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At least 253 records · Page 14Linked to original sources
PubMed2003

Diacylglycerols affect substrate oxidation and appetite in humans.

BACKGROUND: Meals rich in diacylglycerols (DGs) instead of triacylglycerols (TGs) show beneficial effects on lipid metabolism and energy balance. These effects are probably attributable to differences in DG and TG metabolism, especially postprandial fat oxidation. OBJECTIVE: We assessed the effects of partial replacement of TGs with DGs on substrate oxidation, energy expenditure (EE), relevant blood variables, and appetite. DESIGN: Twelve healthy, dietarily unrestrained women participated in a single-blind, placebo-controlled, randomized trial with crossover design. For 3 d before and throughout a 36-h stay in a respiration chamber, subjects were fed energy-maintenance amounts of a diet consisting of 55% of energy from carbohydrate, 15% from protein, and 30% from fat. In the respiration chamber, 40% of the fat was consumed as DG-rich (80% DGs) oil or as TG-based control oil with a similar fatty acid profile. RESULTS: Fat oxidation was significantly higher with DG treatment than with TG treatment. Appetite profiles during day 1 (24 h) did not differ significantly between the DG and TG treatments; however, feelings of hunger, appetite, estimated prospective food intake, and desire to eat were all significantly lower on day 2 (12 h) with DG treatment. Mean plasma beta-hydroxybutyrate tended to be higher with DG treatment, and the difference between the 2 treatments was significant at 1130 on day 2. Plasma lipid concentrations and resting and 24-h EE did not differ significantly between the 2 treatments. CONCLUSION: Consumption of DGs in place of TGs does not alter EE but produces metabolic effects, particularly increases in fat oxidation, which may be associated with improved appetite control and energy balance.

3-Hydroxybutyric Acid↗
PubMed1997

Altered concentrations of appetite regulators may contribute to the development and maintenance of HIV-associated wasting.

OBJECTIVE: To examine the relation of circulating appetite neuropeptides, CCK-8 sulphate (CCK-8s) and beta-endorphin, and the tumour necrosis factor-alpha (TNF-alpha) and soluble TNF receptors (sTNFR) to the anorexia and wasting associated with HIV-infection. DESIGN: Cross-sectional analysis. SETTING: A university-based HIV/AIDS ambulatory clinic in Madrid, Spain. PARTICIPANTS: Thirty-six randomly selected AIDS patients without concomitant diseases or secondary infections were classified into two groups: 19 patients with wasting and 17 with normal body weight, and 18 healthy controls. MEASUREMENTS: Nutritional status was evaluated by anthropometry, laboratory parameters and self-report of appetite. Plasma levels of TNF-alpha and sTNFR proteins p55 (sTNFR-p55) and p75 (sTNFR-p75) were determined by enzyme immunoassay, whereas CCK-8s and beta-endorphin levels were measured by radioimmunoassay. RESULTS: AIDS patients with wasting had significantly higher plasma concentrations of CCK-8s, but lower levels of beta-endorphin when compared to well-nourished AIDS patients (P < 0.01) or controls (P < 0.001). Mean levels of TNF-alpha, and sTNFR-p55 and sTNFR-p75 were greater in AIDS patients with wasting than in asymptomatic AIDS patients or in controls. No significant association was observed between any of these circulating peptides and the parameters of malnutrition. CONCLUSIONS: An activation of the TNF system, together with reciprocal changes in plasma concentrations of two neuropeptides with opposing appetite regulation, that is increased concentrations of CCK-8s but lower levels of beta-endorphin, are associated with the presence of HIV wasting. We hypothesize that these changes may contribute to the development of HIV wasting by producing a pathological inhibition of appetite.

Acquired Immunodeficiency Syndrome↗
PubMed1993

The loss of appetite during depression with melancholia: a qualitative and quantitative analysis.

The loss of appetite occurring severe depression was investigated with an experimental method comparing the eating behaviour of 12 melancholic inpatients to 12 matched normal controls. Food intake and appetite, divided into more basic components such as desire to eat, hunger, satiety, prospective food consumption and pleasure from eating, were monitored during a test meal. Patients ate less than controls, but the difference was not significant. The pattern resulting from the temporal tracking of the appetite ratings indicated that patients were disturbed at the beginning of the meal and showed a decreased desire to eat, hunger and prospective food consumption and an increased satiety and that their pleasure from eating was diminished. These findings suggest that the loss of appetite induced by melancholia follows a specific pattern.

Adult↗
PubMed2006

Gastrointestinal hormones regulating appetite.

The role of gastrointestinal hormones in the regulation of appetite is reviewed. The gastrointestinal tract is the largest endocrine organ in the body. Gut hormones function to optimize the process of digestion and absorption of nutrients by the gut. In this capacity, their local effects on gastrointestinal motility and secretion have been well characterized. By altering the rate at which nutrients are delivered to compartments of the alimentary canal, the control of food intake arguably constitutes another point at which intervention may promote efficient digestion and nutrient uptake. In recent decades, gut hormones have come to occupy a central place in the complex neuroendocrine interactions that underlie the regulation of energy balance. Many gut peptides have been shown to influence energy intake. The most well studied in this regard are cholecystokinin (CCK), pancreatic polypeptide, peptide YY, glucagon-like peptide-1 (GLP-1), oxyntomodulin and ghrelin. With the exception of ghrelin, these hormones act to increase satiety and decrease food intake. The mechanisms by which gut hormones modify feeding are the subject of ongoing investigation. Local effects such as the inhibition of gastric emptying might contribute to the decrease in energy intake. Activation of mechanoreceptors as a result of gastric distension may inhibit further food intake via neural reflex arcs. Circulating gut hormones have also been shown to act directly on neurons in hypothalamic and brainstem centres of appetite control. The median eminence and area postrema are characterized by a deficiency of the blood-brain barrier. Some investigators argue that this renders neighbouring structures, such as the arcuate nucleus of the hypothalamus and the nucleus of the tractus solitarius in the brainstem, susceptible to influence by circulating factors. Extensive reciprocal connections exist between these areas and the hypothalamic paraventricular nucleus and other energy-regulating centres of the central nervous system. In this way, hormonal signals from the gut may be translated into the subjective sensation of satiety. Moreover, the importance of the brain-gut axis in the control of food intake is reflected in the dual role exhibited by many gut peptides as both hormones and neurotransmitters. Peptides such as CCK and GLP-1 are expressed in neurons projecting both into and out of areas of the central nervous system critical to energy balance. The global increase in the incidence of obesity and the associated burden of morbidity has imparted greater urgency to understanding the processes of appetite control. Appetite regulation offers an integrated model of a brain-gut axis comprising both endocrine and neurological systems. As physiological mediators of satiety, gut hormones offer an attractive therapeutic target in the treatment of obesity.

Appetite Regulation↗
PubMed2004

Central localization of plasticity involved in appetitive conditioning in Lymnaea.

Learning to associate a conditioned (CS) and unconditioned stimulus (US) results in changes in the processing of CS information. Here, we address directly the question whether chemical appetitive conditioning of Lymnaea feeding behavior involves changes in the peripheral and/or central processing of the CS by using extracellular recording techniques to monitor neuronal activity at two stages of the sensory processing pathway. Our data show that appetitive conditioning does not affect significantly the overall CS response of afferent nerves connecting chemosensory structures in the lips and tentacles to the central nervous system (CNS). In contrast, neuronal output from the cerebral ganglia, which represent the first central processing stage for chemosensory information, is enhanced significantly in response to the CS after appetitive conditioning. This demonstrates that chemical appetitive conditioning in Lymnaea affects the central, but not the peripheral processing of chemosensory information. It also identifies the cerebral ganglia of Lymnaea as an important site for neuronal plasticity and forms the basis for detailed cellular studies of neuronal plasticity.

Animals↗
PubMedDate not supplied

Reinforcement in an in vitro analog of appetitive classical conditioning of feeding behavior in Aplysia: blockade by a dopamine antagonist.

In a recently developed in vitro analog of appetitive classical conditioning of feeding in Aplysia, the unconditioned stimulus (US) was electrical stimulation of the esophageal nerve (En). This nerve is rich in dopamine (DA)-containing processes, which suggests that DA mediates reinforcement during appetitive conditioning. To test this possibility, methylergonovine was used to antagonize DA receptors. Methylergonovine (1 nM) blocked the pairing-specific increase in fictive feeding that is usually induced by in vitro classical conditioning. The present results and previous observation that methylergonovine also blocks the effects of contingent reinforcement in an in vitro analog of appetitive operant conditioning suggest that DA mediates reinforcement for appetitive associative conditioning of feeding in Aplysia.

Animals↗
PubMed2002

Effects of exogenous corticotropin-releasing factor on antropyloroduodenal motility and appetite in humans.

OBJECTIVES: Corticotropin-releasing factor (CRF) has been shown to affect GI motor function and appetite in animals. We have evaluated the effects of exogenous CRF on antropyloroduodenal motility and appetite in humans. METHODS: On 2 separate days, six healthy volunteers received, in randomized, double-blind fashion, i.v. CRF as a 1.0-microg/kg bolus (0-5 min) followed by a constant infusion (1.0 microg/kg/h) (5-150 min), or an identical volume of saline. At t = 28 min each subject drank 200 ml of a nutrient liquid containing 20 mg/kg of paracetamol. Antropyloroduodenal pressures were measured with sleeve/sidehole manometry and perceptions of appetite by visual analog scales. Venous blood was obtained for measurements of serum cortisol and paracetamol. At t = 150 min the manometric catheter was removed and subjects offered a buffet meal (150-180 min). The amount and macronutrient content of food consumed were quantified. RESULTS: CRF increased serum cortisol (p < 0.001), the number of isolated pyloric pressure waves (p < 0.05), duodenal pressure waves (p < 0.05), and the percentage of antegrade duodenal pressure waves (p < 0.05). CRF had no significant effect on the number of antral pressure waves, basal pyloric pressure, serum paracetamol concentrations, perceptions of appetite, or food intake. CONCLUSIONS: Intravenous CRF stimulates phasic pyloric and duodenal pressure waves in humans.

Acetaminophen↗
PubMed2001

Effect of losartan on sodium appetite of hypothyroid rats subjected to water and sodium depletion and water, sodium and food deprivation.

The involvement of angiotensin AT1 receptors in sodium appetite was studied in hypothyroid rats treated with the angiotensin II antagonist losartan. Losartan was administered chronically by the oral route or acutely by the subcutaneous route after water and sodium depletion or water, sodium and food deprivation. Three days after addition of losartan to the food at the dose of 1.0 mg x g(-1), the rats significantly reduced (P < 0.02) their spontaneous intake of 1.8% NaCl. Increasing the dose of losartan to 2.0 and 4.0 mg x g(-1) did not reduce NaCl intake; in contrast, the intensity of the sodium appetite gradually returned to previous levels. The simultaneous administration of captopril, an angiotensin converting enzyme inhibitor, and losartan significantly increased (P < 0.05) NaCl intake and after captopril removal NaCl intake returned to the levels observed with losartan treatment alone. The administration of losartan 4 days after the beginning of captopril treatment significantly reduced (P < 0.0001) NaCl intake. Following acute administration of losartan, water- and sodium-depleted rats significantly reduced their NaCl and water intake (P < 0.001). The administration of losartan also induced a significant reduction in NaCl and water intake in water, NaCl and food-deprived rats (P < 0.0001 and P < 0.001, respectively). The present results show that chronic treatment with oral losartan inhibited spontaneous sodium appetite in hypothyroid rats. Continuation of treatment rendered rats resistant to the blockade of AT1 receptors. Water and sodium depletion and water, NaCl and food deprivation induced sodium appetite, which in the short term depends on cerebral angiotensinergic activity mediated by the activation of AT1 receptors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1980

Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

1. Prolonged exposure of the brain of the normal Na-replete rat to angiotensin II produced a marked and persistent Na appetite. In a first series of experiments, short-term, repeated systemic injections of isoprenaline or renin (both of which raise circulating angiotensin levels), and repeated intracranial injections of angiotensin II evoked increased ingestion of 2 . 7% NaCl. In the second series of experiments, continuous infusions of angiotensin II directly into the brain evoked extremely large intakes of 3% NaCl. 2. In addition to large intakes of hypertonic NaCl some rats drank daily volumes of water that exceeded their body weight. 3. Not only did the animals drink large volumes of 3% NaCl some rats drank daily volumes of water that exceeded their body weight. 3. Not only did the animals drink large volumes of 3% NaCl during continuous angiotensin II infusion, but after termination of the infusion they continued to ingest NaCl at a rate comparable to that of the adrenalectomized rat. In most of the animals the persistent NaCl intake diminished over several days, but other animals continued to drink NaCl for as long as their intake was measured (up to 7 months). 4. The response to continuous infusion of angiotensin II was dose-dependent. Both water and 3% NaCl intake increased over a dose range of 6 ng h-1 to 6000 ng h-1. The persistence of the sodium appetitite was also dose-dependent across the same range of doses. 5. Angiotensin-induced salt appetite is specific for Na. Animals did not drink 0 . 5 M-NH4Cl and only occasionally drank minimal amounts of 0 . 5 M-KCl during continuous infusion. 6. The large water turnover was not responsible for the Na appetite. Rats given access to 3% NaCl only during infusion of angiotensin copiously. Animals that were not infused but were given saccharine-flavoured water in order to increase their water intakes did not drink 3% NaCl offered at the same time even though fluid intake was high. Rats that did not receive intracranial infusions but were infused intragastrically with volumes of water equal to or exceeding the amounts that were drunk during angiotensin infusion did not drink the 3% NaCl but did drink some water. 7. Records of the drinking by rats infused with angiotensin show that firstly the onset of drinking after the start of angiotensin infusion varied from animal to animal, secondly, NaCl drinking was not temporally linked to water intake, although this was observed occasionally, and thirdly, most of the drinking occurred during the night although angiotensin was infused continuously throughtout the nychthemeron. 8. Therefore, increases in angiotensin levels, probably with other factors such as increased levels of aldosterone or ACTH, result in Na appetite. The hormonal changes may alter the animals' preception of salt making it more acceptable. By means that are not yet understood the increased accceptability of salt persists after the termination of angiotensin infusion.

Angiotensin II↗
PubMed1983

Renin-induced sodium appetite: effects on sodium balance and mediation by angiotensin in the rat.

1. Injection of pig renin or purified renin from the mouse submaxillary gland into the preoptic region or third ventricle of the rat caused thirst within a minute or so of injection followed shortly afterwards by increased sodium appetite. Renin from two widely different sources produced identical responses.2. The stimulating effect of renin on intake of water and hypertonic (2.7%) NaCl was continuous and persisted for at least a week after the largest (265 ng) dose of purified renin.3. The stimulating effect was also very large. A single preoptic injection of less than 0.75 pmol (26.5 ng) purified mouse renin caused mean intakes of 250.4 +/- 26.2 ml water and 44.8 +/- 12.5 ml 2.7% NaCl by five naive rats in 24 h. After the largest dose (265 ng) intakes of water and 2.7% NaCl reached about 80% and 20% body weight respectively.4. Weekly injections of renin resulted in progressively larger intakes of NaCl and water in response to the injections.5. Even after repeated injections, carbachol did not stimulate sodium appetite. The stimulating effect on water intake was quickly over and showed no progressive increase with repeated injections. Overnight intake of water was generally depressed after carbachol.6. Preoptic injection of renin caused some increase in sodium excretion but this was small compared with the stimulating effect on sodium appetite.7. Detailed temporal analysis of fluid and sodium balance shows that the increased intakes of water and 2.7% NaCl were not secondary to renin-induced urinary losses. Increased intakes of water and 2.7% NaCl caused by renin resulted in the rats going into and remaining in positive fluid and sodium balance throughout the 24 h experiment.8. Renin-induced sodium appetite and thirst were inhibited by the converting enzyme inhibitors teprotide or captopril, or by the angiotensin antagonist saralasin. Inhibition was longer lasting after captopril. Carbachol-induced thirst was unaffected.9. In conclusion, renin injected into the preoptic region or third ventricle is a potent stimulus to sodium appetite as well as thirst. The effect is mediated by local generation of angiotensin II and it is not secondary to increased urinary loss.

Angiotensin II↗
PubMed1980

ACTH-elicited sodium appetite in sheep.

Intramuscular injections of long-acting synthetic ACTH (45 U twice daily for 5 days) caused a large increase in the intake of 0.5 M NaCl in sheep. Mean Na intake of the sheep on the last 3 days of treatment approximated 50% of their total extracellular fluid Na. The mineral appetite was specific for NaCl. Intakes of 0.5 M KCl or 0.25 M CaCl2 were not significantly altered. The enhanced appetite for Na induced by ACTH appeared to precede any increase in urinary Na excretion. ACTH treatment was ineffective in adrenalectomized sheep. However, an infusion into adrenalectomized sheep of a combination of adrenal steroid hormones (including aldosterone, deoxycorticosterone, 11-deoxycortisol, cortisol, and corticosterone) that contrived blood levels similar to those, obtained with ACTH treatment in normal sheep did induce Na appetite. Thus, ACTH induces a specific, adrenal-steroid hormone-dependent Na appetite in sheep.

Adrenocorticotropic Hormone↗
PubMed2003

Effects of fat digestion on appetite, APD motility, and gut hormones in response to duodenal fat infusion in humans.

The presence of nutrients in the small intestine slows gastric emptying and suppresses appetite and food intake; these effects are partly mediated by the release of gut hormones, including CCK. We investigated the hypothesis that the modulation of antropyloroduodenal motility, suppression of appetite, and stimulation of CCK and glucagon-like peptide-1 secretion by intraduodenal fat are dependent on triglyceride hydrolysis by lipase. Sixteen healthy, young, lean men were studied twice in double-blind, randomized, crossover fashion. Ratings for appetite-related sensations, antropyloroduodenal motility, and plasma CCK and glucagon-like peptide-1 concentrations were measured during a 120-min duodenal infusion of a triglyceride emulsion (2.8 kcal/min) on one day with, on the other day without, 120 mg tetrahydrolipstatin, a potent lipase inhibitor. Immediately after the duodenal fat infusion, food intake at a buffet lunch was quantified. Lipase inhibition with tetrahydrolipstatin was associated with reductions in tonic and phasic pyloric pressures, increased numbers of isolated antral and duodenal pressure waves, and stimulation of antropyloroduodenal pressure-wave sequences (all P < 0.05). Scores for prospective consumption and food intake at lunch were greater, and nausea scores were slightly less, and the rises in plasma CCK and glucagon-like peptide-1 were abolished (all P < 0.05). In conclusion, lipase inhibition attenuates the effects of duodenal fat on antropyloroduodenal motility, appetite, and CCK and glucagon-like peptide-1 secretion.

Adult↗
PubMed2004

Effects of intraduodenal fatty acids on appetite, antropyloroduodenal motility, and plasma CCK and GLP-1 in humans vary with their chain length.

The gastrointestinal effects of intraluminal fats may be critically dependent on the chain length of fatty acids released during lipolysis. We postulated that intraduodenal administration of lauric acid (12 carbon atoms; C12) would suppress appetite, modulate antropyloroduodenal pressure waves (PWs), and stimulate the release of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) more than an identical dose of decanoic acid (10 carbon atoms; C10). Eight healthy males (19-47 yr old) were studied on three occasions in a double-blind, randomized fashion. Appetite perceptions, antropyloroduodenal PWs, and plasma CCK and GLP-1 concentrations were measured during a 90-min intraduodenal infusion of 1) C12, 2) C10, or 3) control (rate: 2 ml/min, 0.375 kcal/min for C12/C10). Energy intake at a buffet meal, immediately after completion of the infusion, was also quantified. C12, but not C10, suppressed appetite perceptions (P < 0.001) and energy intake (control: 4,604 +/- 464 kJ, C10: 4,109 +/- 588 kJ, and C12: 1,747 +/- 632 kJ; P < 0.001, C12 vs. control/C10). C12, but not C10, also induced nausea (P < 0.001). C12 stimulated basal pyloric pressures and isolated pyloric PWs and suppressed antral and duodenal PWs compared with control (P < 0.05 for all). C10 transiently stimulated isolated pyloric PWs (P = 0.001) and had no effect on antral PWs but markedly stimulated duodenal PWs (P = 0.004). C12 and C10 increased plasma CCK (P < 0.001), but the effect of C12 was substantially greater (P = 0.001); C12 stimulated GLP-1 (P < 0.05), whereas C10 did not. In conclusion, there are major differences in the effects of intraduodenal C12 and C10, administered at 0.375 kcal/min, on appetite, energy intake, antropyloroduodenal PWs, and gut hormone release in humans.

Adult↗
PubMed1986

Salt appetite is suppressed by interference with angiotensin II and aldosterone.

Blockade of central but not peripheral mineralocorticoid receptors, with the antimineralocorticoid RU-28318, reduces but does not suppress salt appetite aroused by sodium depletion in the rat. When central mineralocorticoid blockade is combined with captopril treatment to prevent formation of endogenous angiotensin II the appetite is completely suppressed. Suppression of the appetite occurred without changes in the animals' spontaneous ingestive behaviors, sodium excretion, or insulin-induced food intake. These results demonstrate that a synergy of angiotensin II and aldosterone is responsible for the expression of depletion-induced salt appetite in the rat.

Aldosterone↗
PubMed1987

Attenuated sodium appetite in response to sodium deficiency in Fischer-344 rats.

Fischer-344 (F-344) rats avoid NaCl solutions which are preferred by other strains. The present studies examined Na appetite induced by two methods: maintenance on a Na-deficient diet, and Na depletion by injection of furosemide. In comparison with outbred Wistar rats, F-344 rats showed no evidence of Na appetite induced by Na-deficient diet after the first 15 min (study 1) and demonstrated attenuated Na appetite in response to the natriuretic effects of furosemide (study 2). Since Na loss by Wistar and F-344 rats was similar, it is likely that this reduced Na appetite was due to hedonic differences between the strains rather than to differential renal response to furosemide or Na-deficient diet.

Animals↗
PubMed1996

Rapid elicitation of salt appetite by an intravenous infusion of angiotensin II in rats.

A role for the renal renin-angiotensin system in the direct stimulation of salt appetite in the rat remains controversial because attempts to elicit the behavior by intravenous administration of angiotensin II (ANG II) have been unconvincing. We recently demonstrated that depletion-induced salt appetite was attenuated by selective blockade of peripheral ANG II synthesis with an intravenous dose of converting enzyme inhibitor [captopril (Cap)] that does not block the synthesis of ANG II inside the blood brain barrier. We now show that intravenous ANG II at 30 ng/min rapidly reestablishes salt appetite in Cap-blocked rats. The mean arterial blood pressure (MAP) of unblocked, sodium-depleted rats was normal, but Cap-blocked, depleted rats had low MAP. An intravenous infusion of ANG II in Cap-blocked rats brought MAP into the normal range and elicited water and salt drinking within 90 min. Phenylephrine also normalized MAP but failed to elicit fluid intake in Cap-blocked, sodium-deficient rats. Sodium and water balances tended to be more positive during ANG II than during phenylephrine infusions. Thus circulating ANG II may stimulate both thirst and salt appetite by a direct action on the brain and not by causing natriuresis or by raising the blood pressure.

Angiotensin II↗
PubMed1997

Role of brain angiotensin II in thirst and sodium appetite of sheep.

The contribution of brain angiotensin II (ANG II) to thirst and Na+ appetite of sheep was evaluated. Thirst was stimulated by water deprivation, intracarotid or intracerebroventricular infusion of ANG II, or intracarotid or intracerebroventricular infusion of hypertonic solution. Intracerebroventricular infusion, over 1-3 h, of the ANG II type 1 (AT1) receptor antagonist, losartan, decreased or abolished water intake caused by all of the stimuli tested. Intracerebroventricular infusion of ZD-7155, another AT1-receptor antagonist, blocked ANG II-induced water intake. Neither losartan nor ZD-7155 infused intracerebroventricularly altered the Na+ appetite of Na(+)-depleted sheep. Intracerebroventricular infusion of losartan over 3 h, however, did block the increase in water intake and the decrease in Na+ intake caused by intracerebroventricular infusion of hypertonic NaCl in Na(+)-depleted sheep. Intracerebroventricular infusion of the ANG II type 2 (AT2) receptor antagonist, PD-123319, over 1-3 h, did not alter ANG II-induced water intake or Na+ depletion-induced Na+ intake. These results are consistent with the proposition that brain ANG II, working via AT1 receptors, is involved in the neural system controlling some aspects of physiological thirst and Na+ appetite. A role for AT2 receptors in physiological thirst or Na+ appetite is not supported by the present results.

Analysis of Variance↗
PubMed1997

Polyethylene glycol-induced calcium appetite.

Polyethylene glycol (PEG) has been used to investigate the physiological basis of sodium intake because it sequesters sodium from the extracellular fluid (ECF) and causes rats to drink concentrated NaCl solutions. To test the hypothesis that PEG also depletes ECF calcium and thus activates calcium intake, male Sprague-Dawley rats received two-bottle tests with a choice between a taste solution and water. Relative to intakes after control injections, rats injected with PEG (5 ml of 30% wt/wt sc) drank significantly greater volumes of several calcium solutions (0.1, 1, 10, or 32 mM CaCl2 or 10 or 100 mM calcium lactate). They also drank more 10 mM SrCl2, 300 mM NaCl, and 100 mM KHCO3, drank less 10 mM sodium saccharin, and did not alter intakes of 10 or 100 mM KCl, 32 mM NH4Cl, 10 mM AlCl3, 10 mM FeCl2, 100 mM CaCl2, or 1,000 mM NaCl. Thus PEG treatment produced an appetite that was specific to low and moderate concentrations of calcium, sodium, and perhaps bicarbonate. The physiological basis for this appetite was explored. At 24 h after PEG injection, plasma total calcium concentrations were either unaltered or increased, but plasma ionized calcium concentrations were reduced. Concentrations of parathyroid hormone and calcitonin but not 1 alpha, 25-dihydroxyvitamin D3 were elevated. Perhaps one or more of these changes in calcium homeostasis is responsible for the increased calcium intake. Whatever the mechanism, it is clear that PEG treatment induces an appetite for calcium in addition to the well-known appetite for sodium.

Animals↗