This study tests the hypothesis that the metabolic and endocrine shift characterizing the phase II-phase III transition during prolonged fasting is related to a decrease in fatty acid (FA) oxidation. Changes in plasma concentrations of various metabolites and hormones and in lipolytic fluxes, as determined by continuous infusion of [2-3 H]glycerol and [1-14 C]palmitate, were examined in vivo in spontaneously fasting king penguins in the phase II status (large fat stores, protein sparing) before, during, and after treatment with mercaptoacetate (MA), an inhibitor of FA oxidation. MA induced a 7-fold decrease in plasma -hydroxybutyrate and a 2-to 2.5-fold increase in plasma nonesterified fatty acids (NEFA), glycerol, and triacylglycerols. MA also stimulated lipolytic fluxes, increasing the rate of appearance of NEFA and glycerol by 60-90%. This stimulation might be partly mediated by a doubling of circulating glucagon, with plasma insulin remaining unchanged. Plasma glucose level was unaffected by MA treatment. Plasma uric acid increased 4-fold, indicating a marked acceleration of body protein breakdown, possibly mediated by a 2.5-fold increase in circulating corticosterone. Strong similarities between these changes and those observed at the phase II-phase III transition in fasting penguins support the view that entrance into phase III, and especially the end of protein sparing, is related to decreased FA oxidation, rather than reduced NEFA availability. MA could be therefore a useful tool for understanding mechanisms underlying the phase II-phase III transition in spontaneously fasting birds and the associated stimulation of feeding behavior.protein sparing; lipolytic fluxes; isotopic tracers; mercaptoacetate; seabirds PROLONGED FASTING IS CHARACTERIZED by the preferential utilization of lipid, with relative sparing of body protein (4, 6, 25). Previous studies indicated that protein sparing depends on the availability of lipid fuels (17). The conservation of body protein that characterizes the so-called phase II of fasting (9, 17) is no longer maintained when a lower threshold in fat stores is reached (6,17,22,25). Then a metabolic shift occurs, with a simultaneous acceleration in the catabolism of body protein and a decrease in the contribution of lipid to energy production, the signature of the so-called phase III of fasting (6,22,25). Entrance into phase III is also accompanied by hormonal changes, such as an increase in the level of circulating glucocorticoids thought to contribute to the stimulation of protein breakdown (10). How fat store availability determines body protein sparing during phase II or accelerated catabolism during phase III is not well understood. Is protein sparing during phase II linked to the availability of nonesterified fatty acids (NEFA) mobilized from adipose tissue, or does it depend on their oxidation? Arguments suggest that NEFA may specifically modulate the breakdown of myofibrillar proteins independently of their oxidation as a fuel for muscle (26). This suggestion agrees with ...
Groscolas, R. 2001. Restoration of body mass in King Penguins after egg abandonment at a critical energy depletion stage: early vs late breeders. -J. Avian Biol. 32: 303-310.In fasting-incubating seabirds, it has been proposed that egg abandonment and refeeding should be induced when a low body mass (BM) threshold is attained, thus ensuring adult survival at the expense of immediate breeding. In the context of life-history trade-offs in long-lived birds, we have tested this hypothesis by comparing short-term survival and restoration of BM in King Penguins Aptenodytes patagonicus that abandoned their egg to those that were relieved normally by their mate at the end of the first incubation shift. Since King Penguins have an extended laying period, the possible influence of seasonal factors was also examined by comparing early and late breeders. Forty incubating males were experimentally forced to fast until egg abandonment by preventing relief by the female. At egg abandonment of both early and late breeding males, BM was below the BM threshold, fasting duration was eight days (about 30%) longer than for relieved birds, and plasma uric acid level was elevated (signature of increased body protein catabolism, phase III of fasting). All abandoning birds survived and came back from sea at a BM similar to that of relieved penguins. The duration of the foraging trip of abandoning early breeders was the same as that of relieved birds, and some abandoning birds engaged in a new breeding attempt. Abandoning late breeders, however, made foraging trips twice as long as those of relieved males. This difference can be explained by time constraints rather than nutritional constraints, abandoning early breeders having enough time left in the breeding season to engage in a new breeding attempt in contrast to abandoning late breeders. These observations lend support to the suggestion that not only BM but also an internal clock intervene in the decision to engage in breeding or not. By preventing a lethal energy depletion ashore and by acting at a fasting stage where the capacity to restore BM at sea is unaffected, abandonment at a low body condition threshold plays a major role in the trade-off between adult penguin survival and reproduction.
This study aims to determine how glucagon intervenes in the regulation of fuel metabolism, especially lipolysis, at two stages of a spontaneous long-term fast characterized by marked differences in lipid and protein availability and/or utilization (phases II and III). Changes in the plasma concentration of various metabolites and hormones, and in lipolytic fluxes as determined by continuous infusion of [2-3 H]-glycerol and [1-14 C]palmitate, were examined in vivo in a subantarctic bird (king penguin) before, during, and after a 2-h glucagon infusion. In the two fasting phases, glucagon infusion at a rate of 0.025 g ⅐ kg Ϫ1 ⅐ min Ϫ1 induced a three-to fourfold increase in the plasma concentration and in the rate of appearance (R a) of glycerol and nonesterified fatty acids, the percentage of primary reesterification remaining unchanged. Infusion of glucagon also resulted in a progressive elevation of the plasma concentration of glucose and -hydroxybutyrate and in a twofold higher insulinemia. These changes were not significantly different between the two phases. The plasma concentrations of triacylglycerols and uric acid were unaffected by glucagon infusion, except for a 40% increase in plasma uric acid in phase II birds. Altogether, these results indicate that glucagon in a long-term fasting bird is highly lipolytic, hyperglycemic, ketogenic, and insulinogenic, these effects, however, being similar in phases II and III. The maintenance of the sensitivity of adipose tissue lipolysis to glucagon could suggest that the major role of the increase in basal glucagonemia observed in phase III is to stimulate gluconeogenesis rather than fatty acid delivery. lipolysis; ketone bodies; glucose; isotopic tracers; seabirds MAMMALS AND BIRDS adjust to long-term fasting by mobilizing their fat stores and sparing body proteins (8,14,21). However, the conservation of body protein that characterizes the so-called phase II of fasting is no longer maintained when a lower threshold of fat stores is reached. Then a metabolic shift occurs, and animals enter a new fasting state (phase III) corresponding to a simultaneous acceleration in the catabolism of protein and a decrease in the contribution of lipid to energy production (21, 46). This shift has been described in experimentally fasted laboratory mammals (21, 34) and in birds that spontaneously fast for prolonged periods at certain stages of their annual cycle, such as penguins (23, 37). Nevertheless, the way the metabolic shift is triggered and how the utilization of the metabolic fuels is regulated during phase II and phase III are poorly understood.Among the various hormones that could intervene to regulate fuel utilization, glucagon is likely to play a major role. Although the evidence for a lipolytic action in humans is scarce (10), glucagon stimulates lipolysis in vitro in mammals (38,52) and is the main lipolytic hormone in birds (9,22,36). It therefore plays a key role in the mobilization of fatty acids (FA) from adipose tissue. In mammals, glucagon also appears to influen...
This study aims to determine whether glucose intervenes in the regulation of lipid metabolism in long-term fasting birds, using the king penguin as an animal model. Changes in the plasma concentration of various metabolites and hormones, and in lipolytic fluxes as determined by continuous infusion of [2-3H]glycerol and [1-14C]palmitate, were examined in vivo before, during, and after a 2-h glucose infusion under field conditions. All the birds were in the phase II fasting status (large fat stores, protein sparing) but differed by their metabolic and hormonal statuses, being either nonstressed (NSB; n = 5) or stressed (SB; n = 5). In both groups, glucose infusion at 5 mg.kg-1.min-1 induced a twofold increase in glycemia. In NSB, glucose had no effect on lipolysis (maintenance of plasma concentrations and rates of appearance of glycerol and nonesterified fatty acids) and no effect on the plasma concentrations of triacylglycerols (TAG), glucagon, insulin, or corticosterone. However, it limited fatty acid (FA) oxidation, as indicated by a 25% decrease in the plasma level of beta-hydroxybutyrate (beta-OHB). In SB, glucose infusion induced an approximately 2.5-fold decrease in lipolytic fluxes and a large decrease in FA oxidation, as reflected by a 64% decrease in the plasma concentration of beta-OHB. There were also a 35% decrease in plasma TAG, a 6.5- and 2.8-fold decrease in plasma glucagon and corticosterone, respectively, and a threefold increase in insulinemia. These data show that in fasting king penguins, glucose regulates lipid metabolism (inhibition of lipolysis and/or of FA oxidation) and affects hormonal status differently in stressed vs. nonstressed individuals. The results also suggest that in birds, as in humans, the availability of glucose, not of FA, is an important determinant of the substrate mix (glucose vs. FA) that is oxidized for energy production.
Continuous infusions of 2-[3H]glycerol and 1-[14C]palmitate were performed in vivo in rainbow trout to measure the effects of prolonged swimming on (1) the rate of appearance of glycerol (Ra glycerol or lipolytic rate), (2) the rate of appearance of non-esterified fatty acids (Ra NEFA) and (3) the rate of triacylglycerol:fatty acid cycling (TAG:FA cycling or re-esterification). Our goals were to test the hypothesis that sustained exercise for up to 4 days causes the progressive mobilization of triacylglycerol reserves to supply fuel to contracting muscles, and to assess whether TAG:FA cycling plays a role in the regulation of NEFA availability in teleosts. Contrary to expectation, the rates of lipolysis and fatty acid release in resting trout are not affected by endurance exercise. Unlike mammals, which increase the rate of lipolysis by two- to fourfold during submaximal exercise, these active teleosts do not mobilize triacylglycerol reserves beyond resting levels to supply more NEFAs to working muscles. Furthermore, they maintain Ra glycerol and Ra NEFA well in excess of oxidative fuel requirements even at rest. More than two-thirds of the NEFAs produced are re-esterified, but the results show that TAG:FA cycling is not involved in the regulation of NEFA availability during or after swimming. We propose that the observed high rates of re-esterification represent an important feature of ectothermic metabolism that allows the restructuring of membrane phospholipids to be synchronized with frequent changes in body temperature.
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