per ten islets. Hypothermia highly inhibited glucose-induced insulin secretion and glucose utilization. Inhibition of insulin secretion was partial at 27 degrees C since it was 2.5 times lower than that at 37 degrees C, and it was complete at 17 degrees C. Glucose oxidation in the tricarboxilic acid cycle was markedly inhibited by hypothermia since the inhibition coefficient (Q10) between 37 and 27 degrees C was 5. In contrast, glucose oxidation in the pentose phosphate shunt was enhanced at 27 degrees C, reaching 92 +/- 17 pmol/2 h per ten islets, and it was inhibited relatively little at 17 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of low temperatures on glucose-induced insulin secretion and ionic fluxes in rat pancreatic islets.

The direct effect of cold on the inhibition of B cell secretion is well known in hibernating and experimentally hypothermic mammals. This temperature dependency may result from the inhibition of ion transport across the membranes. In order to verify this hypothesis, ionic effluxes and insulin secretion from rat islets loaded with 86Rb+ and 45Ca+ were measured during perifusion. At 37 degrees C, the rise in glucose concentration from zero to 16.7 mmol/l provoked a rapid decrease in 86Rb+ efflux, an early fall and subsequent rise in 45Ca2+ efflux and a typical biphasic pattern of insulin secretion. At 27 degrees C, glucose induced only a very slight increase in insulin secretion, while the fluxes of radioactive ions were not significantly modified in amplitude but were clearly delayed. At 17 degrees C, no insulin response to glucose was observed and the decrease in K+ conductance indicated by 86Rb+ flux decrease was less temperature-dependent than the movement of Ca2+. After supplementary stimulation with a high extracellular concentration of Ca2+, insulin secretion was enhanced at 27 degrees C and reached levels induced by glucose alone at 37 degrees C. An increase in hormone secretion occurred even at 17 degrees C, but only during a first phase of secretion. Regular increases in temperature potentiated insulin secretion and provoked changes in ionic fluxes which suggest that B cell depolarization (86Rb+ flux decrease) induced by glucose can occur at 15 degrees C but cannot induce the opening of voltage-dependent Ca2+ channels (increase in 45Ca2+ efflux) until temperatures higher than 27 degrees C are reached.(ABSTRACT TRUNCATED AT 250 WORDS)

[Antiulcerogenic properties of bran rice oil in rats]. / Estudio de las propiedades antiulcógenas del aceite de salvado de arroz (ASA) en la rata.

A study was made of the effect of rice chaff oil (ASA) on gastroduodenal ulcer (UGD) induced by different techniques: cysteaminium chloride, indomethacin, artificial gastric juices and stress (acidity, histamine, pepsin and volume of gastric juice were evaluated). For each technique the same protocol was followed: four days before the experiment 20 Wistar rats (180-220 g) were divided into a control group (0.2 ml/day of saline solution per os) and a treated group (0.2 ml/day of oral rice chaff oil). After quantitation of the ulcers and statistical analysis of the data, the ulcer index was found to be smaller in the treated group than in controls, both for stress ulcers (p less than 0.01) and for those induced by indomethacin (p less than 0.001) and artificial gastric juice (p less than 0.001). As for the cysteaminium chloride technique, an evaluation was made of the ulcer per se and the inflammatory halo; in both cases there were significant differences (p less than 0.05 and p less than 0.01 respectively) between the treated group and controls. No significant differences were found on comparing the values off histamine, pepsin and the volume of gastric juices, but there were differences in hydrogen ion concentration (p less than 0.05). An analysis is made of the physiologic aspects studied in each technique, emphasizing the possible implication of prostaglandins (PG) and alpha-tocopherol after treatment with rice chaff oil.