Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat

The present studies investigated the influence of presystemic signals on the control of thirst, salt appetite, and vasopressin (VP) secretion in rats during nonhypotensive hypovolemia. Rats were injected with 30% polyethylene glycol (PEG) solution, deprived of food and water overnight, and then allowed to drink water, 0.15 M NaCl, or 0.30 M NaCl. The PEG treatment, which produced 30-40% plasma volume deficits, elicited rapid intakes in an initial bout of drinking, but rats consumed much more 0.15 M NaCl than water or 0.30 M NaCl. In considering why drinking stopped sooner when water or concentrated saline was ingested, it seemed relevant that little or no change in systemic plasma Na(+) concentration was observed during the initial bouts and that the partial repair of hypovolemia was comparable, regardless of which fluid was consumed. In rats that drank 0.15 M NaCl, gastric emptying was fastest and the combined volume of ingested fluid in the stomach and small intestine was largest. These and other observations are consistent with the hypothesis that fluid ingestion by hypovolemic rats is inhibited by distension of the stomach and proximal small intestine and that movement of dilute or concentrated fluid into the small intestine provides another presystemic signal that inhibits thirst or salt appetite, respectively. On the other hand, an early effect of water or saline consumption on VP secretion in PEG-treated rats was not observed, in contrast to recent findings in dehydrated rats. Thus the controls of fluid ingestion and VP secretion are similar but not identical during hypovolemia.     

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.     

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.     

Elevated dietary salt suppresses renin secretion but not thirst evoked by arterial hypotension in rats

Increased dietary salt intake was used as a nonpharmacological tool to blunt hypotension-induced increases in plasma renin activity (PRA) in order to evaluate the contribution of the renin-angiotensin system (RAS) to hypotension-induced thirst. Rats were maintained on 8% NaCl (high) or 1% NaCl (standard) diet for at least 2 wk, and then arterial hypotension was produced by administration of the arteriolar vasodilator diazoxide. Despite marked reductions in PRA, rats maintained on the high-salt diet drank similar amounts of water, displayed similar latencies to drink, and had similar degrees of hypotension compared with rats maintained on the standard diet. Furthermore, blockade of ANG II production by an intravenous infusion of the angiotensin-converting enzyme inhibitor captopril attenuated the hypotension-induced water intake similarly in rats fed standard and high-salt diet. Additional experiments showed that increases in dietary salt did not alter thirst stimulated by the acetylcholine agonist carbachol administered into the lateral ventricle; however, increases in dietary salt did enhance thirst evoked by central ANG II. Collectively, the present findings suggest that hypotension-evoked thirst in rats fed a high-salt diet is dependent on the peripheral RAS despite marked reductions in PRA.     

Thirst and salt appetite responses in young and old Brown Norway rats

Male Brown Norway rats aged 4 mo (young) and 20 mo (old) received a series of experimental challenges to body fluid homeostasis over approximately 3 mo. Water was available for drinking in some tests, and both water and 0.3 M NaCl were available in others. The series included three episodes of extracellular fluid depletion (i.e., furosemide + 20 h of sodium restriction), two tests involving intracellular fluid depletion (i.e., hypertonic saline: 1 or 2 M NaCl at 2 ml/kg body wt sc), one test involving overnight food and fluid restriction, and testing with captopril adulteration of the drinking water (0.1 mg/ml) for several days. Old rats were significantly heavier than young rats throughout testing. Old rats drank less water and 0.3 M NaCl after sodium deprivation than young rats, in terms of absolute and body weight-adjusted intakes. Old rats drank only half as much water as young rats in response to subcutaneous hypertonic NaCl when intakes were adjusted for body weight. Old rats drank less 0.3 M NaCl than young rats after overnight food and fluid restriction when intakes were adjusted for body weight. In response to captopril adulteration of the drinking water, young rats significantly increased daily ingestion of 0.3 M NaCl when it was available as an alternative to water and significantly increased daily water intakes when only water was available, in terms of absolute and body weight-adjusted intakes. Old rats had no response to captopril treatment. These results add important new information to previous reports that aging rats have diminished thirst and near-absent salt appetite responses to regulatory challenges.     

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).     

Inhibition of thirst when dehydrated rats drink water or saline

The present experiments sought to identify the physiological signals that inhibit thirst when dehydrated rats drink water or NaCl solution. Rats were deprived of drinking fluid but not food overnight. When allowed to drink again, the dehydrated animals consumed water or saline (0.05 M, 0.10 M, 0.15 M, or 0.20 M NaCl solution) almost continuously for 5-8 min before stopping. The volumes consumed were similar regardless of which fluid they ingested, but blood analyses indicated that increased plasma osmolality and decreased plasma volume, or both, still remained when drinking terminated. These results suggest that the composition of the ingested fluid is less significant than its volume in providing an early signal that inhibits thirst and fluid consumption by dehydrated rats. Analyses of the gastrointestinal tracts revealed that the cumulative volume in the stomach and small intestine correlated highly with the amount consumed regardless of which fluid was ingested. These and other results suggest that the volume of fluid ingested by dehydrated rats is sensed by stretch receptors detecting distension of the stomach and small intestine, which provide an early inhibitory stimulus of thirst.     

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.     

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.     

Inhibition of vasopressin secretion when dehydrated rats drink water

The present study determined whether vasopressin (VP) secretion is inhibited by an oropharyngeal signal associated with swallowing fluids when dehydrated rats drink water, as it is when dehydrated dogs are used as experimental subjects (Thrasher, TN, Keil LC, and Ramsay DJ. Am J Physiol Regul Integr Comp Physiol 253: R509-R515, 1987). VP levels in systemic plasma (pVP) fell rapidly when rats drank water after overnight water deprivation. Systemic plasma Na+ concentration (pNa) also fell, but that change likely contributed little to the early inhibition of VP secretion. In contrast, consumption of water by dehydrated rats with an open gastric fistula had no effect on pVP, nor did consumption of isotonic saline by dehydrated rats; in neither case was pNa affected by fluid consumption. These findings provide no evidence that the act of drinking inhibits VP secretion in dehydrated rats. Thus some post-gastric effect of the ingested water seems to be responsible for the inhibitory signal. These results are consistent with previous suggestions that an early inhibitory stimulus for VP secretion in rats is provided by post-gastric visceral osmo- or Na+ receptors that sense the composition of the ingested fluid.     

Difference in rehydration process due to salt concentration of drinking water in rats

Albino rats were thermally dehydrated (approximately 8% of body wt), divided into five groups, and given tap water or 0.2, 0.45, 0.9, or 2.0% NaCl solution ad libitum for 16 h. Rats given 0.9 or 0.45% NaCl solution regained fluid loss completely in 3-3.5 h, whereas those given 0.2% solution became fully rehydrated at 10 h. The rats in the tap water and 2.0% NaCl groups were only 78 and 59% rehydrated, respectively, within 16 h. Na balance was positive in the 0.9% NaCl group by about five times the amount of the cations lost during the dehydration period. A positive balance of Na was also observed in the 0.45 (approximately 250%) and 2.0% NaCl groups (300%), whereas the 0.2% NaCl group regained lost water and Na simultaneously at 10 h. With tap water, additional loss of cations was observed. These findings show that for the replacement of water due to thermal dehydration there is a range of NaCl concentration with which the rats can rehydrate with the mutual cooperation of thirst, salt appetite, and kidney function.     

Parallel effects of DOCA on salt appetite, thirst, and blood pressure in sheep

Salt appetite was quantified in sheep by measuring the relative amounts of high-salt (266 meq/kg) and low-salt (6 meq/kg) pelleted alfalfa that they ate. Given a choice of these two foods, normal sheep ate twice as much low-salt as high-salt pellets. Following DOCA administration the sheep rapidly developed an increased salt appetite, and after 10 days they ate approximately three times as much high-salt as low-salt pellets. Their choice rapidly reverted to control values after the end of the DOCA treatment. The changes in salt appetite were accompanied by changes in thirst and mean arterial pressure. We hypothesize that these effects of DOCA reflect changes that parallel those this mineralocorticoid causes in the hypothalamic regulatory centers for salt appetite, thirst, and blood pressure.     

NMDA receptor participation in control of food intake by the stomach

We previously reported that MK-801 (dizocilpine), an antagonist of N-methyl-D-aspartate (NMDA)-type glutamate receptors, increased meal size and duration in rats. MK-801 did not increase sham feeding or attenuate reduction of sham feeding by intraintestinal nutrient infusions. These results suggested that the MK-801-induced increase in meal size did not depend on antagonism of postgastric satiety signals. Consequently, we hypothesized that the NMDA antagonist might increase food intake by directly antagonizing gastric mechanosensory signals or by accelerating gastric emptying, thereby reducing gastric mechanoreceptive feedback. To test this hypothesis, we recorded intake of 15% sucrose in rats implanted with pyloric cuffs that could be closed to prevent gastric emptying. Sucrose intake was increased when the pyloric cuffs were open, allowing the stomach to empty. However, intake was not increased when the pyloric cuffs were inflated, causing gastric retention of all ingested sucrose. Direct measurements of gastric emptying revealed that MK-801 accelerated the emptying of 5-ml loads of 0.9% NaCl and 15% sucrose. Furthermore, MK-801 also accelerated the rate of emptying of freely ingested sucrose regardless of the volume ingested. Taken together with our previous findings, these results indicate that blockade of NMDA receptors with MK-801 does not increase food intake by antagonizing gastric mechanosensation. Rather, it accelerates gastric emptying, and thereby may indirectly reduce gastric mechanoreceptive cues, resulting in prolongation of eating. Modulation of gastric emptying rate by NMDA receptors could play an important role in the control of meal sizes.     

Continuous measurement of Na concentration in CSF during gastric water infusion in dehydrated rats.

To assess the differential stimulus to central and intravascular osmoreceptors during recovery from thermal dehydration, we measured Na concentrations in cerebrospinal fluid ([Na]CSF) and plasma ([Na]p) continuously and compared these during simulated drinking by gastric water infusion (INF) in euhydrated and thermally dehydrated rats under anesthesia. Continuous measurement of [Na]CSF was obtained with a double-barreled Na electrode placed in the lateral ventricle. Continuous measurement of [Na]p was obtained from a flow cell Na electrode in an extracorporeal shunt. Measurements were made during 10 min of INF (2.5 ml/100 g body wt) into the stomach and during 20 min of recovery. Changes in [Na]CSF always lagged behind those in [Na]p and were quantitatively smaller after INF. The decrease in [Na]CSF occurred sooner in dehydrated than in euhydrated rats in response to the decrease in [Na]p (P < 0.01). These results suggest that water and/or Na movement between blood and CSF is accelerated during restitution from thermal dehydration, acting to prevent overhydration during the early phase of rehydration.     

Thermogenic drinking: mediation by osmoreceptor and angiotensin II pathways

Exposure of rats to air at 5 C for 1-12 days is accompanied by a relative dehydration in spite of the continued presence of water. Dehydration during exposure to cold was manifested by: 1) a reduction in the ratio of water/food ingested; 2) an increase in the ratio of urine excreted/water ingested; 3) an increased evaporative water loss; 4) an increased serum osmolality and chloride concentration; and 5) a striking thirst and ingestion of water after transfer from cold to air at 26 C. Drinking began within 15 min and lasted approximately 1 h. Thermogenic drinking persisted for at least 120 days of exposure to cold. It was not thwarted by preventing access to water for either 1 or 2 h after transfer to warm air, but either intragastric or intraperitoneal administration of a water load equal to 3% of body weight inhibited water intake after transfer. These characteristics of thermogenic drinking are similar to those observed after 24 h of dehydration at 26 C; they also suggest that the cold-exposed rat is dehydrated relative to controls. These results suggest that osmoreceptors may play a role in the induction of thermogenic drinking. However, angiotensin II receptors may also play a role. Thermogenic drinking was inhibited by a beta 2-adrenergic, but not a beta 1-adrenergic, antagonist as well as by captopril, an inhibitor of the conversion of angiotensin I to angiotensin II. Further, plasma renin activity increased fourfold within 15 min after removal from cold. This suggests that an additional component involved in thermogenic drinking is the angiotensin II receptor. The extent to which thermogenic drinking is mediated by each pathway is unknown and will require additional studies.     

Circadian Variation in the Gastric-Emptying Response to Eating in Rats Previously Fed Once or Twice Daily

Four experiments dealt with circadian variation in the gastric emptying (GE) response to eating, among rats accustomed to eating once (1X) or twice daily (2x). In measuring GE response, a test meal [10 g accustomed diet per (kg body weight)^3/4] was fed close to a scheduled eating time or after a delay of up to 24 h. GE response was the fraction of the ingested test meal emptied per hr, up to a known degree of emptying, e.g., 50-58% of the test meal. Animals accustomed to the prescribed eating patterns ate promptly and at similarly rapid rates at all times of day. GE response, as plotted against time of response, fit a 24-h cosine model. Acrophase (time of maximum GE response of the fitted model) was similar, being 1.5 and 2.1 h, respectively, after the starting time of the accustomed dark-span meal for 1X and 2x rats, while amplitude (1/2 the maximum-to-minimum difference) was 41 and 24% of the MESOR (rhythm-adjusted mean). Characteristics of the GE rhythm appeared to be unchanged among 1X rats, severely versus minimally restricted in food intake during a final 9 days.     

Food preference in surgically desalivated rats; texture versus taste

Texture and taste cues guiding oral sensory selection of foodsby desalivated rats were investigated. The major salivary glandswere removed in 15 males. Five days later the operated animalsand 12 sham-operated and six intact males (250 g starting bodyweight) were exposed to various two-choice, 48-h diet selectiontests. These included: plain powdered dry; plain greasy (lubricatedwith 20% weight white vaselin or vegetable oil); sweet-powdereddry (0.5% Na saccharin); bitter greasy (0.25% quinine HCl) testfoods, based on standard rat chow. Operated and control animalsdisplayed similar intakes and no significant differences inbody growth could be seen during a follow-up of 60 post-operativedays. Volume of pilocarpine-stimulated salivary flow measuredafter testing indicated that surgical procedure was successful.Desalivated rats were found to be guided, in establishing foodpreference, more by texture than by taste cues. Both controland desalivated animals showed a clear preference towards thegreasy diet. No gross changes in the oral mucosa or in the tonguepapillation could be detected in the desalivated animals.     

Flavonoid-induced reduction of ENaC expression in the kidney of Dahl salt-sensitive hypertensive rat

Flavonoid, a plant extract, exhibits various biological actions. Dietary flavonoid intake is reported to reduce an elevated blood pressure, however the mechanism is unknown. The epithelial Na+ channel (ENaC) in the kidney plays a key role in the regulation of blood pressure by contributing to the Na+ reabsorption in renal tubules. Thus, we investigated the effect of quercetin, a flavonoid, on ENaC mRNA expression in the kidney of hypertensive Dahl salt-sensitive rats. Dahl salt-sensitive rats of 8 weeks were acclimated for 1 week in a metabolic cage and were subsequently kept for 4 weeks under four different conditions: (1) normal salt diet (0.3% NaCl), (2) normal salt diet with quercetin (10 mg/kg/day), (3) high-salt diet (8% NaCl), and (4) high-salt diet with quercetin. Quercetin diminished the alphaENaC mRNA expression in the kidney associated with reduction of the systolic blood pressure elevated by high-salt diet, suggesting that one of the mechanisms of the flavonoid's antihypertensive effect on salt-sensitive hypertension would be mediated through downregulation of ENaC expression in the kidney.     

Redistribution of extracellular water and sodium may contribute to saline tolerance in wild ducks

The compartmentalization of body fluids was measured in three species of ducks that differ in saline tolerance. Half of the birds of each species drank freshwater, while the other half drank saline (300 mM NaCl). Among ducks that drank freshwater, total body water (TBW) was similar among all species, but Barrow's goldeneyes (Bucephala islandica), the most marine species, had larger extracellular fluid volume (ECFV) than freshwater mallards (Anas platyrhynchos) or estuarine canvasbacks (Aythya valisineria). When acclimated to saline, only goldeneyes shifted extracellular water and Na+ into the intracellular compartment. ECFV was correlated with plasma aldosterone concentration in goldeneyes, but not in canvasbacks (aldosterone was not measured in mallards). Data summarized from the literature showed that TBW does not differ among terrestrial, freshwater, or marine species, but marine species have a larger part of their TBW in the extracellular compartment. Saline induced movement of extracellular water and Na+ into the cells only in goldeneyes. ECFV and redistribution of extracellular water and Na+ into the cells may be important components in saline tolerance of marine birds.     

Dietary Obesity Caused by a Specific Circadian Eating Pattern

The eating pattern is altered by high-fat diet-induced obesity. To clarify whether this is dependent on the fatty acid profile of the diet, the authors conducted two studies on adult female Sprague-Dawley rats fed normal-fat chow or high-fat diets with varying fatty acid composition. Eating pattern and body weight were assessed in rats fed canola-based (low in saturated fatty acids) or lard-based (moderate in saturated fatty acids) diets for 7 days, and in animals fed chow or canola- or butter-based diets (rich in saturated fatty acids) for 43 days. These parameters were also determined when restricted amounts of low-fat canola- or butter-based diets were consumed for 25 days. Early exposure to canola or lard high-fat feeding or prolonged access to canola- or butter-based fat-rich diets (relative to chow feeding) did not alter the normal light-dark distribution of food and energy intake. All animals ingested most of their food during the dark phase. However, feeding the high-fat canola- and butter-based diets produced an altered eating pattern during the light phase characterized by a smaller number of meals, longer intermeal interval, and enhanced satiety ratio, and consumption of shorter-lasting meals than chow-fed animals. Relative to canola or chow feeding, butter-fed animals consumed a lower number of meals during the dark phase and had a higher eating rate in the light phase, but ate larger meals overall. Only butter feeding led to overeating and obesity. When given a restricted amount of low-fat canola- or butter-based diet at the start of the light phase, rats ate most of their food in that phase and diurnal rather than nocturnal feeding occurred with restriction. These findings underscore the role of saturated fatty acids and the resulting eating pattern alteration in the development of obesity. (Author correspondence: louise.thibault@mcgill.ca)