Effect of colostral fat level on fat deposition and plasma metabolites in the newborn pig.

The effects of colostral fat level on fat deposition and plasma concentrations of glucose, insulin, and free fatty acids (FFA) were determined in 28 newborn pigs during the first postnatal day. Soon after birth, pigs were allotted to four treatments groups. Group 1 was killed at birth. The remaining pigs were fed intragastrically sow colostrum that contained high (10.2%; HFC), normal (4.8%; NFC) or low (1.0%; LFC) levels of total fat at the rate of 15 to 18 g/kg birth weight at 65- to 70-min intervals. A total of 21 feedings was provided and pigs were killed 1 h after the last feeding. Body fat deposition increased linearly (P less than .01) with the amount of ingested fat by .32 (+/- .04) g per 1-g increase in fat intake. Fatty acid composition of the pigs changed toward that of the colostrum with increased fat in colostrum. More liver glycogen was lost (P less than .01) in pigs given LFC. Plasma concentrations of glucose and insulin were similar in pigs fed HFC and NFC. After the 11th feeding (14 h postnatal), LFC resulted in lower plasma glucose concentrations (P less than .05) than HFC or NFC. Plasma insulin concentrations also were lower in pigs fed LFC. Plasma FFA concentrations remained unchanged in pigs fed LFC but increased with both fat content in colostrum (P less than .05) and time (P less than .05) in the other two groups. Colostral fat plays a major role in the supply of energy and in glucose homeostasis in the neonatal pig.

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)