Dietary obesity in adult and weanling rats following removal of interscapular brown adipose tissue

In order to investigate the role of brown adipose tissue (BAT) in diet-induced thermogenesis (DIT), a selection of palatable, energy-dense foods (Cafeteria diet) was used to increase the energy intakes of adult and weanling male rats, from some of which interscapular BAT (IBAT) had been surgically excised. Removal of IBAT had no effect upon energy intakes of the cafeteria-fed rats, nor of controls fed a pelleted stock diet. The rate of weight gain of intact controls was similar for the two diets, but adults with IBAT removed and fed with the cafeteria diet gained weight more rapidly than those fed the stock diet. Similarly, although intact weanlings did not exhibit excess weight gain when fed the cafeteria diet, removal of IBAT did result in more rapid weight gain of the cafeteria-fed weanlings relative to their stock-fed siblings. Nevertheless, total carcass energy was increased by some 20% in cafeteria-fed animals, irrespective of whether they had had IBAT removed. Thus there was no evidence for removal of IBAT having improved the efficiency of energy utilisation for growth. The failure to find evidence for altered levels of energy expenditure following removal of IBAT does not necessarily contradict the hypothesis that BAT mediates DIT, however, since, following removal of IBAT, there was hypertrophy of remaining BAT sites which may have compensated for the BAT removed.     

Lack of diet-induced thermogenesis following lesions of paraventricular nucleus in rats

The effects of electrolytic lesions in the hypothalamus paraventricular nucleus were studied in adult male and female Sprague-Dawley rats, fed different diets, consisting of either palatable human food plus chow (cafeteria diet) or chow alone. The results showed that both cafeteria diet and lesions induced an increase in energy intake and weight gain in rats of both sexes. Oxygen consumption rate and colonic temperature were significantly decreased by lesions, while cafeteria diet increased the same parameters only in intact animals. The lesion decreased weight, protein and DNA, and temperature of brown adipose tissue, while cafeteria diet increased the values considered in brown adipose tissue of sham-injured rats, but not in lesioned animals. The response to norepinephrine administration was significantly greater in intact rats and those fed cafeteria diet. The results suggest that the larger body weight gain observed in lesioned rats, particularly evident in rats fed cafeteria diet, is partly due to the disappearance of diet-induced thermogenesis that depends on the reduced mass and functional activity of brown adipose tissue.     

A maternal cafeteria diet during gestation and lactation promotes adiposity and impairs skeletal muscle development and metabolism in rat offspring at weaning

We examined the effects of a maternal cafeteria diet on skeletal muscle and adipose tissue development in the offspring at weaning. Rats born to mothers fed the cafeteria diet either during gestation alone or during both gestation and lactation exhibited a 25% reduction in muscle cross-sectional area with approximately 20% fewer fibres compared with pups fed a balanced chow diet. Maintaining the cafeteria diet during lactation increased intramuscular lipid content and fat pad weights characterized by adipocyte hypertrophy but not hyperplasia. These pups also had elevated muscle IGF-1, IGF-1 receptor, and PPARγ mRNA levels, which may indicate an attempt to maintain normal insulin sensitivity. The increased adiposity and elevated IGF-1, IGF-1 receptor and PPARγ mRNAs were not seen in the pups rehabilitated to the balanced diet during lactation. However, these pups exhibited reduced muscle cell proliferation (PCNA) with reduced insulin receptor and a trend towards reduced glucose transporter (GLUT)-4 mRNAs when compared with pups fed a balanced chow diet, indicating possible alterations in glucose uptake by muscle tissue. Therefore, rats born to mothers fed a cafeteria diet during gestation alone or during both gestation and lactation exhibited impaired skeletal muscle development and metabolic disorders normally associated with insulin resistance as early as the weaning stage.     

Lack of diet-induced thermogenesis in brown adipose tissue of obese medial hypothalamic-lesioned rats

Radiofrequency heat lesions were made in the medial hypothalamus of 12-week old male and female Holtzman rats. Two to three days later rats were offered a palatable cafeteria diet in addition to chow or were fed chow alone for the next 3-4 weeks. Male lesioned rats were only slightly hyperphagic on the chow diet and gained little extra weight. When fed the cafeteria diet, energy intake of male lesioned rats almost doubled in comparison with chow-fed lesioned rats and a very rapid extra weight gain occurred. Despite the marked hyperphagia, thermogenesis in brown adipose tissue was suppressed in the cafeteria-fed lesioned rats, as indicated by low mitochondrial guanosine diphosphate (GDP) binding. In female rats, lesions induced much greater hyperphagia and body weight gain than in male rats, particularly when they ate the cafeteria diet. Again, thermogenesis in brown adipose tissue was suppressed in the cafeteria-fed female lesioned rats. The proportion of energy derived from carbohydrate was not altered by the cafeteria diet in either male or female rats, whether lesioned or not, but there was an increase in the proportion of energy derived from fat at the expense of protein. No sex differences in food selection were observed. The accumulation of body fat was always greater in female lesioned rats than in male lesioned rats for similar food intakes. It is concluded that medial hypothalamic lesions prevent the normal occurrence of diet-induced thermogenesis in brown adipose tissue despite extreme overeating by the rats of a palatable cafeteria diet.     

Effects of a gastric implant on body weight and gastrointestinal hormones in cafeteria diet obese rats

In order to evaluate the effectiveness of a gastric implant in an animal model of dietary obesity, silicone implants (2.5 ml) were inserted into the stomachs of male rats maintained on a chow or "cafeteria" diet. At the time of implantation, the cafeteria fed rats weighed 14% more than chow fed controls. Overweight cafeteria fed animals lost weight in response to the gastric implant, whereas control chow fed animals did not. Both implant groups had significant increases in stomach weights in contrast to sham implant groups, but the increase was much less in the cafeteria diet group. The fasting plasma levels of the gastrointestinal hormones, gastrin and pancreatic polypeptide, and oxytocin (a marker of vagal afferent function) were measured by radioimmunoassay. Cafeteria fed sham or implanted animals had significantly higher fasting levels of plasma oxytocin and gastrin, and significantly lower plasma levels of pancreatic polypeptide than the chow fed groups. These studies demonstrate that the gastric implant has more effect on weight in overweight animals on a palatable mixed diet, perhaps related to both mechanical and neural factors.     

Neurological and stress related effects of shifting obese rats from a palatable diet to chow and lean rats from chow to a palatable diet

Rats exposed to an energy rich, cafeteria diet overeat and become obese. The present experiment examined the neural and behavioural effects of shifting obese rats from this diet to chow and lean rats from chow to the cafeteria diet. Two groups of male Sprague Dawley rats (n=24) were fed either highly palatable cafeteria diet or regular chow (30% vs. 12% energy as fat) for 16 weeks. Half of each group (n=12) was then switched to the opposing diet while the remainder continued on their original diet. The effects of diet switch on the response to restraint stress were assessed and rats were euthanised nine days after diet reversal. After 16 weeks of cafeteria diet, rats were 27% heavier than controls. Rats switched from chow to cafeteria diet (Ch-Caf) became hyperphagic and had increased dopamine D1, D2 and tyrosine hydroxylase mRNA expression in the ventral tegmental area (VTA) compared to rats switched from cafeteria to chow (Caf-Ch). Caf-Ch rats were hypophagic with significant reductions in white (16%) and brown (32%) adipose tissue mass, plasma leptin (34%) and fasting glucose (22%) compared to rats remaining on the cafeteria diet (Caf-Caf). Caf-Caf rats had an elevated plasma corticosterone response to restraint stress compared to Ch-Caf rats indicating that acute but not chronic consumption of palatable cafeteria diet may protect against stress. Caf-Ch rats had increased corticotropin releasing hormone mRNA expression in the dorsal hypothalamus compared to Ch-Ch rats implying that removal of the palatable diet activated the HPA axis. The results were discussed in terms of the links between palatability of diet, obesity and stress.     

Neurological and stress related effects of shifting obese rats from a palatable diet to chow and lean rats from chow to a palatable diet

Rats exposed to an energy rich, cafeteria diet overeat and become obese. The present experiment examined the neural and behavioural effects of shifting obese rats from this diet to chow and lean rats from chow to the cafeteria diet. Two groups of male Sprague Dawley rats (n = 24) were fed either highly palatable cafeteria diet or regular chow (30% vs. 12% energy as fat) for 16 weeks. Half of each group (n = 12) was then switched to the opposing diet while the remainder continued on their original diet. The effects of diet switch on the response to restraint stress were assessed and rats were euthanised nine days after diet reversal. After 16 weeks of cafeteria diet, rats were 27% heavier than controls. Rats switched from chow to cafeteria diet (Ch–Caf) became hyperphagic and had increased dopamine D1, D2 and tyrosine hydroxylase mRNA expression in the ventral tegmental area (VTA) compared to rats switched from cafeteria to chow (Caf–Ch). Caf–Ch rats were hypophagic with significant reductions in white (16%) and brown (32%) adipose tissue mass, plasma leptin (34%) and fasting glucose (22%) compared to rats remaining on the cafeteria diet (Caf–Caf). Caf–Caf rats had an elevated plasma corticosterone response to restraint stress compared to Ch–Caf rats indicating that acute but not chronic consumption of palatable cafeteria diet may protect against stress. Caf–Ch rats had increased corticotropin releasing hormone mRNA expression in the dorsal hypothalamus compared to Ch–Ch rats implying that removal of the palatable diet activated the HPA axis. The results were discussed in terms of the links between palatability of diet, obesity and stress.     

Effect of pre- and postweaning nutrition on dietary induced obesity in B6D2F2 mice

Our purpose was to ascertain whether a phase of postnatal overfeeding would interact with preweaning litter size in influencing dietary induced obesity in mice. Male and female B6D2F2 mice, reared in small (Sm = 4), medium (Md = 8) and large (Lg = 12) litters were maintained on high fat (HF) or control diets (C) for 6 weeks, beginning at weaning. After a further 4 weeks on lab chow, all animals were fed a cafeteria diet for another 6 week period. Body weight at weaning indicated Lg less than Md and Sm animals. Lg animals gained more weight during the postweaning period but their body weight remained lower than the Sm. HF animals from all litter sizes consumed more calories and gained more weight than C animals. During the period of cafeteria feeding the Sm animals gained more weight than the Md and Lg. Although males were heavier than females, the sexes responded similarly to treatment. The postweaning dietary regimen had no effect on the weight gained in response to cafeteria feeding.     

Resocialisation of isolation-reared rats does not alter their anxiogenic profile on the elevated X-maze model of anxiety

Rats were reared from weaning either in isolation or in social groups for 30 days and their behaviour on the elevated X-maze was studied. Isolation-reared rats displayed an anxiogenic profile on the X-maze compared to socially reared controls. Resocialisation of isolation-reared rats for a further 30 days did not reverse this anxiogenic profile, and isolation of the socially reared rats for 30 days did not produce an anxiogenic behavioural profile, indicating that the differences observed may be a result of a permanent developmental change. The locomotor hyperactivity induced by isolation was specific to the rearing conditions. It remains to be determined what neurochemical events are involved in the sustained effects of rearing in isolation.     

Energy intake of rats fed a cafeteria diet

The proportion of lipid, carbohydrate and protein energy self-selected by male and female rats from a cafeteria diet has been studied for a 48-day period (36-day in female rats). The diet consisted in 12 different items and was offered daily, in excess and under otherwise standard conditions, to rats--caged in groups of three--from weaning to adulthood. Groups of control animals were studied in parallel and compared with the cafeteria groups. Cafeteria diet fed groups of rats ingested more energy and lowered their metabolic efficiency with age. Male rats ate more than females and increased their body weight even after female practically stopped growing. There was a wide variation in the aliments consumed each day by the cafeteria-fed rats. However, the proportion of lipid, protein and carbohydrate the rats ate remained constant. Male rats ingested more lipid than females. Carbohydrate consumption was constant in control and cafeteria fed groups of rats independently of sex. Protein consumption was higher in cafeteria rats than in controls, but the differences were not so important as with liquid. Fiber content of the cafeteria diet was lower than that of the control diet. The cafeteria diet selected by the rats was, thus, hypercaloric and hyperlipidic, with practically the same amount of carbohydrate than the control diet, slightly hyperproteic and, nevertheless, remarkably constant in its composition with respect to time. Cafeteria rats had a higher water intake than controls. All these trends were maintained despite the observed changes in the animals' tastes and their differential consumption of the ailments of the diet.     

Effects of age,sex, and prior body weight on the development of dietary obesity in adult rats

Adult male and female rats were fed either lab chow (Groups 2 and 3) or lab chow and an assortment of palatable supermarket foods (Group 1) during Days 1–60 of the experiment. All rats were maintained on only lab chow during Days 61–90. Group 1 and 3 rats were then given the supermarket diet during Days 91–150, while Group 2 rats continued on lab chow only. The rats fed the supermarket diet significantly more body weight than did the lab chow fed rats, and this dietary obesity was greater in the older rats (i.e., during the Days 91–150 of the experiment) than in the younger rats (Days 1–60). Male rats gained as much or more weight on the supermarket diet as did the females, but compared to the same-sexed chow fed rats females displayed greater weight gains than did males. Finally, during Days 91–150 Group 1 and 3 rats gained similar amounts of weight on the supermarket diet despite the fact that the Group 1 rats had previous experience with the diet and had been overweight as a result. The findings demonstrate that age and sex, but not prior experience with palatable foods and overweight, are important factors in the development of dietary obesity in adult rats. The similarity between dietary obesity and hypothalamic obesity with respect to these three factors is discussed.     

Early onset of obesity induces reproductive deficits in female rats

The incidence of obesity is increasing rapidly all over the world and results in numerous health detriments, including disruptions in reproduction. However, the mechanisms by which excess body fat interferes with reproductive functions are still not fully understood. After weaning, female rats were treated with a cafeteria diet or a chow diet (control group). Biometric and metabolic parameters were evaluated in adulthood. Reproductive parameters, including estradiol, progesterone, LH and prolactin during the proestrus afternoon, sexual behavior, ovulation rates and histological analysis of ovaries were also evaluated. Cafeteria diet was able to induce obesity in female rats by increasing body and fat pad weight, which resulted in increased levels of triglycerides, total cholesterol, LDL and induced insulin resistance. The cafeteria diet also negatively affected female reproduction by reducing the number of oocytes and preantral follicles, as well as the thickness of the follicular layer. Obese females did not show preovulatory progesterone and LH surges, though plasma estradiol and prolactin showed preovulatory surges similar to control rats. Nevertheless, sexual receptiveness was not altered by cafeteria diet. Taken together, our results suggest that the cafeteria diet administered from weaning age was able to induce obesity and reduce the reproductive capability in adult female rats, indicating that this obesity model can be used to better understand the mechanisms underlying reproductive dysfunction in obese subjects.     

Isolation-rearing retards the acquisition of schedule-induced polydipsia in rats

Rats were reared from weaning either in isolation or in social groups for 10 weeks and were then tested for the acquisition of schedule-induced polydipsia (SIP). Isolation-reared rats were impaired in the development of this behaviour when compared to socially-reared controls. This reduction in drinking was specific to this test situation. Home cage water consumption and drinking in the SIP test chamber without a schedule of food delivery were unaltered and home cage drinking following water deprivation was significantly higher in the isolates. Housing adult rats in isolation did not impair SIP. The locomotor hyperactivity induced by isolation was also specific to rearing conditions. The inverse relationship between water consumption on the last day of testing and plasma corticosterone levels observed in both the socially-reared and socially-housed rats was absent in both the isolation-reared and isolation-housed rats.     

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.     

Altered sympathetic activity during development of diet-induced obesity in rat

Sprague-Dawley rats developed diet-induced obesity (DIO) after 3 mo on a high-fat, high-sucrose diet (DIO diet), with associated increases in total body and interscapular brown adipose tissue (IBAT) lipid content. After 7 days on the DIO diet, rats had increased levels of tyrosine hydroxylase (TH; 34%), norepinephrine (NE; 34%), and NE turnover (94%; estimated by alpha-methyl-p-tyrosine inhibition of TH) in their IBAT compared with chow-fed controls. After 3 mo on the DIO diet, NE levels and/or turnover were reduced by 27-50% in aortas, hearts, and pancreata in obese rats. While IBAT NE turnover was normal, TH inhibition failed to increase the lipid content of IBAT in obese rats as it did in controls, suggesting a postsynaptic defect in basal NE-stimulated lipolysis in this thermogenically active tissue. When obese rats were switched from the DIO diet to rat chow for 3 days, NE levels remained depressed in their hearts (25%) and aortas (14%) but were increased by 36-45% in IBAT, pancreata, and white adipose tissue. NE turnover rates and/or constants were increased by 37-110% in hearts, aortas, pancreata, and IBAT of these obese rats while there were increased IBAT TH (20%) and dopamine-beta-hydroxylase (87%) activities compared with chow-fed controls. Therefore, sympathetic activity varied markedly as a function of both dietary composition and relative body weight during the development of DIO.     

Effects of diet and exercise training on thermogenesis in adult female rats

The effects of a cafeteria diet on body weight gain, food intake, resting metabolic rate (RMR) and the thermic effect of food (TEF) were compared in female Charles River albino rats that were either sedentary or exercise-trained. The food intakes of the exercise-trained rats on the cafeteria diet were increased to the same degree as those of the sedentary rats, however, they gained less body weight and body fat than sedentary controls. The exercise training increased RMR independent of diet, but differentially increased TEF in rats given the cafeteria diet. Conversely, sedentary rats on the cafeteria diet had significantly lower RMR, but their TEF were not different from control animals on lab chow. Thus, in addition to the direct cost of the exercise, training increased thermogenesis (RMR and TEF) which also helped prevent the dietary obesity which normally occurs with cafeteria diets.     

Brown adipose tissue response to cafeteria diet-feeding involves induction of the UCP2 gene and is impaired in female rats as compared to males

Noradrenaline-dependent brown adipose tissue (BAT) thermogenesis is activated by the cold and excess energy intake, largely depends on the activity of the uncoupling protein 1 (UCP1), and is mediated mainly through the beta3-adrenoceptor (beta3-AR). We investigated the expression of ucp2, a gene that encodes a putative UCP1-like uncoupling protein, along with that of ucp1 and beta3-ar, in the interscapular BAT (IBAT) of male and female rats chronically fed a cafeteria diet. After 3 months on this diet, male rats attained a 34% excess body mass and showed IBAT hypertrophy and increased IBAT thermogenic potential, in terms of both UCP1 and UCP2 mRNA expression (both by 1.6-fold), UCP1 protein expression (by 1.75-fold) and GDP binding to IBAT mitochondria (by 2.2-fold); female rats attained a larger excess body weight (50%) and their IBAT, although hypertrophied, showed no signs of increased thermogenic potential per gram of tissue. Interestingly, the IBAT of female rats was already activated compared to males. Treatment of mouse brown adipocytes in primary culture with noradrenaline also triggered a dose-dependent increase of the levels of UCP1 mRNA and UCP2 mRNA. Retroregulatory down-regulation of the beta3-AR mRNA levels was found in the two models used. The results support a physiological role for UCP2, along with UCP1, in rodent BAT thermogenesis.     

Effects of diet and handling on initiation of independent ingestion in rats

The present study examined the effects of dietary manipulation on the age of onset of weaning in rat pups. In Experiment 1, female rats were placed on a standard chow (SC) or high-fat (HF) diet 1 week following mating. Pups were weighed daily from birth to Day 12, then animals were placed into specialized cages for separate recording of food intake of pups and dams. Pups were offered the same diet as their dam, and food intake and body weight were determined twice daily until Day 25. The results demonstrated that pups reared by dams fed the HF diet initiated independent ingestion on Day 16, approximately 24 hr before pups reared by dams fed the SC diet. There were no differences in body weight in pups across the two diets. While few differences were noted across diets in pups' or dams' behavior, HF pups appeared to demonstrate a delay in the establishment of circadian patterns of food intake. In Experiment 2, all dams were maintained on an SC diet until the day after parturition. At that time, dams and litters were placed into specialized cages and divided into four groups: HF/HF, HF/SC, SC/SC, and SC/HF (dam's diet/pup's diet, respectively). The results demonstrated that dams given the HF diet had pups that initiated food intake approximately 2 days before the pups of dams given the SC diet. In addition, pups offered the HF diet, independent of the dam's diet, initiated food intake approximately 0.8 days prior to pups offered the SC diet. Further, by Day 12, HF dams had pups that were heavier than SC dams. The results suggest that the onset of weaning in rats is affected by maternal diet and the weaning diet available to the pup.     

Effects of sucrose, caffeine, and cola beverages on obesity, cold resistance, and adipose tissue cellularity

Rats consuming Coca-Cola and Purina chow ad libitum increased their total energy intake by 50% without excess weight gain. Their resistance to cold was markedly improved. These phenomena were characterized by significant increases in interscapular brown adipose tissue weight (IBAT) (91%), cellularity (59%), triglyceride content (52%), protein content (94%), and cytochrome oxidase activity (167%). In contrast, Coca-Cola consumption did not significantly affect the cellularity or triglyceride content of parametrial white adipose tissue (PWAT), although it slightly augmented PWAT weight. The effects of Coca-Cola on cold resistance, IBAT cellularity, and composition were entirely reproduced by sucrose, but not caffeine, consumption. Although caffeine also increased IBAT cellularity and composition, it significantly decreased the rate of body weight gain, PWAT weight, and adipocyte size. Moreover, it markedly inhibited adipocyte proliferation in PWAT thereby mimicking the effects of exercise training and food restriction (Bukowiecki et al., Am. J. Physiol. 239 (Endocrinol. Metab. 2): E422-E429, 1980). It is concluded a) that sucrose and Coca-Cola consumption improve the resistance of rats to cold, most probably by increasing brown adipose tissue cellularity, and b) that moderate caffeine intake might be useful for inhibiting proliferative activity in white adipose tissue, thereby preventing obesity.     

Refeeding after various times of ingestion of a low protein diet: effects on food intake and body weight in rats

Rats born of protein-deprived mothers were fed on a low protein (LP) diet (5% casein) from weaning. In each time sequence (0, 1, 3, 5, 8 and 16 weeks after weaning), 12 of them were refed on an isocaloric well-balanced diet (18% casein) for 2 weeks. Food intake, body and adipose tissue weights and protein efficiency ratio (PER) were measured in the refed rats as well as in 12 LP rats. At weaning and after one week, refed (RF) rats immediately increased their food intake. This increase was delayed at weeks 3, 5 and 8 occurred during the second week of refeeding only. At week 16, there was a significant decrease during the first week when compared with LP rats. Body weight increased regularly during each refeeding period without any significant augmentation of the proportion of adipose tissue. During all the experiment (except at week 16), PER in the RF group remained high (about 3 g body weight/g protein) during the first week of refeeding, and fell to 2.0-2.5 g/g during the second week. It was particularly significantly greater than that of the LP rats between week 3 and 5 where an important decrease was observed in this group (1.99 +/- 0.36 vs. 3.23 +/- 0.58 g body weight/g protein during the 1-3 weeks period). It appeared therefore that protein restriction during gestation and lactation in dams had no effect on the mechanisms controlling food intake of their offspring at weaning.(ABSTRACT TRUNCATED AT 250 WORDS)