+ All Categories
Home > Documents > Hyperphagia (Abstracts)

Hyperphagia (Abstracts)

Date post: 03-Jan-2017
Category:
Upload: truongbao
View: 213 times
Download: 0 times
Share this document with a friend
4
Appetite 1980, 1, 85-88 Hyperphagia (Abstracts) A round-table meeting at Leeds University, U.K., on 27 March 1979, convened by J. E. Blundell Investigation of food selection and meal parameters during the development of dietary induced obesity. PETER J. ROGERS and JOHN E. BLUNDELL (Psychology Department, Leeds University, Leeds LS2 9JT, U.K.). Adult female rats (Lister Hooded) offered bread and chocolate along with normal laboratory diet (Oxoid 41B) increased their food intake by 60% and energy intake by over 84%. After 120 days these animals weighed 116 g (49%) more than control rats fed only lab. diet. In more precise investigations the feeding of these animals was continuously monitored for 24-h periods at different stages during the development of the obesity. The foods (in crumb form) were presented separately in food cups (in the horne. cage) with each cup being fitted with a photocell device enabling the timings and duration of feeding visits to be recorded. The time spent at each cup was found to be highly correlated with the amount of the particular food eaten from that cup. For the analysis of meal patterns an interneal interval criterion of > 15 min established from log survivorship functions of non-feeding intervals was used. The hyperphagia seen on the first day of introduction of the varied diet was associated with an increase in both meal frequency and meal size. Subsequently, average meal size continued to increase and by day 30 accounted completely for the hyperphagia since meal frequency had decreased and was by then not different from that of animals feeding on the control diet (i.e. 12-13meals/day). Closer examination revealed that the increase in average meal size was due predominantely to the inclusion of a few large meals in the feeding pattern. These large meals were characterised by consumption of substantial amounts of at least two of the food items, whilst in contrast in the majority of all meals there was significant intake of only a single item. Analysis also showed that a meal in which one food type was preferred rarely followed or preceded a meal eaten mostly of that food type. Rate of consumption of both bread and chocolate was always higher than that of the control diet. Thus effects on feeding of the variety of this diet and the palatability of its individual items per se were evident in the behavioural analysis. Both these factors may contribute to the dramatic and persistent hyperphagia seen with the diet. Finally, when the obese rats were returned to the control diet they became hypophagic and rapidly lost weight-both meal size and frequency being decreased, though when compared to control rats feeding on the lab. diet only meal frequency was found to be significantly lower. Specific satiety and its influence onfeeding. BARBARA J. ROLLS, E. T. ROLLS and E. A. ROWE (Department of Experimental Psychology, University of Oxford, Oxford OXI 3UD, U.K.). While measuring the effects of satiety on lateral hypothalamic neurones which respond to the sight and/or taste offood in the alert behaving monkey, it was observed 0195--{i663/80/010085 + 04 $02'00/0 © 1980 Academic Press Inc. (London) Limited
Transcript
Page 1: Hyperphagia (Abstracts)

Appetite 1980, 1, 85-88

Hyperphagia (Abstracts)

A round-table meeting at Leeds University, U.K., on 27 March 1979,convened by J. E. Blundell

Investigation offood selection and meal parameters during the development of dietaryinduced obesity. PETER J. ROGERS and JOHN E. BLUNDELL (Psychology Department,Leeds University, Leeds LS2 9JT, U.K.).

Adult female rats (Lister Hooded) offered bread and chocolate along with normallaboratory diet (Oxoid 41B) increased their food intake by 60% and energy intake byover 84%. After 120 days these animals weighed 116 g (49%) more than control rats fedonly lab. diet.

In more precise investigations the feeding of these animals was continuouslymonitored for 24-h periods at different stages during the development of the obesity.The foods (in crumb form) were presented separately in food cups (in the horne. cage)with each cup being fitted with a photocell device enabling the timings and duration offeeding visits to be recorded. The time spent at each cup was found to be highlycorrelated with the amount of the particular food eaten from that cup. For the analysisof meal patterns an interneal interval criterion of > 15 min established from logsurvivorship functions of non-feeding intervals was used.

The hyperphagia seen on the first day of introduction of the varied diet wasassociated with an increase in both meal frequency and meal size. Subsequently, averagemeal size continued to increase and by day 30 accounted completely for thehyperphagia since meal frequency had decreased and was by then not different fromthat of animals feeding on the control diet (i.e. 12-13 meals/day). Closer examinationrevealed that the increase in average meal size was due predominantely to the inclusionof a few large meals in the feeding pattern. These large meals were characterised byconsumption of substantial amounts of at least two of the food items, whilst in contrastin the majority of all meals there was significant intake of only a single item. Analysisalso showed that a meal in which one food type was preferred rarely followed orpreceded a meal eaten mostly of that food type. Rate of consumption of both bread andchocolate was always higher than that of the control diet.

Thus effects on feeding of the variety of this diet and the palatability of its individualitems per se were evident in the behavioural analysis. Both these factors may contributeto the dramatic and persistent hyperphagia seen with the diet.

Finally, when the obese rats were returned to the control diet they becamehypophagic and rapidly lost weight-both meal size and frequency being decreased,though when compared to control rats feeding on the lab. diet only meal frequency wasfound to be significantly lower.

Specific satiety and its influence onfeeding. BARBARA J. ROLLS, E. T. ROLLS and E. A.ROWE (Department of Experimental Psychology, University of Oxford, Oxford OXI3UD, U.K.).

While measuring the effects of satiety on lateral hypothalamic neurones whichrespond to the sight and/or taste offood in the alert behaving monkey, it was observed

0195--{i663/80/010085 + 04 $02'00/0 © 1980 Academic Press Inc. (London) Limited

Page 2: Hyperphagia (Abstracts)

86 LEEDS ABSTRACTS

that the responses of these neurones became attenuated to the food on which the animalwas satiated (e.g. glucose), but continued to respond to other foods which had not beenused to produce satiety. The relevance of such specific satieties to human feeding hasbeen investigated.

Subjects rated eight foods and then ate one of the foods to satiety. Two and 20minafter the end of the meal all eight foods were rated again and it was found that at bothtimes the ratings for the food eaten had decreased significantly more than for the foodsnot eaten. The depression in rating was relatively specific to the food eaten, even if thefoods were of the same basic type (e.g. protein, carbohydrate, fat).

These findings are consistent with the view that, though working in conjunction withinternal satiety signals, external factors such as the sight, smell, taste and texture offoodprovide some degree of specificity to satiety. A normal function of specific satieties maybe to ensure that a good balance of nutrients is consumed. The finding implies,however, that because satiety is specific, over-eating may occur if a wide variety offoodsis readily available. To test this hypothesis the intakes of subjects offered a variety offood in succession during a meal were compared to intakes when the same food wasoffered throughout. Subjects ate a third more when offered sandwiches with fourdifferent fillings than when just one filling was available (p<O·OOl). In another studysubjects ate a third more when offered three different flavours of yogurt in successionthan when they were offered just one of the flavours (p < 0'01). Having a variety offoodsreadily available may contribute to the development of obesity because of thespecificity of satiety.

(Supported by the Medical Research Council.)

Persistent dietary obesity and regulatory challenges. E. A. ROWE and BARBARA J. ROLLSDepartment of Experimental Psychology, University of Oxford, Oxford OX1 3UD,U.K.

The provision of varied and palatable high energy foods leads to hyperphagia and anaccumulating positive energy balance in adult rats. Sedentary male hooded Lister rats,10 weeks of age, became obese when offered a mixed supermarket diet (i.e. crisps,biscuits, etc.) for 90 days. The obesity persisted when the high energy foods werewithdrawn and laboratory chow alone was available. After enforced weight reductionby dietary restriction, the experimental rats consumed quantities of chow whichreinstated the obesity. The elevated body weight was not simply due to increasedgrowth because 18 weeks after withdrawal of the mixed diet carcass analysis indicatedthat the experimental rats had a significantly higher percentage of body fat, but not fatfree solids, than the control rats. The development of the obesity was initiallyassociated with elevated fasting plasma insulin and glucose levels, but the levels ofglucose and insulin were not factors associated with the persistence of obesity.

When energy expenditure was increased through voluntary exercise in a runningwheel, female, but not male rats, developed dietary obesity. Although the obesitypersisted in sedentary females, the exercising female rats exhibited significant weightloss when the mixed diet was withdrawn. The effect of environmental temperature onthe development and persistence of 0 besity was investigated in rats housed at either19°C or 27°C. At both temperatures the experimental rats gained significantly moreweight than the controls kept at the same temperature; however, the controls housed at

Page 3: Hyperphagia (Abstracts)

HYPERPHAGIA 87

19°C became significantly lighter than those at 27°C. The rats housed at the lowertemperature lost slightly more weight than those at the higher temperature when themixed diet was withdrawn. At the higher temperature most ofthe elevated weight in theexperimental rats was accounted for by fat; at the lower temperature, although therewas a persistent increase in body weight and fat, much of the surplus weight wasattributable to an increase in fat free body mass. Thus changes in energy expenditurecan influence both the development and the persistence of dietary obesity.

(Supported by the Medical Research Council.)

Reversible obesity induced by "cafeteria" diets. NANCY J. ROTHWELL (Department ofPhysiology, Queen Elizabeth College, University of London W8 7AH, U.K.).

Feeding a varied diet utilising over 40 food items to adult rats results in hyperphagiaand excessive body weight gain. The hyperphagia results from an increase in the weightoffood eaten as well as the greater energy density of the cafeteria diet. Nutrient intakes(% total ME intake) on typical experiments is fat 44, carbohydrate 45, and protein 11.Excess weight gains of 60 g can be achieved in as little as 17 days on the cafeteria dietand all ofthe excess weight can be accounted for as fat. Withdrawal of the cafeteria dietresults in rapid loss of body fat and weight with an eventual return to control values.Short-term repetitive sequences of cafeteria feeding and recovery ("bouncing obesity")produces identical patterns of gain and loss with each "bounce".

Experimental hyperphagia and obesity-some anomalies. MICHAEL J. STOCK(Department of Physiology, Queen Elizabeth College, University of London, LondonW8 7AH, U.K.).

Excessive fat gains induced in mice by treatment with gold-thioglucose (GTG) ormono-sodium glutamate (MSG) are not necessarily due to hyperphagia and do notalways result in greater body weight gains. Mice treated with GTG are initiallyhyperphagic but thereafter eat no more than control animals whilst still maintaining ahigher rate ofbody energy retention. The excessive weight and fat gains ofGTG mice ismainly due to a fourfold increase in the efficiency of energy utilisation. MSG has noeffect on energy intake but causes a twofold increase in the efficiency of energyutilisation. The resultant increase in lipid deposition occurs at the expense of bodywater and protein and thus produces obesity (or adiposity) without an increase in bodyweight. The relevance of these findings to the concepts and definitions of hyperphagiaand obesity were discussed.

Role of taste in long-term control of food intake. DAVID A. LEVITSKY (Division ofNutritional Sciences and Department of Psychology, Cornell University, Ithaca, NY14853, U.S.A.). Currently on leave at the Dunn Clinical Nutrition Centre, Cambridge.

The role of "hedonically" positive and aversive taste was examined in a series ofstudies in rats. In a self-selection experiment, the addition of a bitter tasting, butpharmacologically inert substance, sucrose octacetate, had no effect on 24-h consump-

Page 4: Hyperphagia (Abstracts)

88 LEEDS ABSTRACTS

tion of calories and only a very small effect in depressing protein intake. It was alsofound that rats could detect the presence of SOA at concentrations far smaller thanwould affect their food preference.

In another study, an hedonically positive food, sucrose, was offered to rats inaddition to their regular food supply. When the regular food was a single compositediet, the addition of sucrose caused a small, but significant increase in 24-h caloricconsumption continually for a month. When the animals were self-selecting their dietfrom protein, carbohydrate, and fat sources, the addition of sucrose had no effect ontotal calories consumed, although it profoundly altered the consumption of thecarbohydrate. From these and other studies, we conclude that taste, per se, has a verysmall effect on the long-term consumption of calories.

Stress-induced eating; fact or fiction? T. W. ROBBINS and P. J. FRAY (PsychologicalLaboratory, University of Cambridge, Cambridge CB2 3EB, UK.).

Two questions were addressed; (1) can motivational states other than that of food­deprivation produce eating? (2) if there is non-specificity of motivation, can the eatingbehaviour induced by other states be considered as a "coping" response whichalleviates stress or anxiety?

Initially, evidence was reviewed from the animal and human literature indicatingthat eating may be elicited by a variety ofnon-specific stimuli and conditions, includingelectric shock, noise, novelty or stimulus-change, electrical stimulation of the brain,tail-pinch, social isolation and social facilitation, various drugs, and by the lesioning ofthe ventromedial hypothalamus, which, it was argued, produces non-specific be­havioural effects.

The role of anxiety-reduction as a possible means of motivation of such eatingbehaviour was then assessed. It was held that since anxiety-reduction per se cannotexplain the persistence of shock-avoidance behaviour in animals, it is unlikely to beable to explain the persistence of compulsive eating. In common with contemporarylearning theory, we emphasised the positive incentive properties of "avoidance"behaviour and suggested that compulsive eating is maintained not by anxiety­reduction, but by anticipatory changes in metabolism and by external incentivesaccompanying the eating response itself.

Received 3 August, 1979


Recommended