Cafeteria Feeding Research Articles

Cafeteria diet-induced sleep is blocked by subdiaphragmatic vagotomy in rats.

Feeding rats a cafeteria diet results in increased food intake and excess sleep. Furthermore, vagal afferent activity is altered by a variety of gastrointestinal factors, and vagal stimulation can induce sleep. We investigated, therefore, the hypothesis that the vagal nerve plays a critical role in mediating the sleep-inducing effects of cafeteria feeding. We examined the effects of a cafeteria diet on sleep, electroencephalographic (EEG) slow-wave activity (SWA), and brain temperature (Tbr) in control and vagotomized rats. EEG, electromyogram, and Tbr were recorded for 7 consecutive days. Day 1 was considered a baseline day; normal rat chow was available ad libitum. On days 2-4, the animals were fed, in addition to normal chow, a mixed, energy-rich diet (cafeteria diet). On days 5-7, the rats were again fed only normal rat chow. In control rats, the cafeteria diet resulted in an increase in non-rapid eye movement sleep (NREMS), which was the result of a significant lengthening of the NREMS episodes. In contrast, feeding vagotomized rats the cafeteria diet resulted in a decrease in NREMS. Cafeteria feeding decreased REMS and EEG SWA and increased Tbr in both control and vagotomized rats. These results suggest that an intact vagus plays a key role in the NREMS-inducing effects of the cafeteria diet.

Effects on energy utilization of a beta3-adrenergic agonist in rats fed on a cafeteria diet.

The antiobesity potential of a new beta3-adrenergic agonist (Trecadrine) was assessed in a cafeteria model of obesity through body composition, thermogenesis and oxygen consumption indicators. Animals fed on a cafeteria diet for 75 days increased body weight and fat content, while muscle mass as a percentage of body weight was reduced in relation to control fed rats. In addition, in vitro brown adipose tissue (BAT) and white adipose tissue (WAT) oxygen consumption was increased in these obese animals as compared with controls. Trecadrine administration reduced weight gain, BAT and WAT stores as well as the respiratory quotient, which was accompanied by an increase in WAT and BAT oxygen consumption and rectal temperature. Moreover, muscle mass as a percentage of body weight maintained the same values as non-obese animals, while an increase in absolute muscle weight was found in Trecadrine-treated obese rats. However, liver weights and in vitro oxygen consumption remained unaltered after cafeteria feeding and Trecadrine administration. Since chronic administration of Trecadrine had no effect on food intake, the stimulation of thermogenesis and oxygen consumption by the beta3-adrenergic agonist in white and brown adipose tissue are apparently responsible for the rise in energy expenditure as well as for the lower weight gain and fat deposition in obese treated rats. Thus, Trecadrine exhibits some promise as a potential treatment for obesity.

Damage from the Larkspur Mirid Deters Cattle Grazing of Larkspur

The larkspur mirid (Hopplomachus affiguratus) is host specific to tall larkspur (Delphinium barbeyi Huth). These insects suck cell solubles from leaves and reproductive racemes, causing flowers to abort and leaves to desiccate. Cattle generally prefer lark spur flowering heads, pods, and leaves, and are frequently poisoned. The objective of this experiment was to determine if cattle would avoid eating mirid-damaged larkspur. A 2-choice cafeteria feeding trial was conducted to determine preference for mirid-damaged and undamaged larkspur. Four cows were offered a choice of the 2 types of larkspur in 10 min. feeding trials in the morning and evening for 5 days. Cows preferred the undamaged larkspur plants (0.8 kg +/- 0.08, SE) over mirid-damaged plants (0.1 kg +/- 0.03, SE). The cows were then turned out into a larkspur-infested pasture and consumption of mirid-damaged and undamaged larkspur was quantified by bite count. The cows did not select any mirid-damaged larkspur. Consumption of undamaged larkspur peaked at 17% of bites on the second day of the grazing trial, then declined as mirid damage on the plants increased. If the density of mirids on larkspur is sufficiently high to damage most of the leaves and flowering racemes, grazing by cattle may be deterred, and subsequent poisoning avoided.

Consumption of a High Fat Diet Impairs Reproductive Performance in Sprague-Dawley Rats , ,

Rats made obese by cafeteria feeding have poor reproductive outcomes. To investigate this phenomenon in animals fed a more nutritionally adequate diet, female rats were fed either a high fat (HF) (modified AIN-76ATM, 35 g fat/100 g diet) or a control (C) (AIN-76ATM, 5 g fat/100 g diet) diet, beginning at 27 d of age. To assess reproductive performance, rats were studied at d 0, 5 and 18 of pregnancy and on d 3 of lactation. Pregnancy rates were significantly (P < 0.001) lower in the high fat–fed rats than in the control-fed rats (56.4 and 89.1%, respectively). There was no difference between groups in total pregnancy weight gain or the proportion of weight gained during pregnancy that was retained by the dam. High fat–fed dams tended to gain weight more rapidly early in gestation than control-fed dams and then less rapidly than control-fed dams during the last week of gestation. Litter number and pup weight at birth did not differ between groups, but of high fat–fed pups had significantly higher (P < 0.04) mortality rates than pups of control-fed dams (16.5 and 7.7%, respectively) over the first 3 d of life. Control-fed dams experienced the expected reduction (P < 0.05) in plasma insulin concentrations between the end of pregnancy and early lactation, but high fat-fed dams did not. Thus, physiological mechanisms controlling distribution of metabolic fuels may not be functioning properly in high fat–fed dams. Therefore, consuming a high fat diet reduces a rat's capacity to conceive and ability to maintain her litter during the perinatal period.

Changes in fatty acid composition in rat adipose tissue induced by dietary obesity.

The aim of the study was to evaluate the effects of cafeteria feeding on the composition of fatty acids in retroperitoneal fat pad and also to determine what happens to fatty acids when rats previously fed the cafeteria diet are returned to regular rat chow. The study of the post-cafeteria rats enabled us to determine the effects of dietary induced excess weight in the absence of artefactual interferences from the diet because these rats, unlike the cafeteria obese rats, ate the same diet as controls. In response to cafeteria feeding there were increases in the majority of adipose tissue fatty acids. However, significant decreases were observed in the relative proportions of 18:2n-6 and in two related n-6 polyunsaturated fatty acids (18:3n-6 and 20:3n-6), as well as in 16:1. In the post-cafeteria obesity model the previous dietary influence on fatty acid composition was still evident. The maintenance of both the high levels and proportions of 18:1 and the decrease of 16:1 percentage in the post-cafeteria rats argues in favour of an alteration in the activity of the elongation metabolic pathway. Certain changes affecting polyunsaturated fatty acid adipose depot composition of obese rats, mainly the decreased levels of 18:2n-6, are long lasting and could be related to the maintenance of the obese status. On the whole, although the fatty acid composition of adipose tissue is influenced by the composition of the diet, there are some differences in both the maintenance of the effects and also in the selectivity of adipose tissue for the different fatty acids of obese and lean rats.

The effect of cafeteria feeding on energy balance in lean and obese zucker rats

A 6-item cafeteria diet was given to 30-day lean and obese Zucker rats for two successive 15-day periods, the consumption of energy and metabolic substrates and different foods was compared with those of rats fed a standard reference diet. Cafeteria feeding and obesity had a partly superimposable effect on lean body mass and fat accrual. Rats' intake was grossly hyperlipidic when receiving a cafeteria diet, but their protein and total carbohydrate intake were similar in absolute terms to those of controls. More than half the carbohydrate sweet foods than lean animals. There was a direct relationship established between the amount of oligosaccharides consumed and the share of absorbed energy being deposited as fat. Both obesity and cafeteria feeding induced hyperphagia. The energy available (heat) in each group was, nevertheless, higher in cafeteria-fed obese rats than in those on the reference diet, but most differences were lost in obese rats when expressed as a function of LBM −0.75 (lean body mass). This uniform value was higher than that of lean rats on the reference diet, suggesting that the heat production per unit of lean body mass of obese rats was not influenced by diet. Heat production was maintained as a way to keep the thermal homeostasis of the rat within functional levels

Studies on mechanisms of hepatic insulin resistance in cafeteria-fed rats.

Whether hyperinsulinemia causes insulin resistance or vice versa is controversial. The development of hyperinsulinemia and insulin resistance was tracked in the cafeteria-fed rat to determine which occurred first. After 3 days of cafeteria feeding the rats were obese, manifested a small but significant decrease in fasting glucose levels, and showed no change in fasting insulin levels, basal hepatic glucose production (HGP), insulin binding to hepatic membranes, and glucose utilization during a euglycemic hyperinsulinemic clamp, but the rats did demonstrate an increased glucose disappearance rate associated with an enhanced insulin response to intra-arterial glucose and hepatic insulin resistance during the clamp. After 7 days of cafeteria feeding, the results were similar except that fasting hyperglycemia and hyperinsulinemia, an enhanced basal HGP, and decreased insulin binding developed. After 6 wk of cafeteria feeding, both hepatic and peripheral insulin resistances were present. After 7 days of cafeteria feeding in rats given streptozotocin or etomoxir, an inhibitor of free fatty acid (FFA) oxidation, hepatic insulin resistance persisted despite elimination of hyperinsulinemia and reduction of FFA oxidation. These data do not support a causal role for either hyperinsulinemia or enhanced lipolysis of hypertrophied fat stores and subsequent FFA oxidation in the liver in the development of hepatic insulin resistance in this animal model of obesity.

Body composition and brown adipose tissue in sedentary and active mice

The influence of exercise on body composition, brown adipose tissue (BAT) activity and energy balance was studied in young female CD1 Swiss albino mice. Mice were divided into 2 groups with different levels of activity; Sedentary Controls (SC) were housed in standard mouse cages while the Active (A) group had free access to activity wheels. All mice were fed stock diet and after 6 weeks (Stock Period), energy intake, body composition and BAT were analyzed in half of the mice. The remaining mice continued in their same activity groups but were encouraged to overeat by cafeteria feeding with highly palatable human foods. Energy intake, energy balance, body composition and BAT were again measured after 2 weeks (Cafeteria Period). The Active group spent considerably more time in physical activity and consumed 18% more kJ during the Stock Period than the Sedentary Controls. Despite different levels of exercise and food intake, both groups had similar carcass energy content and BAT activity during the Stock Period. The SC group increased energy intake by 52% in response to cafeteria feeding while the A group increased energy intake by only 28%. The SC mice accumulated significantly more carcass fat than the A mice during the Cafeteria Period; SC, 15.1±1.2% and A, 9.0±0.4% carcass fat. The Active mice were better able to maintain body weight and energy balance when fed an energy dense diet. BAT activity was increased by cafeteria feeding (diet-induced hyperphagia) but was not affected by exercise (activity-induced hyperphagia).

Sustained changes in blood alpha amino nitrogen compartmentation during recovery from cafeteria feeding in rats

We have previously reported that blood urea and blood cell amino acids levels are reduced in rats obese by feeding a palatable cafeteria diet. In order to distinguish whether these changes result from the altered diet, or from the obesity per se, we have studied cafeteria fed rats after returning to standard diet. As in previous studies, obesity induced by cafeteria feeding (for 90 days) was maintained when the cafeteria diet was removed and rats were fed standard diet only. After removal of the cafeteria diet, blood urea levels of 24 h starved obese rats were lower (23%) than those of starved control rats. Blood cell amino acid levels of obese were lower than control ones from day 50 onwards, during and after cafeteria feeding (21% lower on day 100 of life), and thus coincided with divergence of body weights; these differences were maintained despite removal of cafeteria diet. The effects of starvation on plasma amino acid levels were more marked in obese than control rats, during and after cafeteria feeding. Thus the effects on blood amino acids and urea levels in cafeteria diet induced obese rats are related to the obese status rather than to the diet composition.

Effect of selection for growth, body composition and food intake in mice: Utilization of increased energy intake by “cafeteria” feeding

Genetic differences in energy partition, in response to increases in levels of energy intake in excess of maintenance, were investigated in mouse lines selected high (H) or low (L) for either: 4–6-week food intake, corrected for 4-week body weight (A); fat content (F); total lean mass (P); or 8–10-week food intake corrected for mean 8 and 10-week weight (M). In each line, either a varied high energy food of stock diet, walnuts and cheese (cafeteria) or stock diet alone (control) was fed ad libitum during the period from 4 to 6 weeks of age, an age interval representing the period of fastest growth. In general, cafeteria feeding resulted in increased energy intake, weight gain, basal metabolic rate and fat deposition, in all lines. The cafeteria-fed AH line mice ate more and had higher basal metabolic rate than their counterparts in the AL line. The FH line gained most in proportion to body weight and deposited the most fat of all the lines on the cafeteria diet. The PH line had the highest absolute increase in growth and had a lower basal metabolic rate, in relation to body weight, than the PL line. The MH and ML lines had similar food intake and body weight, but MH had a higher metabolic rate than ML. These results show that there is physiological variation in the partitioning of feed energy between the different populations, with a tendency for increase in efficiency in the PH line mice with increased energy intake.

Estrous cycle irregularities in overfed rats

Hypothalamic and genetic obesities in rodents are usually associated with reproductive impairments, but the underlying etiology of the latter is not clear because of concomitant metabolic abnormalities in these animal models. In the present study metabolically intact rats were used and obesity was developed by offering the rats a cafeteria-type diet. Purina chow-fed animals were used as control. Cafeteria feeding was associated with hyperphagia and an increased brown adipose tissue (BAT) thermogenesis, in association with long estrous cycles ( p<0.01). The latter was accounted for by a long diestrous phase ( p<0.02). Replacement of the cafeteria diet with purina rat chow corrected the estrous cycle irregularities, as caloric consumption and body weight were reduced. We propose, as a working hypothesis, that reproductive functions are finely tuned with body temperature, and that an excess feeding-induced BAT thermogenesis may underlie the disruption in estrous cycle observed during overfeeding.

THERMOGENESIS AND THE EFFECT OF INJECTED CATECHOLAMINES ON THE OXYGEN CONSUMPTION OF CAFETERIA‐FED RATS

1. The oxygen consumption (VO2) of unrestrained rats given a 'cafeteria' (high energy, high fat) or control diet was studied. The resting values of VO2 were the same in each dietary group, whether maintained at 26 degrees C or 6 degrees C. This negative finding suggests that cafeteria feeding is not an important cause of diet-induced thermogenesis (DIT). 2. The response of each group of rats to injected noradrenaline or dopamine was also studied. Each catecholamine could increase VO2 values but the response was much less in cold-adapted rats measured at 6 degrees C. In all experimental circumstances the dopamine response exceeded that of noradrenaline. There was no evidence that the cafeteria diet consistently increased the response to either catecholamine. 3. These results suggest that DIT cannot be equated with non-shivering thermogenesis (NST). Furthermore, it is suggested that dopamine would be a better agent for measuring the oxygen equivalent of NST, since it would stimulate the dopamine receptors as well as the alpha- and beta-adrenoreceptors of brown fat.

Reduced obligatory nitrogen loss in rats made obese by cafeteria feeding

Rats made obese by fat feeding have been shown to have a lower urinary mitrogen excretion when fasting than non-obese animals (1). However, it is not clear whether this reduced metabolism of protien is the effect (2) or the cause (3) of the obese state nor are its implications understood. We report here that the induction of obesity by cafeteria feeding in rats is also assosited with a lower fasting urinary nitrogen loss (FUNL) than relative to matched non-obese controls and that these changes are paralled by changes in obligatory nitrogen loss (ONL) of the animals when fed a protein free diet. Our results suggest that the reduced net nitrogen losses are a consequence of obesity and, since ONL is the dominant component of the protein requirements, that obese subjects may have a reduced protein requirement as well as a lower propensity to catabolise protein when fasting. Thus, the adiposity of the subject may need to be considered when estimates of protein requirement are made.

Stimulation of S14 mRNA and lipogenesis in brown fat by hypothyroidism, cold exposure, and cafeteria feeding: evidence supporting a general role for S14 in lipogenesis and lipogenesis in the maintenance of thermogenesis.

In liver, thyroid hormone rapidly induces S14 mRNA, which encodes a small acidic protein. This sequence is abundantly expressed only in lipogenic tissues and is thought to have some function in fat metabolism. In the euthyroid rat, we measured 20-fold higher levels of S14 mRNA in interscapular brown adipose tissue than liver. Furthermore, whereas in liver or epididymal fat, hypothyroidism resulted in an 80% fall in S14 mRNA, in brown fat the level of this sequence increased a further 3-fold. In all three tissues, the expression of S14 mRNA correlated well with lipogenesis, as assessed by 3H2O incorporation. Physiological activation of brown fat by chronic cold exposure or cafeteria feeding increased the concentration of S14 mRNA in this tissue and again this was accompanied by a greater rate of fatty acid synthesis. Overall, in liver and white and brown adipose tissue, S14 mRNA and lipogenesis were well correlated and strongly suggest a function of the S14 protein related to fat synthesis. These studies suggest that the S14 protein and lipogenesis may be important for thyroid hormone-induced and brown adipose tissue thermogenesis and that stimulation of these functions in hypothyroid brown fat is a consequence of decreased thyroid hormone-induced thermogenesis elsewhere.

Studies on the role of insulin in N metabolism changes in cafeteria-fed rats

The present work studies the serum insulin response to cafeteria feeding and the possible role of this hormone in the marked N retention induced by cafeteria feeding. Rats fed a cafetaria diet for periods of 10, 20 and 30 days showed a significant and progressive increase in serum insulin levels. In order to elucidate the possible intervention of this hormone in the marked N retention induced by cafeteria feeding we studied the changes in N metabolism in non-diabetic and streptozotocin-diabetic rats fed a cafeteria diet for 10 days. The amount of N ingested was the same in all experimental groups. Our results suggest that insulin is not absolutely indispensible in the N retention exhibited by cafeteria-fed rats, inasmuch as cafeteria feeding also promotes a decrease in N excretion in streptozotocin-diabetic rats. This is in accordance with the reduction in urea excretion and the activities (U/g liver) of the ureogenic enzymes in streptozotocin-diabetic rats fed a cafeteria diet.

Body composition in mice maintained with cyclic periods of food restriction and refeeding

The effect of cyclic periods of underfeeding and overfeeding on body composition and energy efficiency was investigated in adult female CD1 Swiss mice. Four groups of mice were studied for 8 weeks: 1) Controls, fed stock diet ad libitum, 2) Overfed, fed stock diet plus a varied selection of highly palatable human foods (cafeteria feeding), 3) Cyclic-fed, given restricted amounts of stock diet (80% of controls) and cafeteria diet on alternate weeks, and 4) Restricted, fed 80% of the food consumed by the controls. The restricted mice had lower body weight, carcass energy content and energy expenditure than the other groups. The overfed mice had increased energy intake, energy expenditure, food efficiency, carcass fat and energy stores. The cyclic-fed mice had higher food intake than the controls but lower intake than the overfed mice. The cyclic-fed mice had increased food efficiency, increased carcass fat and carcass energy compared to the controls but values were less than for the overfed mice. Carcass energy was 224±8 kJ, controls; 314±18 kJ, overfed; 277±14 kJ, cyclic-fed and 173±9 kJ, restricted mice. Carcass energy was highly correlated with total energy consumed (r=0.592, p<0.001). Both regular and periodic consumption of an energy dense diet did increase energy intake, energy efficiency and carcass energy stores. However, there was no evidence that repeated periods of food restriction and refeeding increased body fat stores.

Effect of Pre- and postweaning nutrition on dietary induced obesity in B6D2F 2 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 B6D2F 2 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 < 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.

Acetaminophen sulfation deficit in obese rats overfed an energy-dense cafeteria diet.

The current studies examine acetaminophen pharmacokinetics and biotransformation in obese animals for possible shifts in metabolic conjugation reactions. Obesity was produced in Sprague-Dawley rats with an energy-dense cafeteria feeding regimen. Acetaminophen half-life remained unchanged and apparent volume of distribution increased slightly in obese versus pellet-fed control rats following an ip dose of 287 mg/kg. However, obese animals exhibited lower plasma concentrations of acetaminophen sulfate and excreted less sulfate conjugate but more glucuronide conjugate in urine. Absolute clearance of acetaminophen from plasma was similar for both groups of rats but formation clearance of acetaminophen sulfate was lower and formation clearance of acetaminophen glucuronide and was higher than control in obese rats. Renal clearance of unchanged drug and both conjugated metabolites appeared to rise with the degree of obesity. The many parallels in acetaminophen disposition shared with the obese human show the overfed rat to be a promising model for metabolic and physiologic changes associated with human obesity.

Egg quality and hen performance responses to protein-calcium deficiency, cafeteria feeding, and cage density.

Single Comb White Leghorn (SCWL) hens were given feeds (2975 kcal ME/kg) that were marginally deficient in protein (15%) and calcium (3.0%). Negative control was as a mash, whereas an experimental mixture had the same formulation, but 5 of the 15% protein was soybean pellets in place of the meal and 2 of the 3% calcium was oyster shell flakes. A complete cafeteria system acted as a positive control and provided pellets, oyster shell, and a 10% protein-1% calcium mash (2975 kcal ME/kg) separately in a three-compartment trough. Feed treatments were imposed from 24 to 40 weeks of age on hens kept one and two/cage. Performance effects, because of the feed treatments, were not apparent until after 8 weeks of experimentation. Production was sustained by the pellet-oyster shell feed mixture when birds given the complete mash declined. Feeds had immediate effects on egg quality. Egg shell deformation and albumen Haugh values were highest with the complete mash and lowest for the cafeteria system, while the complete mixture was generally between these extremes. Hens kept two/cage consumed more feed than those one/cage and responded similarly to each treatment, but the reduced performance associated with increased density was not alleviated.

Thermogenesis and sympathetic activity in BAT of overfed rats after adrenalectomy.

Resting oxygen consumption was elevated by 30% in young rats fed a cafeteria diet compared with their chow-fed controls and by 22% in cafeteria-fed, adrenalectomized (ADX) rats compared with the ADX chow-fed group, but injection of propranolol reduced oxygen consumption in the cafeteria-fed animals and abolished these differences. Brown adipose tissue (BAT) mass was increased by cafeteria feeding, and the activity of the mitochondrial proton conductance pathway (assessed from purine nucleotide binding) was enhanced by adrenalectomy and by cafeteria feeding. Norepinephrine turnover in BAT (determined from the time-dependent loss of tissue [3H]norepinephrine specific activity) was increased by 105% in sham-operated, cafeteria-fed rats, by 142% in chow-fed ADX rats, and by 400% in cafeteria-fed ADX rats, compared with chow-fed controls. Cardiac norepinephrine turnover was elevated by 80% in sham-operated, cafeteria-fed rats, but unaffected by adrenalectomy. These data indicate that the enhanced thermogenesis and BAT activity induced by adrenalectomy in chow- or cafeteria-fed rats is due to increased sympathetic activity in the tissue.