Influence of lipoprotein-lipase activity on plasma triacylglycerol concentration and lipid storage in three genotypes of ducks.

The lipoprotein-lipase (LPL) hydrolyses the triacylglycerols (TG) secreted by the liver and, thus, allows the storage of lipids onto the extrahepatic tissues. The LPL activity has been studied by injection of LPL antibodies in three genotypes of ducks (Muscovy (Cairina moschat), Pekin (Anas plathyrhynchos) and Mule (hybrids of male Muscovy ducks and female Pekin ducks)) under overfeeding condition. The results show a similar weight gain between injected and control animals. A higher liver steatosis is observed in Mule ducks (616+/-18 g; 8.79% of body mass (BW)) and Muscovy ducks (514+/-13 g; 7.05% BW) compared to Pekin ducks (353+/-21 g; 5.89% BW, p<0.05). Pekin ducks showed a much marked extrahepatic fattening of abdominal and subcutaneous adipose tissues. The LPL activity was evaluated by comparing the evolution of the plasma TG concentrations after injections of saline (control animals) or injections of specific LPL-antibodies. Inhibition of LPL activity performed by intravenous injections of LPL-antibodies showed a spectacular increase in the plasma TG concentrations in the three genotypes. That increase was considerably higher in Pekin ducks (98+/-10 g/L) compared to Muscovy ducks (35+/-2 g/L, p<0.01) and Mule ducks (30+/-4 g/L, p<0.01). Those data suggest that a high export of lipids synthesized in liver and a high LPL activity occur in overfed Pekin ducks, which can favour the extrahepatic fattening to the detriment of the liver steatosis, and conversely in overfed Muscovy and Mule ducks.

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)

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 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.

[In vitro studies of the effect of temperature on insulin secretion in the rat, the active and the lethargic hedgehog (author's transl)]. / Etude in vitro de l'influence de la température sur la secrétion de l'insuline par le pancréas du rat, du hérisson actif et du hérisson en léthargie.

The study of insulin secretion by the technic of perifusion of pieces of pancreas at increasing temperature allowed us to point out that the pancreas of the lethargic hedgehog is more sensitive to temperature than that of the active hedgehog or that of the Rat.

Effects of dietary fructose on liver steatosis in overfed mule ducks.

Overfeeding of some waterfowl species results in obesity, which is mainly characterized by a dramatic hepatic steatosis induced by strong accumulation of lipids synthesized from dietary glucose in the liver. In mammals, fructose is known to be able to raise plasma triacylglycerol concentrations significantly; consequently, this may induce obesity. The aim of this study was to assess the effect of partial replacement of dietary glucose provided by corn starch with fructose on metabolism and fatty liver production in the Mule ducks. On the basis of 9.5 kg maize (132,920 kJ) given twice a day for 14 days, a supplementation of 9,800 kJ was provided in form of glucose, sucrose or high fructose corn syrup (HFCS: 50 % glucose, 42 % fructose and 8 % other saccharides). Fatty liver weight in ducks fed with glucose supplementation was 499 +/- 21 g. Sucrose or HFCS supplementation brought about a significant increase in liver weight (+ 18.7 % and + 16.3 % vs. glucose supplementation respectively, p < 0.05). These results suggest that the dietary fructose favors the liver steatosis by increasing hepatic lipogenesis. Postprandial plasma insulin concentrations were similar in ducks fed diets with or without fructose, suggesting that the effect of fructose on liver steatosis is not mediated by insulin.

[Regulation of endocrine pancreas secretions (insulin and glucagon) during the periodic lethargy-waking cycle of the hibernating mammal]. / Régulation des sécrétions du pancréas endocrine (insuline et glucagon) au cours du cycle léthargie-réveil périodique du mammifère hibernant.

In winter, hibernating mammals enter a long phase of lethargy which is characterized by low body temperature, depressed metabolism and minimal release of metabolic substrates from endogenous fuel stores. Periodically, they spontaneously warm themselves to regain the euthermic state. These arousals are, by contrast, times of high release and consumption of endogenous substrates. Insulin and glucagon may contribute to the control of both contrasting metabolic periods. The secretion and metabolic effects of these two hormones were investigated in two hibernators: the hedgehog (Erinaceus europaeus) and the edible dormouse (Glis glis). During lethargy, blood glucose, insulin and glucagon concentrations were low. In vivo and in vitro studies showed that the secretion of both hormones was markedly depressed by low temperatures. Insulin secretion was not stimulated by glucose, although glucagon secretion remained reactive to arginine. Blood glucose was not regulated by insulin but pharmacological doses of glucagon increased blood glucose concentrations. The tissues were found to be highly insulin-resistant, preventing the fall of blood glucose and consequently limiting the depletion of glucidic substrates during the long periods of starvation. During arousal, blood glucose, insulin and glucagon levels increased at the end of rewarming while glucose turnover gradually increased above a body temperature of 15 degrees C. The effects of glucagon and insulin on glucose metabolism increased markedly beyond this stage. Thus the metabolic effect of both hormones are temperature-dependent. Insulin and glucagon allow an increase in glucose availability for the active metabolic processes which occur during arousal.

In vitro B cell response to glucose in the hibernating hedgehog: comparison with the homeothermic hedgehog and the rat.

The effect of glucose and temperature on insulin secretion was studied using pieces of pancreas from hibernating hedgehogs, homeothermic hedgehogs and rats. The rewarming of the perfusion medium progressively stimulated insulin release from the pancreases from lethargic hedgehogs above 13 degrees C even in the absence of glucose. At low temperature (20 degrees C), insulin probably resulted from labile compartments as suggested by the great first phase of glucose-induced insulin secretion from pancreases from lethargic hedgehogs. The insulin release from pancreases from homeothermic animals (hedgehogs and rats) was temperature dependent only above 23-25 degrees C and only with stimulating glucose concentrations (100 or 300 mg/100 ml). These main differences between B cell physiology of lethargic or homeothermic animals suggest that hibernation induces modifications in the secretory processes which facilitate insulin secretion during the in vivo spontaneous arousal from lethargy.

Plasma glucose and insulin in the hibernating hedgehog.

Plasma glucose and insulin have been studied during lethargy and spontaneous arousal of hibernating hedgehogs. During lethargy, plasma glucose and insulin were low and showed no variation. Glucose and insulin injections given during lethargy showed no effects on plasma insulin and glucose respectively but confirmed a very low plasma clearance of glucose and insulin. During spontaneous arousal, the increase in plasma insulin occured before the increase in blood glucose and at about the time that utilization of blood glucose was restored.

[Plasma Ca, Na, and K levels during the hibernation of hedgehogs, common dormice, and garden dormice]. / Evolution du Ca, Na et K plasmatiques au cours de l'hibernation des hérissons, des loirs et des lérots

The plasmatic rate of Ca, Na and K are nearly constant during the deep lethargy of hedgehogs, common dormice and garden dormice and little differ from those measured in the active animals at 22 degrees C. Only the kaliemies of the hibernating common dormice and garden dormice are very low. The evolution of the three parameters during the alternance lethargy and periodic arousal has been analysed in terms of the metabolic and endocrinian changes which occur at those moments.

Plasma glucagon, glucose, and free fatty acid concentrations and secretion during prolonged hypothermia in rats.

Impairment of metabolic substrate mobilization and utilization may be a factor limiting survival in hypothermia. Using a newly developed technique for maintaining stable low body temperature (Tb), substrate profiles and their regulation by glucagon were examined in hypothermic rats (Tb 19 +/- 0.3 degrees C) over 20 h. During cooling, plasma glucagon, glucose, and free fatty acid (FFA) concentrations increased significantly (536 +/- 55 pg/ml, 304 +/- 26 mg/100 ml, and 844 +/- 81 mueq/l, respectively). Plasma glucagon and glucose concentrations continued to increase up to 8 h (peaks 810 +/- 103 pg/ml and 451 +/- 33 mg/100 ml, respectively) and remained high throughout the rest of the hypothermic period. FFA concentrations decreased steadily during the hypothermic period. Exogenous glucagon (20 micrograms/kg) induced significant increases in plasma glucose (+129 +/- 31 mg/100 ml) and FFA concentrations (+351 mueq/l) at 2 h but had no effect at 15 h of hypothermia. In vitro evaluation of pancreatic alpha-cell function indicated that glucagon secretion is independent of temperature between 37 and 19 degrees C. Our data indicate that hypothermia is characterized by a disturbed substrate metabolism, which is likely due to an imbalance in pancreatic alpha- and beta-cell function and a time-dependent decrease in tissue sensitivity to glucagon. These deleterious changes may limit survival in hypothermia.

Insulin secretion and substrate homeostasis in prolonged hypothermia in rats.

In hypothermia, impairment of metabolic substrate mobilization and utilization may be a factor limiting survival. By use of a newly developed technique, substrate profiles and their regulation by insulin were examined in hypothermic rats (body temperature 19 degrees C) over 24 h. Plasma glucose concentrations increased to approximately 300 mg/dl during cooling and remained high throughout the period of hypothermia. Free fatty acid (FFA) concentration was not altered during cooling or during the first 10 h of hypothermia (approximately 700 mu eq/l) but progressively decreased thereafter, reaching 420 mu eq/l by 20 h. Plasma insulin decreased dramatically during cooling and remained very low (9 +/- 2 microU/ml) during the whole period of hypothermia, reflecting the suppression of insulin secretion by isolated islets at low temperatures. To test he hypothesis that suppression of endogenous insulin secretion may hamper glucose utilization and thus limit survival in hypothermia, exogenous insulin was administered. At doses of 0.1, 0.5, and 1 U/kg intravenously, insulin slowly decreased plasma glucose and FFA. However, at 0.1 and 1 U/kg intraperitoneally, insulin resulted in a dose-dependent decrease in survival time in the hypothermic rat. It is possible that the antilipolytic effect of insulin may have outweighed any beneficial effect of improving glucose utilization in hypothermia.

Pancreatic A and B cell stimulation in euthermic and hibernating marmots (Marmota flaviventris): effects of glucose and arginine administration.

In euthermic and hibernating marmots (Marmota flaviventris), the pancreatic A and B cells respond in the appropriate secretory manner to glucose or arginine injection. Although reduced, this response, is clearly present in hibernating marmots. When glucose is administered to euthermic or hibernating marmots, plasma insulin concentrations rise and glucagon levels fall. While similar results are obtained in hibernation, the time period of the response is much longer due to the slowing of temperature dependent metabolic processes. Injection of L-arginine stimulates an increase in plasma glucose, insulin, and glucagon as expected. Measurements of plasma glucose, insulin, and glucagon under basal conditions, suggest that there are no significant differences between any phase of hibernation (eg. entrance, deep hibernation, arousal) and euthermia. These results provide indirect evidence that the pancreatic A and B cells of hibernating marmots continue to function in order to help regulate plasma glucose concentration.

Glucose oxidation by adipose tissue of the edible dormouse (Glis glis) during hibernation and arousal: effect of insulin.

1. The effect of insulin on U-14C-glucose oxidation by adipose tissue isolated from hibernating or arousing edible dormouse has been studied. 2. CO2 production derived from radioglucose was analysed point by point during in vitro rewarming (from 6 to 37 degrees C). 3. The rate of temperature increase was 2 degrees/5 min in order to mimic the rate of rewarming during the spontaneous arousal of the dormouse. 4. Insulin did not increase the glucose oxidation by the adipose tissue from hibernating dormouse whereas adipocytes from active animal present high insulin sensitivity. 5. These results suggest that insulin resistance occurs during hibernation.

Pancreatic hormonal and metabolic responses in overfed ducks.

When overfed at their maximum (intensive overfeeding) or at only 80% (moderate overfeeding) of food intake capacity, Mule ducks developed strong liver steatosis, whereas Pekin ducks showed very marked extrahepatic fattening. During overfeeding, evolution of plasma glucose and triacylglycerol concentrations suggested a very strong increase in the hepatic lipogenesis as well as genotype- and diet-independent lipoprotein secretion. In contrast, lipoprotein-lipase activity was dependent on alimentary status (the intensive overfeeding induces the highest activities), and Pekin ducks showed higher lipoprotein-lipase activity than Mule ducks, which could favor extrahepatic fattening to the detriment of hepatic steatosis. In Pekin ducks, plasma pancreatic hormone concentrations are related to diet levels and blood sugar. With similar food intake, Mule ducks (moderately overfed) showed global blood insulin lower than that of Pekin ducks (intensively overfed) despite similar blood sugar levels, suggesting a trend towards reduced pancreas response to glucose in Mule ducks. This may result from their lower lipoprotein-lipase activity as previously shown in these two ducks overfed at only 60% of their maximal food intake capacity (unpublished results). These results suggest that high plasma insulin concentrations may be necessary to induce an optimum lipoprotein-lipase activity in overfed ducks.

Hormonal control of lipolysis from the white adipose tissue of hibernating jerboa (Jaculus orientalis).

1. Plasma glucose, glycerol, free fatty acids and total lipid content of the white adipose tissue were measured in euthermic and hibernating jerboa. 2. During hibernation, plasma glucose and glycerol were low compared to the euthermic animals, whereas there was no obvious difference in plasma free fatty acids. The white adipose tissue lipid content was strongly reduced in the hibernating state. 3. The effect of lipolytic hormones (norepinephrine and glucagon) and antilipolytic hormone (insulin) on in vitro glycerol release by adipose tissue isolated from hibernating or euthermic jerboa has been studied. 4. The white adipose tissue from hibernating jerboa presented a higher sensitivity to norepinephrine and glucagon than that of euthermic jerboa; insulin did not modify either basal glycerol release or lipolysis induced by the two lipolytic hormones at low temperatures (7 degrees C) and during the rewarming (from 7 degrees C to 37 degrees C) of the tissue slices. 5. These results suggested that white adipose tissue constitutes an important source of substrates derived from lipolysis during hibernation.

Pancreatic A cell response to arginine in the hibernating hedgehog (Erinaceus europaeus).

Pancreatic A cell response to arginine was measured in hedgehogs during the periods of lethargy and arousal and then during activity. Spontaneous plasma glucagon concentrations were lower during lethargy than during activity, and they increased during arousal. Arginine administration induced a slight, but significant delayed increase in plasma glucagon concentration in the lethargic hedgehog (body temperature: 6 degrees). During arousal, in vitro glucagon secretion was temperature dependent suggesting that body rewarming might, in itself, be an important stimulating factor of the A cells. In the presence of arginine, the glucagon output of the pancreas of lethargic hedgehogs was high at low temperatures. It decreased to a nadir at 19 degrees and increased up to 37 degrees. However, the basal or arginine-stimulated glucagon secretion of animals in lethargy was higher than that of animals in activity. These characteristics suggested the presence of a particular pool of cold-adapted enzymes in the A cells of lethargic hedgehogs.