Inhibition of NaCl appetite when DOCA-treated rats drink saline

Marked increases in the consumption of concentrated NaCl solution were elicited in rats by daily injection of the synthetic mineralocorticoid, deoxycorticosterone acetate (DOCA). DOCA-treated rats drank different volumes of NaCl solution depending on its concentration (between 0.15 M and 0.50 M), with less consumed (in milliliters) the more concentrated the fluid was. In consequence, total Na(+) intake (in milliequivalents) was roughly similar in all groups. Gastric emptying of Na(+) also diminished as the concentration of the ingested NaCl solution increased, and the delivery of Na(+) to the small intestine was remarkably similar in all groups. Cumulative volume of ingested fluid in the stomach and small intestine was very closely related to intake (in milliliters) of the concentrated NaCl solutions. Systemic plasma Na(+) levels did not increase until after rats stopped consuming concentrated NaCl solution, although they were elevated at the onset of water ingestion. The situation appeared to be different when 0.15 M NaCl was consumed. This isotonic solution emptied and was absorbed relatively rapidly, and DOCA-treated rats drank larger amounts of it throughout a 1-h test period than when they drank concentrated NaCl solutions. Collectively, these findings suggest that saline consumption by DOCA-treated rats may be inhibited by two presystemic factors, one related to the volume of ingested fluid (i.e., distension of the stomach and small intestine) and one related to its concentration (i.e., elevated osmolality of fluid in the small intestine and/or in adjacent visceral tissue).     

Ontogeny of hypertonic preabsorptive inhibitory control of intake in neonatal rats

The ontogenetic development of postingestive inhibitory control of ingestion by the osmotic load of a preload was examined in rats. On postnatal days 6 (P6) and 12 (P12), pups were deprived for either 6 or 24 h. Gastric preloads (5% body wt) of water, mannitol (a sugar alcohol that is not absorbed) in six concentrations [from 0.125 M (hypotonic) to 1.0 M (hypertonic)], or sham preloads were administered 5 min before a 30-min intake test. Compared with sham treatment, isotonic mannitol (0.25 M), a probe of volumetric control, significantly reduced intake on P12, but not on P6. Compared with isotonic mannitol, the three highest hypertonic concentrations (0.5, 0.66, and 1.0 M) significantly decreased intake on P12, at both levels of deprivation. On P6, 0.66 and 1.0 M mannitol reduced intake after 24 h, but not after 6 h, of deprivation. Thus, on P6, the hypertonic control was detectable only after prolonged deprivation and the volumetric control was not present. On P12, both controls were observed and the hypertonic control was more potent than on P6.     

Gestational and early postnatal dietary NaCl levels affect NaCl intake, but not stimulated water intake, by adult rats

We examined body fluid regulation by weanling (21-25 days) and adult (>60 days) male rats that were offspring of dams fed chow containing either 0.1, 1, or 3% NaCl throughout gestation and lactation. Weanling rats were maintained on the test diets until postnatal day 30 and on standard 1% NaCl chow thereafter. Ad libitum water intake by weanlings was highest in those fed 3% NaCl and lowest in those fed 0.1% NaCl. Adult rats maintained on standard NaCl chow consumed similar amounts of water after overnight water deprivation or intravenous hypertonic NaCl (HS) infusion regardless of early NaCl condition. Moreover, baseline and HS-stimulated plasma Na(+) concentrations also were similar for the three groups. Nonetheless, adult rats in the early 3% NaCl group consumed more of 0.5 M NaCl after 10 days of dietary Na(+) deprivation than did rats in either the 1% or 0.1% NaCl group. Interestingly, whether NaCl was consumed in a concentrated solution in short-term, two-bottle tests after dietary Na(+) deprivation or in chow during ad libitum feeding, adult rats in the 3% NaCl group drank less water for each unit of NaCl consumed, whereas rats in the 0.1% NaCl group drank more water for each unit of NaCl consumed. Thus gestational and early postnatal dietary NaCl levels do not affect stimulated water intake or long-term body fluid regulation. Together with our previous studies, these results suggest that persistent changes in NaCl intake and in water intake associated with NaCl ingestion reflect short-term behavioral effects that may be attributable to differences in NaCl taste processing.     

Taste, salience, and increased NaCl ingestion after repeated sodium depletions

Previous studies have shown that repeated sodium depletions using the natriuretic-diuretic furosemide induce progressive increases in NaCl ingestion. We investigated the role of taste in this behavioral sensitization in Sprague-Dawley rats using short-term lickometer testing along with 2-h stimulated intake tests. Our results show maximal licking across a range of NaCl concentrations after each of the three depletions, regardless of whether the solutions contained sucrose or were presented alone. Similarly, the presence of sucrose did not affect stimulated NaCl intake in long-term tests, although ingestion of NaCl solutions increased progressively with successive depletions. Finally, both licking and ingestion returned to baseline levels during need-free conditions. These results suggest that sodium imbalance acutely increases the salience of sodium taste and thereby the likelihood of NaCl ingestion, which may, in turn, contribute to progressive increases in NaCl intake that occur with multiple furosemide-induced sodium depletions.     

Effects of lead shot ingestion on selected cells of the mallard immune system

The immunologic effects of lead were measured in game-farm mallards (Anas platyrhynchos) that ingested lead shot while foraging naturally, mallards intubated with lead shot, and unexposed controls. Circulating white blood cells (WBC) declined significantly in male mallards exposed to lead by either natural ingestion or intubation, but not females. Spleen plaque-forming cell (SPFC) counts were significantly lower in mallards intubated with lead pellets compared to controls. Declines in WBC and SPFC means with increasing tissue lead concentrations provide further evidence that lead exposure reduced immunologic cell numbers. Hormonal activity and diet may have influenced the immunologic effects of lead exposure in this study.     

Early osmoregulatory stimulation of neurohypophyseal hormone secretion and thirst after gastric NaCl loads

Cerebral osmoreceptors mediate thirst and neurohypophyseal secretion stimulated by increases in the effective osmolality of plasma (P(osmol)). The present experiments determined whether an intragastric load of hypertonic saline (ig HS; 0.5 M NaCl, 4 ml) would potentiate these responses before induced increases in P(osmol) in the general circulation could be detected by cerebral osmoreceptors. Adult rats deprived of water overnight and then given intragastric HS consumed much more water in 15-30 min than rats given either pretreatment alone, even though systemic P(osmol) had not yet increased significantly because of the gastric load. In other rats pretreated with an intravenous infusion of 1 M NaCl (2 ml/h for 2 h), plasma levels of vasopressin and oxytocin were considerably elevated 15 and 25 min after intragastric HS treatment, whereas systemic P(osmol) was not increased further. These and other findings are consistent with previous reports that hepatic portal osmoreceptors (or Na(+) receptors) stimulate thirst and neurohypophyseal hormone secretion in euhydrated rats given gastric NaCl loads and indicate that these effects are potentiated when animals are dehydrated.     

Osmoregulation in water-deprived rats drinking hypertonic saline: effect of area postrema lesions

Rats drank rapidly when 0.3 M NaCl was the only drinking fluid available after overnight water deprivation, consuming approximately 200 ml/24 h. Although such large intakes of this hypertonic solution initially elevated plasma osmolality, excretion of comparable volumes of urine more concentrated than 300 meq Na(+)/l ultimately appears to restore plasma osmolality to normal levels. Rats drank approximately 100 ml of 0.5 M NaCl after overnight water deprivation, but urine Na(+) concentration (U(Na)) did not increase sufficiently to achieve osmoregulation. When an injected salt load exacerbated the initial dehydration caused by water deprivation, rats increased U(Na) to void the injected load and did not significantly alter 24-h intake of 0.3 or 0.5 M NaCl. Rats with lesions of area postrema had much higher saline intakes and lower U(Na) than did intact control rats; nonetheless, they appeared to osmoregulate well while drinking 0.3 M NaCl but not while drinking 0.5 M NaCl. Detailed analyses of drinking behavior by intact rats suggest that individual bouts were terminated by some rapid postabsorptive consequence of the ingested NaCl load that inhibited further NaCl intake, not by a fixed intake volume or number of licks that temporarily satiated thirst.     

The response of plasma gastric-inhibitory polypeptide (GIP) to slow and fast glucose ingestion in Billroth II resected patients and normal controls

Eight Billroth II resected patients and 8 normal controls were given two oral glucose loads, one ingested within 2 min, and the other ingested slowly over 80 min. In the Billroth II resected group, the integrated plasma GIP release was significantly higher after the fast than after the slow glucose ingestion. In this group the integrated plasma GIP release was also significantly higher than in the control group, but only after the fast glucose ingestion. These findings indicate that the rate of glucose delivery into the intestine may be of importance in the plasma GIP response to oral glucose.     

NaCl concentration alters temporal patterns of drinking and eating by rats

To obtain an understanding of the role of taste in NaCl preference-aversionunder standard laboratory feeding conditions, we characterizedthe eating and drinking patterns of rats maintained on powderedfood, water, and NaCl solution. The concentration of NaCl wasvaried systematically from 0.01 to 0.4 M with a single concentrationpresent for four consecutive days. In addition to daily intake,the number and duration of ingestion bouts, and the number ofswitches between food and fluid and between water and salinewere recorded throughout the day/night cycle. The availabilityof NaCl solution did not alter the typical pattern of night-timefeeding and prandial (drinking after a meal) drinking. As shownpreviously, NaCl intake was highest for 0.15 M NaCl and declinedat both stronger and weaker concentrations. Variations in drinkingbout number and duration determined amount consumed. Drinkingbout duration was highest for 0.2 M NaCl then declining progressivelyat both stronger and weaker concentrations. The number of drinkingbouts was highest for 0.04 M NaCl, a concentration slightlyabove the adapting salivary sodium concentration, declininglinearly thereafter with stronger NaCl concentrations. The availabilityof NaCl solution influenced the amount of food consumed, aswell as the number and duration of food bouts. Food bout numberwas highest in the presence of the weakest 0.01 M NaCl solution,while food bout duration was highest in the presence of hypertonicNaCl concentrations. Most switching behavior occurred betweenmeal consumption and drinking and little between drinking fluids.When 0.01–0.08 NaCl solutions were available, the ratsdrank saline after a meal; when hypertonic 0.3–0.4 M NaClsolutions were available, they drank water after a meal. Inthe presence of intermediate NaCl concentrations (0.15–0.20),the choice of fluid consumed after a meal was more equivocalto the extent that there was increased switching between waterand saline and vice versa. The significance of these differencesin the micromolar features of eating and drinking are discussedin relationship to taste and postingestional control mechanismsof ingestion.     

Effect of a protein preload on food intake and satiety feelings in response to duodenal fat perfusions in healthy male subjects

The control of food intake and satiety requires a coordinated interplay. Oral protein and duodenal fat inhibit food intake and induce satiety, but their interactive potential is unclear. Our aim was therefore to investigate the interactions between an oral protein preload and intraduodenal (ID) fat on food intake and satiety feelings. Twenty healthy male volunteers were studied in a randomized, double-blind, four-period crossover design. On each study day, subjects underwent one of the following treatments: 1) water preload plus ID saline perfusion, 2) water preload plus ID fat perfusion, 3) protein preload plus ID saline perfusion, or 4) protein preload plus ID fat perfusion. Subjects were free to eat and drink as much as they wished. An oral protein preload significantly reduced caloric intake (19%, P < 0.01). Simultaneous administration of an oral protein preload and ID fat did not result in a positive synergistic effect with respect to caloric consumption, rejecting the initial hypothesis that the two nutrients exert a positive synergistic effect on food intake. An oral protein preload but not ID fat altered the feelings of hunger and fullness. These data indicate that the satiety effect of an oral protein preload is not amplified by ID fat; indeed, the effect of a protein preload does not seem to be mediated by cholecystokinin, glucagon-like peptide-1, or peptide YY. Much more information is necessary to understand the basic physiological mechanisms that control food intake and satiety.     

Neuroendocrine factors in salt appetite.

We dedicate this paper to Curt P. Richter, father of the study of salt appetite, who died recently at the age of 94. Richter first demonstrated that the adrenalectomized rat's voracious appetite for salt kept it alive (1936) and showed the same in humans (1940). Our first paper in 1955 demonstrated that salt appetite was an innate response to salt depletion. Since then, we have pursued the notion that the neuroendocrine consequences of sodium depletion create a brain state that raises salt appetite. In Epstein's laboratory, it was shown that angiotensin and aldosterone, the hormones of salt retention in the periphery, act synergistically in the brain to produce salt appetite in the rat. Block either hormone and the appetite is reduced by half; block both and the appetite is eliminated despite severe bodily need. With repeated depletions or treatments of the brain with angiotensin and aldosterone, salt ingestion increases, reaching an asymptote by the third depletion. Need-free intake of NaCl also increases, especially in female rats which ingest more NaCl than male rats. In Stellar's laboratory, running speed to salt solutions in a runway is used as a measure of salt appetite. When the appetite is raised with large doses of DOCA, a mimic of aldosterone, rats run rapidly for a taste of strong salt solutions as high as 24% (almost 4 molar). Using ingestion as a measure, the role of the atrial natriuretic peptide (ANP), an antagonist of angiotensin's physiological effect, was investigated as a modulator of salt appetite. When angiotensin is involved is producing salt appetite, following sodium depletion by a diuretic combined with a low-salt diet, ANP reduced salt intake by 40%. When salt appetite was raised by DOCA, however, ANP either had no effect or reduced salt ingestion by only 10%. The subfornical organ, the lateral preoptic area, and the central and medial nuclei of the amygdala are being investigated as major components of the limbic circuit underlying salt appetite produced by the actions of angiotensin, aldosterone and ANP in the brain.     

Intravenous infusion of glucagon-like peptide-1 potently inhibits food intake, sham feeding, and gastric emptying in rats

Glucagon-like peptide-1(7-36)-amide (GLP-1) is postulated to act as a hormonal signal from gut to brain to inhibit food intake and gastric emptying. A mixed-nutrient meal produces a 2 to 3-h increase in plasma GLP-1. We determined the effects of intravenous infusions of GLP-1 on food intake, sham feeding, and gastric emptying in rats to assess whether GLP-1 inhibits food intake, in part, by slowing gastric emptying. A 3-h intravenous infusion of GLP-1 (0.5-170 pmol.kg(-1).min(-1)) at dark onset dose-dependently inhibited food intake in rats that were normally fed with a potency (mean effective dose) and efficacy (maximal % inhibition) of 23 pmol.kg(-1).min(-1) and 82%, respectively. Similar total doses of GLP-1 administered over a 15-min period were less potent and effective. In gastric emptying experiments, GLP-1 (1.7-50 pmol.kg(-1).min(-1)) dose-dependently inhibited gastric emptying of saline and ingested chow with potencies of 18 and 6 pmol.kg(-1).min(-1) and maximal inhibitions of 74 and 83%, respectively. In sham-feeding experiments, GLP-1 (5-50 pmol.kg(-1).min(-1)) dose-dependently reduced 15% aqueous sucrose intake in a similar manner when gastric cannulas were closed (real feeding) and open (sham feeding). These results demonstrate that intravenous infusions of GLP-1 dose-dependently inhibit food intake, sham feeding, and gastric emptying with a similar potency and efficacy. Thus GLP-1 may inhibit food intake in part by reducing gastric emptying, yet can also inhibit food intake independently of its action to reduce gastric emptying. It remains to be determined whether intravenous doses of GLP-1 that reproduce postprandial increases in plasma GLP-1 are sufficient to inhibit food intake and gastric emptying.     

Adrenal modulation of the inhibitory effect of corticotropin releasing factor on feeding

Corticotropin releasing factor (CRF) reduces food intake in rats after central administration. In these studies we examined whether the adrenal gland and the vagus were involved in CRF suppression of intake. One hour intake was reduced by a 5 μg (ICV) injection of CRF in sham but not adrenalectomized rats maintained on 0.9% NaCl. In a separate experiment on rats maintained on tap water, the inhibitory effect of CRF (5 μg) lasted at least 4 hours in sham rats whereas adrenalectomized rats did not significantly differ from controls. These experiments suggest that the adrenal gland modulates the feeding response to CRF. As replacement with corticosterone (0.75 mg/kg) in total adrenalectomized rats did not restore responsiveness to 5 or 10 μg of CRF, we next studied whether the adrenal medulla was responsible for the decreased responsiveness to CRF. In rats lacking the adrenal medulla only, food intake was reduced by a 5 μg injection of CRF; in sham rats, intake was significantly reduced by doses as low as 0.1 μg of CRF. An additional experiment examined the effect of gastric vagotomy on the CRF feeding response. Vagotomized rats were as responsive to 5 and 10 μg injections of CRF as sham rats, which suggests that the effect is not dependent on the vagus nerve. These findings indicate that the adrenal gland, primarily the medulla, plays an intermediate role in the reduction of food intake caused by central injections of CRF. This conclusion is consistent with the known effect of CRF on adrenomedullary discharge.     

Bottle-choice tests in Sprague-Dawley rats using liquid diets that differ in oil and sucrose contents

Bottle choice tests using liquid diets were done with Sprague-Dawley (SD) rats. SD rats ingested more oil-and-sucrose-enriched milk (hi-fat) and less oil-enriched milk (hi-fat-no-carb) than sucrose-enriched (hi-carb) milk by two-bottle choice tests after they were habituated to liquid diets for 4 days. Chronic food restriction didn't increase hi-fat ingestion but hi-fat-no-carb. Rats ingested less without habituation, and overnight food deprivation increased intake. This increment was maintained after rats were free-fed. The difference in fat content of the maintenance diet had little effect on fat preference. These results showed SD rats prefer a sweet and fatty liquid diet than a sweet and lean liquid diet. Habituation and food restriction were more important than the composition of the maintenance diet to demonstrate a clear preference for the fatty liquid diet.     

Downregulation of melanocortin-4 receptor during refeeding and its modulation by adrenalectomy in rats

Melanocortin system and corticotropin releasing hormone (CRH) are implicated in the control of feeding behavior. Besides its anorexigenic effect on food intake, CRH is one of the most important regulators of hypothalamic-pituitary-adrenal (HPA) axis activity. Therefore, there could be an interplay between HPA axis activity and melanocortin system. We investigated the expression of melanocortin-4 receptor (MC4-R) mRNA in the hypothalamus of rats after 14 days of food restriction or after a fasting-refeeding regimen, in sham or adrenalectomized rats. Male Wistar rats were subjected to free access to food or food ingestion restricted for 2 h a day (8-10 AM) during 14 d, when plasma corticosterone, ACTH, insulin, leptin concentrations, and MC4-R mRNA expression were determined before and after refeeding. Another set of rats was fasted for 48 h, followed by refeeding during 2 or 4 h on the seventh day after adrenalectomy (ADX) or sham surgery. On the day of the experiment, rats were anesthetized and perfused and the brain processed for MC4-R mRNA by in situ hybridization. Long-term reduction of food intake, either secondary to food restriction or adrenalectomy, reduced body weight gain and also leptin and insulin plasma concentrations. Food ingestion reduced MC4-R expression in the paraventricular nucleus in naive rats subjected to food restriction and also in sham rats fasted for 48 h. However, after ADX, MC4-R expression was not changed by refeeding. In conclusion, the present data indicate that MC4-R expression is downregulated by food ingestion and this response could be modulated by glucocorticoid withdrawal.     

Behavioral and electrophysiological taste responses change after brief or prolonged dietary sodium deprivation

Dietary Na+ deprivation elicits a hormonal response to promote sodium conservation and a behavioral response to increase sodium ingestion. It has generally been accepted that the former occurs within 24 h after sodium deprivation, while the latter is delayed and may not appear until as much as 10 days later. Na+ deprivation of similar duration also decreases the sensitivity of the chorda tympani nerve (CT) to NaCl, suggesting that changes in CT responses are necessary for increased NaCl intake. However, previous work from our laboratory showed that licking responses to NaCl solutions increase after only 2 days of Na+ deprivation, suggesting rapidly occurring changes in response to NaCl taste. The present experiments examined the effects of 2 days of dietary Na+ deprivation on CT responses to NaCl and patterns of NaCl consumption and found that Na+-deficient rats licked significantly more during the first NaCl intake bout compared with control rats. CT responses to NaCl were reduced at all concentrations after brief Na+ deprivation compared with Na+-replete control rats and did not decrease further with prolonged (10 days) dietary Na+ deficiency. Moreover, amiloride, which suppressed CT responses to NaCl by approximately 30% in control rats, had virtually no effect on CT responses in Na+-deprived rats. Thus, 2 days of Na+ deprivation is sufficient to alter patterns of ingestion of concentrated NaCl and to reduce gustatory responses to NaCl. Furthermore, changes in gustatory responses to NaCl during dietary Na+ deprivation may involve the amiloride-sensitive component of the CT.     

Fluid consumption, electrolyte excretion and heart remodeling in rats with myocardial infarct maintained on regular and high sodium intake.

The purpose of the study was to determine effect of high sodium intake on fluid and electrolyte turnover and heart remodeling in the cardiac failure elicited by myocardial infarction (MI). The experiments were performed on four groups of Sprague Dawley rats maintained on food containing 0.45% NaCl and drinking either water (groups 1, 2) or 1% NaCl (groups 3, 4). Groups 1 and 3 were sham-operated while in groups 2 and 4 MI was produced by the coronary artery ligation. In each group food and fluid as well as sodium intake, urine (Vu), sodium (UNaV), potassium (UKV) and solutes (UosmV) excretion were determined before and four weeks after the surgery. Size of the infarct, left ventricle (LV) weight and diameter of LV and right ventricle (RV) myocytes were determined during post-mortem examination. Before the surgery groups 3 and 4 ingested significantly more fluid and sodium, had higher Vu, UNaV, UKV and UosmV than the respective groups 1 and 2. In groups 2 and 4 MI resulted in significant decrease in Vu, UNaV and UosmV in comparison to the pre-surgical level. In Group 4 MI resulted also in a significant decrease of food and sodium intake. The MI size did not differ in groups 2 and 4 while diameter of LV myocytes was significantly greater in groups 2 and 4 than in groups 1 and 3, and in group 4 than in group 2. The study reveals that prolonged high sodium consumption increases fluid and electrolyte turnover both in the sham and in the MI rats and that the MI causes decrease in food and sodium intake in rats on high but not on regular sodium intake. In addition high sodium diet promotes development of greater post-MI hypertrophy of the LV myocytes.     

Water ingestion provides an early signal inhibiting osmotically stimulated vasopressin secretion in rats

Dehydrated dogs are known to inhibit secretion of vasopressin (VP) within minutes after drinking water, before plasma osmolality (P(osmol)) diminishes. The present studies determined whether water ingestion causes a similar rapid inhibition of neurohypophyseal hormone secretion in rats. Adult rats were infused with 1 M NaCl (2 ml/h iv) for 240 min to stimulate VP and oxytocin (OT) secretion. After 220 min of infusion, rats were given water to drink for 5 min, and blood samples were taken 5 and 15 min later for RIA. Plasma VP (pVP) was much lower when rats ingested water than when they drank nothing even though P(osmol) was not significantly altered. Plasma OT (pOT) was affected similarly. In contrast, no effects on pVP or pOT occurred when rats drank isotonic NaCl solution for 5 min in amounts comparable to the water intakes (approximately 5.5 ml). These results suggest that neurohypophyseal secretion of VP and OT in rats is inhibited rapidly by water drinking, and that this inhibition is mediated by a visceral signal of osmotic dilution rather than by the act of drinking per se.     

NaCl intake and preference threshold of spontaneously hypertensive rats.

Both male and female spontaneously hypertensive (SH) rats have an appetite for NaCl solution. The appetite is present when a choice is offered between distilled water and either isotonic or hypertonic (0.25 M) NaCl solution to drink. Total fluid intake (water plus NaCl solution) was greater for SH rats than for controls while food intakes (g/100 g body wt/day) of SH rats were not different from controls. Mean body weight of SH rats was always less than that of controls. The appetite for NaCl solution was accompanied by a significant reduction in preference (detection) threshold. SH rats could detect the difference between distilled water and NaCl solution when the concentration of the latter was 12 mEq/liter compared to a control threshold of 30 mEq/liter. The NaCl appetite and reduced NaCl preference threshold induced by spontaneous hypertension is in marked contrast to the NaCl aversion induced by other types of experimentally induced hypertension in rats. The mechanism or mechanisms responsible for these differences remain for further study.     

Rapid calorie metering inad lib rats

Adult wistar rats of either sex housed in individual cages and fedad lib were used to investigate the effects of calorie content and taste on ingestion. A 15 min single-choice solution (water, quinine, sucrose, saccharin) test as well as 1 h mixed diet (stock diet, sucrose-mixed, saccharin-mixed, quinine-mixed) tests were used. Calorically-rich sucrose either in solution or in mixed-diet was preferentially ingested. Tasteper se has not influenced calorie intake, as intake on sweet saccharin (3.4 ±0.4 cal) or on bitter quinine (3.3 ±0.6 cal) was similar to intake on stock diet (4.8 ±0.8 cal). Increased 5 min intake on sucrose solution (4.6 ±0.1 ml) over intake of other test solutions (saccharin 3.5 ±0.2 ml, quinine, 1.2 ±0.3 ml, water 2.1 ±0.1 ml) and calorie intake suppression on 1 h stock diet immediately following sucrose solution intake, indicate rapid calorie metering, probably based on fast-acting specific gustatory signals