Leptin resistance does not induce hyperphagia in the rat

Leptin has been thought to work as a mediator for body weight control by inhibiting food intake. Leptin, however, cannot prevent obesity induced by a high-fat diet (HFD) probably because of leptin resistance. We investigated daily feeding and weight gain when ordinary chow (OC) was changed to a HFD in male rats. Food intake, by weight, significantly increased the next day, but gradually decreased until at 20 days the HFD intake contained the same calories as consumed by the OC-fed control rats. The reduction in food intake occurred only during the night without change of preference for the HFD, even after leptin resistance had developed. Nonetheless, the HFD-fed rats gained more weight than the controls. From the present experiment, it is concluded that leptin resistance does not induce hyperphagia, and suggested that body weight is not regulated to be constant.     

Dietary self-selection in insulin-injected hamsters

Adult male golden hamsters were given access to a variety of nutrient sources and were observed following the administration of regular insulin. It was hypothesized that if insulin produced hyperphagia in hamsters by the activation of a glucoprivic feeding mechanism, a selective increase in carbohydrate consumption would be observed. All animals received subcutaneous injections of 10, 30, 50 and 100 units/kg of insulin as well as a control injection of saline. Food consumption was recorded at +3, +6 and +24 hours after injections. In Experiment 1 hamsters having continuous access to Purina lab chow, fat (Crisco) and sucrose (sugar cubes) increased their total caloric consumption in response to insulin, but did not do so by selectively increasing their carbohydrate intake. In Experiment 2 hamsters maintained on Purina chow and sugar cubes consistently increased their carbohydrate intake as well as their total caloric consumption in response to insulin, but again the increase in carbohydrate intake was not selective; increased consumption of both sugar cubes and Purina chow occurred, and neither the proportion of total calories derived from carbohydrate nor the proportion of total calories derived from sugar cubes was affected by insulin administration. The results support the conclusion that insulin-induced hyperphagia in hamsters results from the activation of a non-glucoprivic feeding mechanism.     

Diet composition determines course of hyperphagia in developing Zucker obese rats

Previous observations from this laboratory indicate that, during growth, the hyperphagia of the male genetically obese Zucker rat reaches a peak or "breakpoint" and then declines. To examine the effect of dietary macronutrient content on the course of hyperphagia, groups of male lean and obese rats were maintained from 5-28 weeks of age on powdered chow, or isocaloric diets (3.6 kcal/g) containing 72% of calories as corn oil, dextrose, or soy isolate protein (n = 5 lean and obese rats/diet). On chow, hyperphagia was maintained at a level of 7-8 g above lean control intake until a "breakpoint" was reached at 17 weeks, and obese intake declined to lean control level. On the fat diet, hyperphagia was increased to 10 g/day when a breakpoint was reached at 8 weeks. On the dextrose and protein diets, hyperphagia at a level of 3-4 g/day reached breakpoints at weeks 18 and 16, respectively. On all diets, the intakes of obese rats were precisely equal to the intakes of lean control rats by weeks 19-20. These data show that the magnitude and duration of hyperphagia in the developing obese rat are influenced by diet composition. Previously, we have proposed that the obese rat's hyperphagia arises from rapid adipocyte filling. Since high-fat diets facilitate adipocyte enlargement, the early "breakpoint" of hyperphagia seen with the high-fat diet may indicate that this feeding stimulation decreases as the fat cells of the obese rat approach maximal size.     

Deafferentation affects short-term but not long-term control of food intake

Deafferentation affects short-term but not long-term control of food intake (PHYSIOL BEHAV XX(X) 000-000, 2005). Rats were treated neonatally with capsaicin (CAP) to investigate the involvement of vagal afferents in food intake control and body weight regulation. In the first set of experiments, rats were offered increasing concentrations of sucrose (10-15-20-40%) in short-term feeding tests of 1 h. At the end, 10% was offered again to see whether CAP rats modified their intake after repeated exposure to different concentrations of sucrose solution. Results demonstrated that CAP animals overconsume persistently compared to vehicle (VEH) controls. This overconsumption is most pronounced and variable at 10% trials. Hypertonic 40% sucrose solution resulted in a small but significant drop in intake in CAP rats. Overall, if the concentration of sucrose solution is more than 10%, sucrose ingestion of CAP and VEH rats does not depend on the concentration of sucrose solution and remains relatively constant during all trials. In another experiment, rats were exposed to a high-fat condensed milk suspension (CMS) for 5 days. CAP rats initially overconsumed from this CMS compared to VEH. This was accompanied by a decreased intake in chow. However, over the 5 day period CAP animals adjusted their CMS and chow intake to control levels. During both experiments there were no differences in body weight gain between CAP and VEH. Together, these results suggest that capsaicin-sensitive vagal C-fibers are involved in the control of volume ingestion and short-term food intake control but are not required for long-term control of energy intake.     

Increased enkephalin in brain of rats prone to overconsuming a fat-rich diet

Recent studies have shown that the opioid enkephalin (ENK), acting in part through the hypothalamic paraventricular nucleus (PVN), can stimulate consumption of a high-fat diet. The objective of the present study was to examine sub-populations of Sprague-Dawley rats naturally prone to overconsuming a high-fat diet and determine whether endogenous ENK, in different brain regions, is altered in these animals and possibly contributes to their behavioral phenotype. An animal model, involving a measure of initial high-fat diet intake during a few days of access that predicts long-term intake, was designed to classify rats at normal weight that are either high-fat consumers (HFC), which ingest 35% more calories of the high-fat than low-fat chow diet, or controls, which consume similar calories of these two diets. Immediately after their initial access to the diet, the HFC compared to control rats exhibited significantly greater expression of ENK mRNA, in the PVN, nucleus accumbens and central nucleus of the amygdala, but not the arcuate nucleus or basolateral amygdala. This site-specific increase in ENK persisted even when the HFC rats were maintained on a chow diet, suggesting that it reflects an inherent characteristic that can be expressed independently of the diet. It was also accompanied by a greater responsiveness of the HFC rats to the stimulatory effect of a PVN-injected, ENK analogue, D-ala2-met-enkephalinamide, compared to saline on consumption of the high-fat diet. Thus, normal-weight rats predicted to overconsume a fat-rich diet exhibit disturbances in endogenous ENK expression and functioning that may contribute to their long-term, behavioral phenotype.     

Dietary fat content affects energy intake and weight gain independent of diet caloric density in rats

Recent considerations of high-fat diet hyperphagia have focused on fat's relatively high energy density as the critical variable which promotes overeating. However, a high-fat (HF) diet has been shown to enhance intake and weight gain relative to a high-carbohydrate (HC) diet when both energy density and palatability are equated [Am. J. Physiol. 269 (1995) R30]. The present studies investigated the generality of this finding across manipulations of diet caloric density, diet physical form, and chow availability. Separate groups of male rats were fed HF or HC at either 2.3 or 1.15 kcal/ml for 16 days; HF feeding enhanced weight gain relative to HC across both levels of energy density. HF hyperphagia also occurred when diets were presented in semisolid (gelled) form, and when chow was available in addition to liquid diet. These findings are consistent with previous observations that an HF diet can enhance daily kilocalorie intake and weight gain at least partly via a mechanism that is unrelated to caloric density.     

Dietary self-selection of golden hamsters in response to acute food deprivation and chronic food restriction

Adult male golden hamsters were maintained on either Purine Rat Chow (Chow diet) or a self-selection diet consisting of high-protein chow, pure fat, and pure carbohydrate (Choice diet). In Experiment 1, animals were deprived of food for single periods of up to 48 hr. Animals on the Chow diet did not increase intake at any time after deprivation; animals on the Choice diet selectively increased their consumption of fat-derived calories and increased their total caloric intake during the first 6 hr of refeeding, but not thereafter. The nature of the diet did not influence the rate at which animals regained weight following deprivation. In Experiment 2, hamsters were placed on food-restriction schedules (access to food either for 1 hr/day only or on alternate days only) until they lost 20% of starting body weight. Chow-fed animals demonstrated little or no change in food intake either during or after food restriction. Hamsters on the Choice diet consumed more calories and lost weight more slowly than did chow-fed animals during 1-hr/day feeding; intake of fat-derived calories was elevated during restriction. Choice hamsters increased total caloric intake only towards the end of the alternate-days restriction schedule. Choice hamsters were hyperphagic following both types of food-restriction schedules, but no increased preference for fat-derived calories was observed. Factors influencing food consumption of hamsters in response to deprivation and restriction are discussed.     

Effects of alternations (10 days) of high-fat with normal diet on liver lipid infiltration, fat gain, and plasma metabolic profile in rats

The purpose of the present study was to test the hypothesis that short-term alternations of high-fat with normal chow feeding result in higher fat accumulation in liver than continuous intake of the same high-fat diet. Male Sprague-Dawley rats (7 weeks of age) were divided into 3 groups according to diet composition: standard chow (SD; 12,5% kcal as fat), high-fat (HF; 42% kcal as fat), and food cycles (FC) consisting of 10-day alternations between HF and SD diets beginning with the high-fat diet. Rats in each of these 3 groups were sacrificed after 10, 30, and 50 days (n = 10 rats/sub-groups). Energy intake, body weight, liver and muscle relative weights were not significantly (P > 0.05) different between FC- and HF-fed rats. Using the total energy intake for the 50-day period, it was calculated that approximately 30% less calories as fat was ingested in the FC- compared to the HF-fed rats. In spite of this, liver lipid infiltration as well as fat accretion in abdominal adipose tissues were increased (P < 0.01) similarly in FC- and HF-fed rats. Plasma FFA and insulin levels depicted strong tendencies (P < 0.07) to be higher in FC- than in continuous HF-fed rats at the end of the 50-day period. These results indicate that, despite a 30% reduction in ingested lipids, alternations of HF with normal chow diet compared to the continuous hyperlipidic diet caused the same level of infiltration of lipids in the liver and in the abdominal adipose tissues and, to a certain extent, may even result in a larger deterioration of the metabolic profile.     

Differential effects of sucrose and fructose on dietary obesity in four mouse strains

We examined sugar-induced obesity in mouse strains polymorphic for Tas1r3, a gene that codes for the T1R3 sugar taste receptor. The T1R3 receptor in the FVB and B6 strains has a higher affinity for sugars than that in the AKR and 129P3 strains. In Experiment 1, mice had 40 days of access to lab chow plus water, sucrose (10 or 34%), or fructose (10 or 34%) solutions. The strains consumed more of the sucrose than isocaloric fructose solutions. The pattern of strain differences in caloric intake from the 10% sugar solutions was FVB > 129P3 = B6 > AKR; and that from the 34% sugar solutions was FVB > 129P3 > B6 ≥ AKR. Despite consuming more sugar calories, the FVB mice resisted obesity altogether. The AKR and 129P3 mice became obese exclusively on the 34% sucrose diet, while the B6 mice did so on the 34% sucrose and 34% fructose diets. In Experiment 2, we compared total caloric intake from diets containing chow versus chow plus 34% sucrose. All strains consumed between 11 and 25% more calories from the sucrose-supplemented diet. In Experiment 3, we compared the oral acceptability of the sucrose and fructose solutions, using lick tests. All strains licked more avidly for the 10% sucrose solutions. The results indicate that in mice (a) Tas1r3 genotype does not predict sugar-induced hyperphagia or obesity; (b) sucrose solutions stimulate higher daily intakes than isocaloric fructose solutions; and (c) susceptibility to sugar-induced obesity varies with strain, sugar concentration and sugar type.     

Fat substitutes promote weight gain in rats consuming high-fat diets

The use of food products designed to mimic the sensory properties of sweet and fat while providing fewer calories has been promoted as a method for reducing food intake and body weight. However, such products may interfere with a learned relationship between the sensory properties of food and the caloric consequences of consuming those foods. In the present experiment, we examined whether use of the fat substitute, olestra, affect energy balance by comparing the effects of consuming high-fat, high-calorie potato chips to the effects of consuming potato chips that sometimes signaled high calories (using high-fat potato chips) and that sometimes signaled lower calories (using nonfat potato chips manufactured with the fat substitute olestra). Food intake, body weight gain and adiposity were greater for rats that consumed both the high-calorie chips and the low-calorie chips with olestra compared to rats that consumed consuming only the high-calorie chips, but only if animals were also consuming a chow diet that was high in fat and calories. However, rats previously exposed to both the high- and low-calorie chips exhibited increased body weight gain, food intake and adiposity when they were subsequently provided with a high fat, high calorie chow diet suggesting that experience with the chips containing olestra affected the ability to predict high calories based on the sensory properties of fat. These results extend the generality of previous findings that interfering with a predictive relationship between sensory properties of foods and calories may contribute to dysregulation of energy balance, overweight and obesity.     

Control of protein intake in golden hamsters

Experiments were performed to investigate the behavioural responses of golden hamsters to manipulations of dietary protein availability. In the first experiment, hamsters were maintained on a protein-free diet and a powdered diet containing 64.8% protein (P64.8). When the P64.8 diet was progressively diluted with cornstarch, hamsters increased their intake of this diet fraction, but protein intake nevertheless declined. When the protein content of the diet was 16.2%, animals derived only 6% of total calories from protein and lost weight despite normal intake of calories. In the remaining experiments, hamsters were maintained on a self-selection regimen of high-protein chow, pure carbohydrate (sugar cubes), and pure fat (vegetable shortening). When high-protein chow was removed for either 5 or 10 days, total caloric intake and body weight declined, and hamsters selectively increased protein intake for several days after high-protein chow was returned. Hamsters allowed access to high-protein chow for only one hour each day markedly increased the amount of high-protein chow they ate during this hour as protein-restriction continued, but still consumed only about 10% of their normal daily protein intake on this schedule and lost 20% of starting body weight in two weeks; when free access to high-protein chow was restored, these animals selectively increased their protein intake above pre-restriction levels. Hamsters given access to high-protein chow only on alternate days demonstrated a relatively modest and slowly developing increase in protein intake, perhaps because they incurred only a moderate protein deficit. The results suggest that when protein intake falls below normal minimum requirements, hamsters will demonstrate an adaptive protein hunger but make only a limited adjustment to the dilution of a protein-containing diet fraction.     

Dietary fat-induced hyperphagia in rats as a function of fat type and physical form

The influence of dietary fat on food intake and weight gain was assessed by feeding adult female rats diets that differed in the type and form of fat, as well as in the availability of other macro- and micronutrients. Compared to chow-fed controls, the various fat diets increased total food intake by 4% to 27%. Specifically, rats fed chow and a separate source of fat (fat option diet) consumed more fat and total calories, and gained more weight when the fat source was emulsified corn oil rather than pure corn oil or was vegetable shortening rather than corn oil. However, corn oil and shortening had similar effects on caloric intake and weight gain when presented as emulsified gels. Also, pure and emulsified-gel forms of shortening did not differ in their effects on caloric intake and weight gain. Supplementing the vegetable shortening with micronutrients, however, enhanced its hyperphagia-promoting effect. The results of two-choice tests revealed that the rats' preferences for the orosensory properties of the various fat sources did not account for the differential hyperphagias obtained. Rather, it appears that long-term fat selection and caloric intake are influenced primarily by postingestive factors. Fat selection and total intake were determined not only by the fat source itself, but also by the other diet options. That is, rats selected more fat and consumed more calories when chow was the alternative food than when separate sources of carbohydrate and protein were available.     

Flavor-cued modulation of intake in rats: role of familiarity and impact on 24-h intake.

Following training with distinctively flavored nutritive solutions that differ in concentration and thus in caloric value, rats demonstrate flavor-postingestive consequence learning by preferentially consuming one of the flavors in two-bottle tests (both flavors in nutrient-identical solutions.) Experiment 1 investigated whether the relative familiarity of the flavor-nutrient combinations encountered in two-bottle tests contributes to the observed preference. One of the training concentrations (rather than the customary intermediate concentration) was used to present the flavors in testing; thus, one of the flavors was in a familiar context while the other was in an unfamiliar context. The results of two independent trials (rats trained with 1 and 5% sucrose; rats trained with 5 and 40% sucrose) confirmed that two-bottle test preference was not a preference for the familiar flavor-nutrient combination. Experiment 2 examined whether caloric expectancies based upon a previously learned flavor-postingestive consequence association would affect total daily intake. On alternating days, rats consumed 30 mL of dilute (5%) and concentrated (40%) sucrose, each distinctively flavored. When given 30 mL of 22.5% sucrose containing each of the flavors on separate test days, they ate less chow and thus fewer total calories over 24 h when given the flavor previously paired with concentrated sucrose. Experiment 3 replicated the design of Experiment 2 except that fat calories were used instead of sucrose; no significant adjustment of chow intake in extinction tests was noted, even when the number of fat calories used in training was increased (Experiment 4). Thus, rats did not exhibit flavor-cued modulation of chow intake when trained with fat, in contrast to responsivity to flavor cues when trained with sucrose. This differential responding to fat versus carbohydrate calories is consistent with previous observations, in a variety of paradigms, that modulation of caloric intake is less energetically appropriate when ingested foods are high in fat relative to high-carbohydrate foods.     

Somatic and metabolic responses of mature female rats with dietary obesity to dorsomedial hypothalamic lesions: Effects of diet palatability

Caloric intake, body weight, obesity status (Lee Index) and incorporation of U-14 C-glucose into liver and retroperitoneal fat pad glycogen and lipid were studied in mature female rats that had received bilateral lesions or sham-operations in the dorsomedial hypothalamic nuclei (DMN) after dietary obesity was well established. Their diet consisted of a high-fat-sucrose chow mix, chocolate chip cookies and a drinking fluid of 32% sucrose in tap water. Comparable groups of DMN lesioned rats (DMNL rats) and sham-operated controls were maintained on lab chow pellets and tap water. Prior to the hypothalamic operation, the animals on the high-caloric regimen consumed significantly more calories than the rats on lab chow and also attained commensurately higher body weights and obesity indices. The bulk of the calories consumed during this time was derived from the cookies. Following DMNL, the animals maintained on lab chow became hypophagic and had lower body weights than the sham-operated rats, as has been previously reported. In rats on the high-caloric regimen, DMNL resulted in hyperphagia in comparison to all other groups. The greatest percentage of the calories during this time was derived from the high-fat-sucrose chow mix and sugar water. Correspondingly, DMNL rats on the high-caloric regimen had higher body weights and obesity indices than all other groups. At sacrifice, both a diet and lesion effect were noted in an elevated incorporation of U 14-C glucose in both fat pad and liver lipid and glycogen. The data are interpreted to mean that (1) when a highly palatable, high-caloric diet is available, DMNL do not exert their usual hypophagic and weight-lowering effects; (2) DMNL and control rats show excessive caloric intake when both groups are fed a highly palatable, high-caloric diet in comparison to their chow-fed counterparts. However, DMNL rats fed high-caloric diet also consume significantly more than controls fed this diet; (3) This excessive caloric intake of the DMNL rats possibly predisposes these animals to exaggerated lipogenesis in liver and adipose tissue; (4) the sham-operated controls on the high-caloric regimen also show greater lipogenesis but at a level intermediate between the chow-fed controls and the DMNL rats on the high-caloric diet.     

Evidence for the involvement of neurotrophins in muscle transdifferentiation and acetylcholine receptor transformation in the esophagus of Myf5(-/-):MyoD(-/-) and NT-3(-/-) embryos.

The primary aim of our study was to determine whether the esophageal innervation (i.e., vagal and enteric) and the skeletal muscle-secreted neurotrophins have a role in smooth-to-skeletal muscle transdifferentiation and in the muscarinic-to-nicotinic acetylcholine receptor type transition. To that end, we used genetically engineered embryos and immunohistochemistry. We found that, in the absence of Myf5 and MyoD, the esophageal muscle cells failed to develop the striated phenotype of acetylcholine receptors. In addition, the development of vagal and enteric innervation was delayed in Myf5(-/-):MyoD(-/-) and NT-3(-/-) mutants, but it was reestablished 2 days before the end of gestation. The smooth muscle cells in the esophagus appeared to be a distinct subpopulation of cells and their ability to transdifferentiate was based on their competence to express neurotrophins and their receptors. Finally, our data suggest a role for NT-3 in the esophageal muscle transdifferentiation.     

Dietary self-selection vs. complete diet: body weight gain and meal pattern in rats.

Food intake and body weight gain of male adult Wistar rats were examined in two groups of animals. One group (n = 14) was allowed to select its diet from separate sources of protein (casein, 3.1 kcal/g), fat (lard and sunflower oil, 7.9 kcal/g) and carbohydrate (CHO, starch and sucrose, 3.3 kcal/g). Another group (n = 10) received a nutritionally complete diet (3.3 kcal/g). After 2 weeks of adaptation to the diets, body weights and meal patterns were recorded for at least 4 days. The total caloric intake was nearly identical for the two groups of rats. Rats given dietary choice gained less weight over 4 days than rats fed chow and showed reduced feed efficiency. During the 24-h period, self-selecting rats consumed 20.8% of calories as proteins, 21% as fats and 58.2% as CHO. Self-selecting rats ate significantly less calories during the day than did rats given chow. The chow diet consisting of 17.3% calories as protein, 7.6% as fat and 75.1% as CHO. When comparing the self-selecting group nutrient intakes to those of chow-fed group it was observed that 24-h protein calorie intakes were identical in both groups. Fat intake was significantly higher and CHO reduced as compared to chow-fed rats. During the day, CHO intake was higher in self-selecting rats, and fat intake was not significantly reduced. During the night, protein and fat intakes were significantly higher in self-selecting rats, while CHO intake was significantly decreased, particularly in the last periods of the night.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early postnatal overnutrition: potential roles of gastrointestinal vagal afferents and brain-derived neurotrophic factor

Abnormal perinatal nutrition (APN) results in a predisposition to develop obesity and the metabolic syndrome and thus may contribute to the prevalence of these disorders. Obesity, including that which develops in organisms exposed to APN, has been associated with increased meal size. Vagal afferents of the gastrointestinal (GI) tract contribute to regulation of meal size by transmitting satiation signals from gut-to-brain. Consequently, APN could increase meal size by altering this signaling, possibly through changes in expression of factors that control vagal afferent development or function. Here two studies that addressed these possibilities are reviewed. First, meal patterns, meal microstructure, and the structure and density of vagal afferents that innervate the intestine were examined in mice that experienced early postnatal overnutrition (EPO). These studies provided little evidence for EPO effects on vagal afferents as it did not alter meal size or vagal afferent density or structure. However, these mice exhibited modest hyperphagia due to a satiety deficit. In parallel, the possibility that brain-derived neurotrophic factor (BDNF) could mediate APN effects on vagal afferent development was investigated. Brain-derived neurotrophic factor was a strong candidate because APN alters BDNF levels in some tissues and BDNF knockout disrupts development of vagal sensory innervation of the GI tract. Surprisingly, smooth muscle-specific BDNF knockout resulted in early-onset obesity and hyperphagia due to increases in meal size and frequency. Microstructure analysis revealed decreased decay of intake rate during a meal in knockouts, suggesting that the loss of vagal negative feedback contributed to their increase in meal size. However, meal-induced c-Fos activation within the dorsal vagal complex suggested this effect could be due to augmentation of vago-vagal reflexes. A model is proposed to explain how high-fat diet consumption produces increased obesity in organisms exposed to APN, and may be required to reveal effects of EPO on vagal function.     

Influence of anterior subdiaphragmatic vagotomy and TPN on rat feeding behavior.

Total parenteral nutrition (TPN) inhibits food intake and feeding behavior. Whether caloric sensory function of the liver contributes to this food intake and feeding behavior regulation via vagal-afferent innervation was tested after performing anterior hepatic vagotomy or sham operation in rats infused with a TPN solution providing 100% of daily energy needs, given continuously for 4 days. Food intake, meal number, size, duration, meal and intermeal sniffs, and eating activity were measured using an automated computerized rat eater meter (ACREM). TPN infusion resulted in a significant decrease of food intake and feeding indexes in both groups. The vagotomized rats showed a significantly higher food consumption, achieved by greater meal frequency, larger meal size, and longer meal duration. Thus, vagotomized rats consumed more than their controls by eating larger meals more often and of longer duration. Data suggest that anterior hepatic vagotomy interrupts hepatic caloric sensory feedback loop, diminishing inhibitory vagal effects on food intake with TPN, leading to an overall increase in food intake.     

A detailed analysis of sucrose drinking in the rat

The present report represents an initial attempt to examine and quantify the eating and drinking patterns of rats presented with water, laboratory chow, and sucrose solution for 23 hours. The concentration of the sucrose solution was systematically increased (0.10 M, 0.25 M, 0.5 M, 1.0 M) with a single concentration being presented to rats in four-day blocks. As has been previously shown, total intake (ml) of sucrose solution increased with concentration to a peak at 0.25 M and then decreased with further rises in concentration. Calories consumed from sucrose monotonically increased with concentration, reaching a maximum at 0.50 M. As calories consumed from sucrose increased with rising concentration, chow intake monotonically decreased. This compensatory decrease in chow intake was primarily attributable to decreases in nighttime chow consumption when the concentration of sucrose available was less than or equal to 0.25 M; when the concentration was greater than 0.25 M, further reductions in chow intake occurred during the day. Moreover, the decrease in chow intake was due solely to a reduction in the number of chow bouts. As the concentration of sucrose increased, the day-to-night ratio of sucrose intake approached unity. Bout volume increased with concentration to a broad peak spanning 0.25-0.5 M, and then decreased with 1.0 M. Bout duration changed with sucrose concentration such that the bout drinking rate (ml/min) was seen to monotonically increase, reaching a stable maximum at 0.5 M. Since the caloric intake per sucrose bout progressively increased with each rise in concentration, the asymptotic portion of the curve describing calories consumed from sucrose was attributable to alterations in sucrose bout number and not sucrose bout size.     

Dietary hyperphagia in rats: role of fat, carbohydrate, and energy content

Dietary energy, fat and carbohydrate content were varied to determine the nutritional factors responsible for hyperphagia induced by feeding rats high-fat diets. In the first experiment, rats were fed isoenergetic high-fat or high-carbohydrate diets for 2 weeks. Weight gain and energy intake were lower in rats given the high-fat diet. When some of the rats were switched to a diet that was high in fat, carbohydrate and energy, gram food intake was initially unchanged, resulting in a substantial increase in energy intake and weight gain. Energy intake gradually declined over the 4 weeks following the switch to the high-energy diet. In the second experiment, rats were fed high-fat diets that were either high or low in carbohydrate content and either high or low in energy content (kcal/g). Rats fed a high-fat diet that was high in energy and carbohydrate ate the most energy and gained the most body weight and carcass fat. In the third experiment, rats were fed high-carbohydrate diets varying in fat and cellulose content. Energy intake and body weight gain varied directly as a function of caloric density regardless of the fat or cellulose content of the diets. It is concluded that hyperphagia induced by feeding high-fat diets is not due to the high dietary fat content alone. Rather, high levels of fat, carbohydrate, and energy interact to produce overeating and obesity in rats fed high-fat diets.