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PubMedDate not supplied

[The role of orexines in appetite regulation].

Anorexia nervosa (AN) belongs to the group of eating disorders. Many different factors are taken into consideration as far as the origin of this disorder is concerned, among them: individual factors (genetic, biological), personality factors, sociocultural factors, family factors. Among the biological factors, the role of neuropeptides is considered. Last few years (1998) have resulted in the discovery of two neuropeptides--orexines OXA and OXB which--apart from being regarded as appetite stimulants--are also supposed to be responsible for the energy metabolism of an organism. Orexines, a.k.a. hypocretins, arise from the disintegration of their common precursor--the polypeptide: preorexine. Their name derives from the Greek word for appetite: orexis. The orexine A (OXA) is a 33 amino acid peptide consisting of 2 chains connected by the Cys 6--Cys 12 and Cys 7--Cys 14 bridges. It is a potential food intake and gastric juice secretion stimulant. The connecting bridges in OXA play a crucial role in the receptor OXA-1 activation. The orexine B (OXB) is a 28 amino acid peptide with no connecting bridges between the chains. It mainly plays a role in the energy metabolism of an organism and does not influence the secretion of gastric juice. The OXR-1 receptor is a selective receptor for OXA, while the OXR-2 receptor is not privileged for any of the two orexines--both of them can connect to it. Orexines are produced by a small number of hypothalamus neurons, mainly in the lateral hypothalamus (LHA), but also the posterior hypothalamus--the so-called "eating center". Orexines control: the wakefulness-sleep state, food intake (OXA over 100 times stronger than OXB) and the neuroendocrine system. Their discovery may help in understanding the mechanism of anorexia nervosa.

Animals↗
PubMed1996

Overconsumption as a cause of weight gain: behavioural-physiological interactions in the control of food intake (appetite).

There is an asymmetry in the operation of physiological processes that maintain body weight. The body exerts a strong defence against undernutrition and weight loss, but applies a much weaker resistance to overconsumption and weight gain. These principles influence how appetite control operates and this constitutes one form of vulnerability to weight gain. The expression of appetite is reflected in an episodic pattern of eating behaviour, the selection of dietary commodities and an associated profile of conscious sensations such as hunger, preferences, aversions and fullness. The onset and termination of eating episodes are subject to facilitatory and inhibitory physiological processes, and are held in place by strong environmental contingencies and habitual routines. Energy intake resulting from physiological and environmental control of behaviour is generally in balance with energy expenditure, although changes in energy expenditure do not inevitably trigger changes in food intake. Excess energy intake over expenditure may be due to aberrant positive drive to seek energy or a permissive response to strong external stimuli. The former could arise from a defect in a lipostatic regulatory system, and the latter from the weakness of inhibitory signals or from strong facilitatory responses to superpotent physical features of food. Taste and textural qualities of food give rise to hedonic responses via opioidergic and aminergic systems. Inhibitory responses to macronutrients include adjustment of gastric volume, rate of gastric emptying, release of cholecystokinin and enterostatin, and changes in plasma levels of products of digestion. These peripheral responses lead to a series of changes in brain neurotransmitter networks. Proteins, fats and carbohydrates generate different sets of physiological responses that produce different effects on the intensity and duration of satiety. The nutrient composition of food and the overall energy density influence control of meal size and post-ingestive inhibition. Particular sensory and nutrient combinations in foods can facilitate passive overconsumption. Overriding physiological satiety signals can lead to a positive energy balance and weight gain.

Animals↗
PubMed1989

Ontogeny of renin-induced salt appetite in the rat pup.

Intracerebroventricular injections of renin in suckling rat pups increased intake of NaCl solutions when they were orally infused 5 hr after injection. The appetite for saline solution was evident in pups as young as 3 days, was greater in females, and was specific insofar as intake of milk, either by suckling or by oral infusion, was not affected. Three-day-old pups increased intake only to 12% NaCl, the acceptable concentration of NaCl becoming lower in older pups. These results suggest, first, that, as is true for feeding and drinking, the brain mechanism for salt appetite is competent for expression of the behavior in the very young rat pup, and second, that its angiotensinergic neural substrate is distinct from that which mediates the dipsogenic effect of the hormone.

Animals↗
PubMed1991

The early presence of food-oriented appetitive behavior in developing rats.

The appetitive behavior of 3- to 6-day-old rat pups was studied by testing their ability to direct their ingestive behavior to a restricted food source. We found that, from 3 days of age, pups were able to feed efficiently from such a source. More specifically, pups that were deprived of nutrition but not of maternal care as well as pups that were dehydrated ingested significantly more than nondeprived animals, and did so whether liquid diet was spread over the entire floor surface beneath them or restricted to a fraction of the floor surface. However, pups that had been nutritionally and maternally deprived were not able to direct their feeding. The general locomotor activation of pups in this latter group appeared to interfere with their ability to direct their behavior to the restricted source. These results indicate that from early ages, developing rats possess the appetitive competence to guide their behavior and suggest that previous findings of poorly directed behavior were a confound of the behavioral activation shown by pups tested in a state of maternal deprivation.

Animals↗
PubMed1979

[Substrate and parasubstrate regulation of physiological processes at various levels of the organization of living systems as illustrated by examples of the regulation of appetite, of the specific dynamic action of food and of the inhibition of processes of absorption].

It was demonstrated that in the organism of higher animals the adaptation regulation of food uptake and nutrient absorption and transport comprises, in addition to the classic mechanisms of substrate regulation, specialized non-substrate and parasubstrate mechanisms which control the uptake of food and other substrates at all three levels (organosystemic, organic and cellular). As to the organosystemic level, it was observed in duodenectomized rats that appetite inhibition is produced not only by a stimulation of the receptors and by an increase in the concentration of the food substrates and of the metabolites in the blood, but also by one of the intestinal appetite-inhibiting hormones, arenterin. As to the organic level, it was evidenced that the enzymatic and transport functions of the small intestine and the numerical composition of the enterocyte population in the different segments are determined by the substrate load on the respective areas of the small intestine as well as by the blood and chyme-mediated intersegmental reactions in the small intestine. As to the tissular and cellular levels, the possibility of a regulation of the enzymatic and transport systems of the microvilli by means of substrates contained in the mucous membrane of the small intestine and endogenous substances (permein and antipermein) was evinced.

Adaptation, Physiological↗
PubMed2005

The hippocampus and appetitive Pavlovian conditioning: effects of excitotoxic hippocampal lesions on conditioned locomotor activity and autoshaping.

The hippocampus (HPC) is known to be critically involved in the formation of associations between contextual/spatial stimuli and behaviorally significant events, playing a pivotal role in learning and memory. However, increasing evidence indicates that the HPC is also essential for more basic motivational processes. The amygdala, by contrast, is important for learning about the motivational significance of discrete cues. This study investigated the effects of excitotoxic lesions of the rat HPC and the basolateral amygdala (BLA) on the acquisition of a number of appetitive behaviors known to be dependent on the formation of Pavlovian associations between a reward (food) and discrete stimuli or contexts: (1) conditioned/anticipatory locomotor activity to food delivered in a specific context and (2) autoshaping, where rats learn to show conditioned discriminated approach to a discrete visual CS+. While BLA lesions had minimal effects on conditioned locomotor activity, hippocampal lesions facilitated the development of both conditioned activity to food and autoshaping behavior, suggesting that hippocampal lesions may have increased the incentive motivational properties of food and associated conditioned stimuli, consistent with the hypothesis that the HPC is involved in inhibitory processes in appetitive conditioning.

Amygdala↗
PubMed1993

Chemosensory function, food preferences and appetite in human liver disease.

We evaluated chemosensory function, food preferences, and appetite in 88 patients with liver disease including those with hepatitis, cirrhosis, primary biliary cirrhosis, and sclerosing cholangitis. Reported chemosensory disturbances were common in the patients with liver disease: over 40% reported recent taste changes, and 27% reported recent changes in smell, compared to only 6% of healthy, age- and gender-matched controls with no history of marked chemosensory malfunction. Compared to controls, a greater proportion of liver patients reported food cravings (47 vs. 17%) and food aversions (33 vs. 16%). Foods with a predominantly bitter taste were specifically less preferred in patients with liver disease compared to healthy controls. Patients were also more likely to report poor to fair appetite than controls (37 vs. 5%). Groups of patients with different types of liver pathology showed varying patterns of food preferences, suggesting that dietary recommendations to liver patients might be tailored to the altered preferences associated with a particular type of hepatic dysfunction.

Adult↗
PubMed1998

Uncoupling the effects of energy expenditure and energy intake: appetite response to short-term energy deficit induced by meal omission and physical activity.

The effects of two methods of inducing an acute energy deficit (exercise and a low-energy breakfast) on appetite were investigated in 11 healthy females, all of whom were regular exercisers and regular breakfast eaters. There were four experimental days: with exercise and a high-energy (500 kcal) breakfast (EHB), exercise and a low-energy (64 kcal) breakfast (ELB), no exercise and a high-energy breakfast (NEHB) and no exercise and a low-energy breakfast (NELB). Hunger and moods were monitored each hour from 8 a. m. until 5 p.m. Energy and macronutrient intake were measured during an ad libitum lunch test meal 4 h after the exercise and breakfast. Heart rate was continuously monitored using the Polar sport tester. The low-energy breakfasts (ELB and NELB) led to increased hunger during the morning and an increase in energy intake at lunch compared with the high-energy breakfasts. Subjects also experienced significantly more food cravings after LBs than after HBs. Exercise failed to have any significant effect on these variables. Thus, two methods of inducing a short-term energy deficit had markedly different effects on appetite. The low-energy breakfast presumably fails to generate the inhibitory satiety signals induced by the 500 kcal breakfast, whereas the metabolic effects of an exercise session failed to generate excitatory signals to hunger and food intake.

Adult↗
PubMed1998

A behavioral economic analysis of fat appetite in rats.

A behavioral economic analysis of rats' consumption of various fat and sweet solutions was conducted in order to assess whether rats' fat appetite is readily modifiable. According to economic demand theory, changes in the price of a reinforcer will produce substantial changes in its consumption under conditions in which a substitutable reinforcer is available. Results from income-compensated price changes revealed that sucrose, mineral oil and saccharin solutions substituted for a corn oil solution: increases in the price of the corn oil led to large decreases in its consumption and sizable increases in consumption of these alternatives. On the other hand, plain water did not substitute for the corn oil solution: increasing the price of the corn oil did not result in nearly as marked a change in its consumption nor in consumption of the water. Neither the strength of preference for the corn oil under baseline conditions nor the caloric content of the alternative solution predicted whether the alternative reinforcer substituted for the corn oil. Rather, palatability appeared to be a dimension along which substitution was based. These results suggest that fat appetite is modified when palatable alternatives are available, independent of how strongly the fat is preferred.

Animals↗
PubMed1999

Chocolate craving and hunger state: implications for the acquisition and expression of appetite and food choice.

The importance of hunger state for the acquisition and expression of chocolate craving was investigated. Seventeen chocolate cravers and 12 non-cravers were supplied with chocolate and instructed to eat some twice a day for 14 days. Within each group, subjects were allocated to one of two conditions, hungry- or full-trained. Hungry-trained subjects were asked to eat the chocolate exclusively at least 2 h after last eating; full-trained subjects were asked only to eat the chocolate 15-30 min after eating a meal. A diary was kept to encourage and allow assessment of compliance. At the start and end of the 2 weeks, subjects rated their craving for and anticipated intake of chocolate prior to eating it; then, on initial tasting, pleasantness of the taste was rated. All subjects made these ratings on one day when hungry and on another when full, as defined above. For cravers and non-cravers who ate chocolate exclusively when hungry, chocolate craving increased post-training, but, at least for cravers, only when ratings were made while hungry. For full-trained subjects, chocolate craving decreased post-training, but this decrease did not depend on whether subjects were currently hungry or full. A similar pattern of results was found for anticipated intake and pleasantness of taste, except that pleasantness did not increase in hungry-trained subjects. The results are interpreted with reference to learned control of appetite and in particular to recent findings on incentive learning processes. Craving for chocolate or other foods may be an expression of a strong appetite elicited by hunger that has been acquired by repeated experience of eating the craved food when hungry.

Adult↗
PubMed1999

Greater appetite control associated with an increased frequency of eating in lean males.

Eight healthy males of age 22.9+/-4.2 years (mean+/-SD) and body weight 73.26+/-11.50 kg, with BMI of 23.11+/-2.84 kg/m(2)underwent two different eating meal frequency patterns on 2 separate days. On both days they were fed approximately 33.3% of their average daily energy requirements as a breakfast pre-load meal: served either as a single meal (SINGLE) or divided into five equal portions (served hourly) (MULTI). Five and a half hours after the initial meal, an ad libitum meal was served. Venous blood was tested to determine plasma glucose and serum insulin concentrations every hour until the ad libitum lunch, and at 15-, 45- and 75-min after lunch. Visual analogue scales (VAS) were completed every hour until the ad libitum lunch, and at 15-, 45- and 75-min after lunch as a measure to determine hunger, appetite and satiety indices. Although both groups were fed isocaloric and identical macronutrient "breakfast pre-loads" (3450+/-466 kJ), the SINGLE group consumed 26.6% more (p<0.02) energy in the ad libitum lunch (5111+/-1502 kJ vs. 3752+/-893 kJ) than the MULTI group did. The pre-load feeding pattern had no effect on blood glucose responses throughout the trial. Following the larger SINGLE pre-load, serum insulin concentration rose to a higher (p<0.01) level compared to the first of the MULTI pre-load meals (123.04+/-61.51 microIU/ml vs. 37. 30+/-26.65 microIU/ml SINGLE vs. MULTI, respectively). Serum insulin rose to a higher (p<0.01) level following the fifth and final of the MULTI pre-load meals compared to the serum insulin levels in the SINGLE group at the same time into the trial (74. 21+/-51.64 microIU/ml vs. 24.98+/-13.46 microIU/ml MULTI vs. SINGLE, respectively). Despite consuming more energy in the ad libitum lunch, the SINGLE group showed no difference in serum insulin concentration following the ad libitum lunch compared to the insulin response of the MULTI group. These data suggest that when the nutrient load was spread into equal amounts and consumed evenly through the day in lean healthy males, there was an enhanced control of appetite. This greater control of satiety when consuming smaller multiple meals may possibly be linked to an attenuation in insulin response although clearly both other physical (gastric stretch) and physiological (release of gastric hormones) factors may also be affected by the periodicity of eating.

Adult↗
PubMed2000

Effect of habitual dietary-protein intake on appetite and satiety.

To investigate whether appetite response to a high-protein test meal varies inversely with habitual protein intake, the satiating influence of dietary protein was investigated in 14 subjects. Subjects were divided into two groups on the basis of habitual protein intake: means of 1.0 g/kg/day (LP) and 1.4 g/kg/day (HP). Appetite was assessed in each group following high protein meals (test a). A 13-day period of dietary manipulation increased differences in protein intake between groups to a mean of 0.75 g/kg/day (LP) and 1.96 g/kg/day (HP) and a second satiety test (b) was performed. A third test (c) was performed in the HP group after protein intakes were reduced for 2 days to a mean of 0.85 g/kg/day. Differences in satiety were most marked, with significant correlations between satiety after the three meals and daily protein intake (r=-0.36). LP satiety was significantly greater than HP after test b (p=0.025), and approached significance when satiety response during LPb was compared with HPc (p=0.07). Results support the hypothesis that the satiating effect of dietary protein varies inversely with habitual protein intake.

Adult↗
PubMed2002

Appetitive instrumental learning is impaired by inhibition of cAMP-dependent protein kinase within the nucleus accumbens.

The medium spiny neurons of the nucleus accumbens receive a unique convergence of dopaminergic and glutamatergic inputs from regions associated with motivational, cognitive, and sensory processes. Long-term forms of plasticity in the nucleus accumbens associated with such processes as appetitive learning and drug addiction may require coactivation of both dopamine D1 and glutamate N-methyl-D-aspartate (NMDA) receptors. This notion implies that an intracellular mechanism is likely to be involved in these long-term neuroadaptive processes. The present series of experiments examined the effects of intra-accumbens microinfusion of protein kinase inhibitors on acquisition of an instrumental task, lever-pressing for food. Male Sprague-Dawley rats were bilaterally implanted with chronic indwelling cannulae aimed at the nucleus accumbens core. Following recovery, animals were food-restricted and subsequently trained for operant responding. The broad-based serine/threonine kinase inhibitor H-7 (5 or 27 nmol per side) dose-dependently impaired learning when infused immediately after testing on days 1-4. Rp-cAMPS, a cAMP-dependent protein kinase (PKA) inhibitor, also impaired learning regardless of whether it was infused immediately before (5 or 20 nmol) or immediately after (10 nmol) testing on days 1-4. Rp-cAMPS (10 nmol) also inhibited learning when infused 1 h after testing, though to a lesser extent than when administered before or immediately after testing. The PKA stimulator Sp-cAMPS (5 or 20 nmol) also impaired learning when infused before testing, suggesting that there is an optimal level of PKA activity required for learning. None of the drugs used produced nonspecific motor or feeding effects. These results provide evidence supporting the involvement of nucleus accumbens PKA in appetitive learning and suggest that this kinase may be involved in long-term changes associated with this and other motivationally based neuroadaptive processes.

Animals↗
PubMed1978

Increased feeding in rats treated with chlordimeform and related formamidines: a new class of appetite stimulants.

Low doses of the formamidine pesticide, chlordimeform (CDM) induce voracious daytime feeding in non-food deprived rats. Following CDM (10 mg/kg), food intakes were five times control intakes after 3 h and 1.1 times control intakes after 24 h. Other selected formamidines, such as the N-demethylated metabolite of CDM, and amitraz, increased 3-h food intake by two and five times control intake, respectively. Anorexia accompanied by excessive CNS stimulation was noted with higher doses of CDM (above 40 mg/kg) and other formamidines. This contrasts with the sedation usually observed with high doses of other structurally diverse appetite stimulants. In addition, hyperphagia was not observed with other CNS stimulants or local anesthetics such as amphetamine, cocaine, and holocaine. Thus the formamidines constitute a new class of appetite stimulants, which should prove to be useful agents for the study of feeding behavior.

Amidines↗
PubMed1982

The effects of chlorpromazine and lithium on appetitive discrimination learning in the rat.

Rats learned one of two appetitive discrimination tasks varying in terms of cognitive difficulty. Contrary to previous reports showing an impairment in the acquisition of avoidance tasks under the effects of either chlorpromazine (CPZ) or lithium, the results of this experiment indicate that neither drug retards the acquisition of appetitive tasks. Instead, at the highest doses used (2 and 3 mg/kg), CPZ decreased the number of trials required for the difficult task. Rats administered CPZ had longer reaction times than rats administered placebo, and therefore might have achieved criterion earlier because they spent more time in front of and on the discriminanda. The contrary results reported with avoidance tests concerning the effects of CPZ are explained in terms of the anxiety-reducing properties of CPZ, which might reduce drive without impairing cognitive ability.

Animals↗
PubMed1975

Salt appetite during the early phase of renal hypertension in rats.

In male Sprague-Dawley rats the left renal artery was constricted by a 0.2mm silver clip while the contralateral kidney was left untouched. 10 days after clipping the animals were offered, in addition to water, 0.9% saline as drinking fluid for 6 days. Hypertensive animals drank twice as much saline as did control rats throughout the period of observation. In the hypertensive animals, 24-hrs saline intake during the first day of the self-selection study was quantitatively related to the actual height of blood pressure and to the preceding blood pressure increase. After 6 days on the self-selection regimen, plasma angiotensin II concentrations in the hypertensive rats were elevated by 50% when compared with control rats. On the basis of these and previously reported findings (i.e. an increased activity of the renin-angiotensin-aldosterone system and sodium retention) it is suggested: a) despite sodium retention salt appetite is enhanced, indicating a disordered regulation of sodium balance during the early phase of renal hypertension in rats; b) elevated plasma concentrations of angiotensin II and aldosterone could have enhanced salt appetite; c) despite greater salt intake than in control rats the activity of the renin-angiotensin system remains elevated in renal hypertensive rats, thereby possibly inducing a sustained high saline intake.

Aldosterone↗
PubMed1975

Double blind cross-over study of a new appetite suppressant AN 448.

The effects of a new appetite suppressant, AN 448, and a placebo have been compared in 30 obese individuals using a fully randomized double-blind cross-over design. 1 mg of AN 448 t.i.d. produced a significant degree of appetite suppression and a mean weight loss of more than 4 kg per individual over a 6 week period. Side effects were few and no haematological, renal or hepatic damage was observed.

Appetite↗
PubMed1991

Is a serotonergic mechanism involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced appetite suppression in the Sprague-Dawley rat?

The major cause of TCDD-induced death in rats is a progressive voluntary feed refusal which has been correlated with reduced gluconeogenesis. Since centrally administered TCDD does not cause death or decreased feed intake in rats, the ability of TCDD to suppress appetite via peripheral mechanisms acting on the central nervous system was examined in two experimental models. First, it was found that the feed intake of rats on scheduled feeding cycles was not decreased by blood transfused from rats with TCDD-induced appetite suppression (8 days after a lethal dose of TCDD, i.p.). In contrast, a similar transfusion from normal, satiated rats did reduce feed intake of recipient rats by approximately 40%, suggesting that TCDD-treated rats are not satiated but rather that they are not hungry. In the second study tryptophan (the amino acid precursor of the neurotransmitter serotonin) was measured in the plasma and tryptophan, serotonin, norepinephrine and dopamine in the hypothalamus as well as dopamine and its metabolites in the striatum 4, 8, and 16 days after TCDD dosage (125 micrograms/kg, i.p.). Progressive time-dependent increases in tryptophan levels in plasma and brain were paralleled by increases in brain serotonin and 5-hydroxyindoleacetic acid (the primary metabolite of serotonin) in TCDD-treated rats. No changes were observed regarding the other biogenic amines. It is suggested based on these data and on substantial evidence from the published literature that a serotonergic mechanism may be involved in TCDD-induced feed intake reduction.

Animals↗