Regulation of food intake by metabolic fuels in white-crowned sparrows

1995 ◽  
Vol 269 (6) ◽  
pp. R1462-R1468 ◽  
Author(s):  
T. Boswell ◽  
R. D. Richardson ◽  
R. J. Seeley ◽  
M. Ramenofsky ◽  
J. C. Wingfield ◽  
...  

Migratory birds rely on increased fat storage and fatty acid utilization to meet seasonal changes of energy expenditure and as a result increase food intake and fat stores before migration. To determine whether their feeding behavior is sensitive to carbohydrate and/or fatty acid utilization, white-crowned sparrows maintained on short daylength (9L15D) were injected intraperitoneally with 2-deoxy-D-glucose (2-DG) or 2,5-anhydro-D-mannitol (2,5-AM). Low doses of 2-DG (25 or 50 mg/kg) had no effect on food intake, and higher doses (100 or 300 mg/kg) significantly suppressed feeding after 1 and 2 h. No dose of 2-DG increased meal size. Similarly, low doses of 2,5-AM (25, 50, or 100 mg/kg) had no effect on food intake, and higher doses (300 and 600 mg/kg) significantly suppressed intake. These data suggest that decreased carbohydrate metabolism does not elicit feeding in this species. Importantly, these drugs, as well as insulin and glucagon, were demonstrated to increase plasma fatty acids as well as to decrease feeding. Injections of tributyrin (100, 300, 600, or 2,000 mg/kg i.p.) or glycerol (300, 450, and 600 mg/kg) also significantly suppressed 60-min and 120-min food intake dose dependently in these birds, and equimolar glucose (1,200 mg/kg) had no effect. We conclude that feeding by the white-crowned sparrow is unresponsive to manipulations of carbohydrate metabolism and is decreased after manipulations that increase plasma lipids.

1984 ◽  
Vol 102 (3) ◽  
pp. 381-386 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe

ABSTRACT To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake. J. Endocr. (1984) 102, 381–386


1991 ◽  
Vol 261 (2) ◽  
pp. R283-R288 ◽  
Author(s):  
M. G. Tordoff ◽  
N. Rawson ◽  
M. I. Friedman

We determined the site at which the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) acts to increase food intake in rats. Rats began eating sooner and ate more food during hepatic portal than during jugular infusions of 2,5-AM (50, 100, or 150 mg/h). After rats were intubated with 2,5-[14C]AM (1.15 microCi in 200 mg/kg), significant quantities of radioactivity were found in liver but not in brain. Hepatic vagotomy prevented the eating response to 200 mg/kg 2,5-AM without altering the effect of the analogue on plasma fuels. These results indicate that low doses of 2,5-AM act in the liver to increase food intake and suggest that the signal for feeding generated in the liver is transmitted to the brain through the hepatic vagus nerve. Taken together, this work provides the strongest evidence to date that a signal initiating feeding behavior originates in the liver.


1965 ◽  
Vol 33 (3) ◽  
pp. 397-404 ◽  
Author(s):  
B. N. PREMACHANDRA

SUMMARY Investigations were carried out to study the effect of reserpine in doses up to 100 μg./100 g. body weight on thyroid function as determined by thyroxine secretion rates (TSR) in the rat, hamster, guinea-pig and mouse. It was found that 20 μg. reserpine/100 g. body weight had no effect on TSR or on body weight. At higher doses (50–100 μg./100 g.) TSR was depressed, greater depression being noted with doses of 100 μg. Food intake was reduced at the higher dosage resulting in significant losses of body weight (up to 33%). In long-term studies in rats, administration of 10 μg. reserpine/100 g. body weight for 6 weeks had no effect on TSR. No dose of reserpine that would inhibit TSR without contributing to body weight loss and depression in food intake was found. Administration of reserpine in these low doses did not influence body temperature. Uniform results were obtained in all the species studied. It is concluded that reserpine, in low doses, has no influence on thyroid function as determined by the rate of thyroxine secretion. Higher doses of reserpine, however, inhibit thyroid secretion, but such an inhibition appears to be secondary to the effects of inanition brought about by a toxic action of the drug and/or its hypothalamic effects.


1991 ◽  
Vol 260 (4) ◽  
pp. R688-R692 ◽  
Author(s):  
T. J. Kalogeris ◽  
R. D. Reidelberger ◽  
V. E. Mendel ◽  
T. E. Solomon

Feeding responses to continuous intravenous administration of graded doses of the COOH-terminal octapeptide of cholecystokinin (CCK-8) and pancreatic glucagon, alone and in combination, were determined in dogs fasted 4 h. Low doses of glucagon (50, 500, 5,000, 6,000 pmol.kg-1.h-1) had no effect on food intake, whereas higher doses (12 and 24 nmol.kg-1.h-1) depressed intake by 50-60%. Of the CCK-8 doses administered (50 and 400 pmol.kg-1.h-1), food intake was depressed only at the higher dose (53%). This effect was blocked by glucagon (50-5,000 pmol.kg-1.h-1). Simultaneous administration of 50 or 500 pmol.kg-1.h-1 of glucagon and 50 pmol.kg-1.h-1 of CCK-8, doses currently thought to produce plasma peptide levels similar to those occurring postprandially in dogs, had no effect on food intake. These results suggest that plasma levels of CCK and glucagon after a meal are not sufficient alone or in combination to produce satiety.


2008 ◽  
Vol 295 (3) ◽  
pp. R799-R805 ◽  
Author(s):  
Abdelhak Mansouri ◽  
Susan Aja ◽  
Timothy H. Moran ◽  
Gabriele Ronnett ◽  
Francis P. Kuhajda ◽  
...  

Central and intraperitoneal C75, an inhibitor of fatty acid synthase and stimulator of carnitine palmitoyl-transferase-1, inhibits eating in mice and rats. Mechanisms involved in feeding inhibition after central C75 have been identified, but little is yet known about how systemic C75 might inhibit eating. One issue is whether intraperitoneal C75 reduces food intake in rats by influencing normal physiological controls of food intake or acts nonselectively, for example by eliciting illness or aversion. Another issue relates to whether intraperitoneal C75 acts centrally or, similar to some other peripheral metabolic controls of eating, activates abdominal vagal afferents to inhibit eating. To further address these questions, we investigated the effects of intraperitoneal C75 on spontaneous meal patterns and the formation of conditioned taste aversion (CTA). We also tested whether the eating inhibitory effect of intraperitoneal C75 is vagally mediated by testing rats after either total subdiaphragmatic vagotomy (TVX) or selective subdiaphragmatic vagal deafferentations (SDA). Intraperitoneal injection of 3.2 and 7.5 mg/kg of C75 significantly reduced food intake 3, 12, and 24 h after injection by reducing the number of meals without affecting meal size, whereas 15 mg/kg of C75 reduced both meal number and meal size. The two smaller doses of C75 failed to induce a CTA, but 15 mg/kg C75 did. The eating inhibitory effect of C75 was not diminished in either TVX or SDA rats. We conclude that intraperitoneal injections of low doses of C75 inhibit eating in a behaviorally specific manner and that this effect does not require abdominal vagal afferents.


1995 ◽  
Vol 268 (6) ◽  
pp. R1418-R1422 ◽  
Author(s):  
R. D. Richardson ◽  
T. Boswell ◽  
B. D. Raffety ◽  
R. J. Seeley ◽  
J. C. Wingfield ◽  
...  

To determine if altered sensitivity to neuropeptide Y (NPY) underlies premigratory fattening, white-crowned sparrows held on short day length (9:15-h light-dark) received injections into the third ventricle (ivt) of saline or several doses of NPY. An inverted-U function occurred with food intake increasing 30 and 60 min after doses of 1.0 and 2.0 micrograms NPY. When photostimulated (20:4-h light-dark), birds increased daily caloric intake and gained weight rapidly. Birds maintained on long day lengths significantly increased food intake after 0.25 and 0.5 micrograms of NPY and did not respond to higher doses. The effective dose range for NPY to increase food intake moved to the left, suggesting an increase in sensitivity to the peptide on long day lengths. In summary, white-crowned sparrows consume more food when administered NPY ivt and have increased sensitivity when photostimulated and gaining weight. Hence NPY may be a natural stimulator of food intake in this species.


The Condor ◽  
2005 ◽  
Vol 107 (2) ◽  
pp. 269-279 ◽  
Author(s):  
Barbara J. Pierce ◽  
Scott R. McWilliams

Abstract It is well established that birds use fat stores to primarily fuel migration; however, few studies have focused on the causes and consequences of observed seasonal changes in fatty acid composition of fat stores in birds. We propose and test two hypotheses that address the causes of these seasonal changes in composition of fat stores: (1) diet composition determines fatty acid composition of fat stores, and (2) birds selectively metabolize and store certain fatty acids during migration in lieu of changing their diet. When we offered Red-eyed Vireos (Vireo olivaceous) choices between diets that differed only in fatty acid composition, vireos preferred diets with more triolein over diets with more tristearin and tripalmitin, and these preferences were similar between seasons. We also collected fat samples six times throughout the year from captive Red-eyed Vireos fed one of two diets differing in fatty acid composition, and found that fatty acid composition of stored fat differed by diet and changed over time, although these changes were not season-specific or consistent with the selective-metabolism hypothesis. Thus, fatty acid composition of stored fat was primarily a product of diet composition; selective metabolism possibly played a minor, but important, role. Given recent evidence that fatty acid composition of birds affects their energy expenditure during intense exercise, the implication is that birds at stopover sites can influence the fatty acid composition of their body fat by selective feeding, and this can significantly affect the energetic cost of migration. Cambios Estacionales en la Composición de las Reservas Lipídicas en Aves Migratorias: Causas y Consecuencias Resumen. Se sabe que las aves utilizan reservas de grasa principalmente como fuente de energía durante la migración; sin embargo, pocos estudios han analizado las causas y consecuencias de los cambios estacionales en la composición de ácidos grasos de las reservas de grasa de las aves. Aquí proponemos y probamos dos hipótesis que se relacionan con las causas de los cambios estacionales en la composición de las reservas de grasa: (1) la composición de la dieta determina la composición de ácidos grasos de las reservas de grasa, y (2) las aves metabolizan y almacenan de manera selectiva ciertos ácidos grasos durante la migración, en lugar de cambiar sus dietas. Ofrecimos a individuos de la especie Vireo olivaceous para que elijan entre dietas que sólo diferían en la composición de ácidos grasos, los cuáles prefirieron dietas con más trioleina que dietas con más tristearina y tripalmitina, y estas preferencias fueron similares entre estaciones. Colectamos además muestras de grasa, en seis oportunidades a lo largo del año, de individuos en cautiverio alimentados con una de las dos dietas disponibles, las que difirieron en la composición de ácidos grasos. Encontramos que la composición de ácidos grasos de las reservas de grasa difirió en relación a las dietas y varió a lo largo del tiempo, aunque estos cambios no fueron estacionalmente específicos ni coherentes con la hipótesis de metabolismo selectivo. Por lo tanto, la composición de ácidos grasos de las reservas de grasa fue principalmente el producto de la composición de la dieta; el metabolismo selectivo probablemente jugó un papel menor, aunque importante. Existe evidencia reciente que sugiere que la composición de ácidos grasos en las aves afecta el gasto energético que tienen durante períodos de ejercicios intensos, lo que implica que las aves pueden influir sobre la composición de los ácidos grasos en sus reservas de grasa al alimentarse de manera selectiva en los sitios de parada migratoria, lo que puede afectar significativamente el costo energético de la migración.


1993 ◽  
Vol 264 (3) ◽  
pp. R573-R577 ◽  
Author(s):  
J. E. Schneider ◽  
D. G. Friedenson ◽  
A. J. Hall ◽  
G. N. Wade

Previous results supported the notion that estrous cycles in Syrian hamsters are responsive to the general availability of metabolic fuels, rather than to either fatty acid or glucose availability per se. To test this idea, we monitored estrous cycles in hamsters that were fed ad libitum and treated with a range of doses of 2-deoxy-D-glucose (2-DG), an inhibitor of glucose utilization. Hamsters treated with 2-DG at doses ranging from 750-1,250 mg/kg showed normal estrous cycles, but higher doses (1,750 or 2,000 mg/kg) induced anestrus. While it is clear from these data that estrous cycles are affected by glucoprivation, it is not clear whether they are responsive to decreased fatty acid availability. Groups of hamsters were fed ad libitum and treated with a range of doses of methyl palmoxirate (MP), an inhibitor of fatty acid utilization. Some of the hamsters that received the highest doses became torpid and thus were not tested for lordosis. None of the euthermic, MP-treated hamsters became anestrous. Other experiments examined the role of glucose availability in fasted hamsters. Hamsters with a high body fat content were protected from fasting-induced anestrus. In contrast, fat food-deprived hamsters treated with low doses of 2-DG (750 mg/kg) became anestrous. Thus fatty acids mobilized from adipose tissue did not prevent fasting-induced anestrus when glucose utilization was blocked. One interpretation is that during fasting fatty acid utilization spares glucose for other tissues involved in the control of estrous cycles.(ABSTRACT TRUNCATED AT 250 WORDS)


1989 ◽  
Vol 61 (03) ◽  
pp. 463-467 ◽  
Author(s):  
G M Smith

SummaryIn this study, 5-hydroxytryptamine (5-HT) caused a dose- dependent fall in the circulating platelet count suggesting that 5-HT receptors are activated in rat platelets to cause platelet adhesion and aggregation. When low doses of adenosine diphosphate (ADP) were simultaneously injected with 5-HT, there was a significant potentiation of the responses to ADR Ketanserin significantly reduced the potentiated responses. When higher doses of ADP were infused with bolus injections of 5-HT there was no potentiation and ketanserin did not reduce these responses. Ketanserin did not inhibit the collagen-induced fall in circulating platelet count, but did significantly increase the rate of return to the basal platelet count compared with control. 5-HT did not cause a fall in platelet count in guinea-pigs


2021 ◽  
Vol 9 (1) ◽  
pp. e002104
Author(s):  
Kenji Takeda ◽  
Hiraku Ono ◽  
Ko Ishikawa ◽  
Tomohiro Ohno ◽  
Jin Kumagai ◽  
...  

IntroductionSodium glucose cotransporter-2 (SGLT2) inhibitors are widely used for diabetes treatment. Although SGLT2 inhibitors have been clinically observed to increase food intake, roles or even the presence of SGLT2 in the central nervous system (CNS) has not been established. We aimed to elucidate potential functions of SGLT2 in the CNS, and the effects of CNS-targeted SGLT2 inhibitors on food intake.Research design and methodsWe administered three kinds of SGLT2 inhibitors, tofogliflozin, dapagliflozin, and empagliflozin, into the lateral ventricle (LV) in rats and evaluated their effects on food intake. We also evaluated the effects of tofogliflozin administration in the third (3V) and fourth ventricle (4V). Intraperitoneal administration of liraglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist known to suppress food intake, was combined with central tofogliflozin to elucidate whether GLP-1 signaling antagonizes the effect of central SGLT2 inhibitors on food intake. To elucidate potential molecular mechanisms mediating changes in feeding, hypothalamic areas associated with food intake regulation were harvested and analyzed after intracerebroventricular administration (ICV) of tofogliflozin.ResultsBolus ICV injection of tofogliflozin induced a robust increase in food intake starting at 1.5 hours postinjection, and lasting for 5 days. No effect was observed when the same dose of tofogliflozin was administered intraperitoneally. ICV dapagliflozin and empagliflozin significantly enhanced food intake, although the strength of these effects varied among drugs. Food intake was most markedly enhanced when tofogliflozin was infused into the LV. Fewer or no effects were observed with infusion into the 3V or 4V, respectively. Systemic administration of liraglutide suppressed the effect of ICV tofogliflozin on food intake. ICV tofogliflozin increased phosphorylation of AMPK and c-fos expression in the lateral hypothalamus.ConclusionsSGLT2 inhibitors in the CNS increase food intake. SGLT2 activity in the CNS may regulate food intake through AMPK phosphorylation in the lateral hypothalamic area.


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