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PubMed1981

A neurochemical theory of appetite and weight changes in depressive states.

The literature concerning appetite and weight changes in depressive illness is reviewed. Diminished appetite and weight loss have for about 100 years been regarded as prominent symptoms of depressive illness. A tendency for some depressives to gain weight has also been recognized. About 85% of depressives lose weight and 15% gain weight. There appears to be a tendency for weight gain to be commoner in milder depressions. Carbohydrate craving is also described in association with some depressed states. The neurochemical control of appetite in health is surveyed. Norepinephrine appears to be necessary for the intake of food, and drugs which raise intrasynaptic levels of norepinephrine stimulate feeding. Serotonin seems to be associated with satiety and in experimental animals decreased intrasynaptic levels of serotonin produce carbohydrate hunger. The neurochemical control of appetite is discussed in relation to the amine theories of depression. A number of hypotheses are drawn from this discussion.

Adult↗
PubMed2007

Milnacipran, a serotonin and norepinephrine reuptake inhibitor, induces appetite-suppressing effects without inducing hypothalamic stress responses in mice.

Milnacipran, a selective serotonin (5-HT) and norepinephrine (NE) reuptake inhibitor, increases extracellular 5-HT and NA levels equally in the central nervous system. Here, we report that systemic administration of milnacipran (20-60 mg/kg) significantly suppressed food intake after fasting in C57BL6J mice. The appetite-suppressing effects of milnacipran were sustained for 5 h. Neither SB242084, a selective 5-HT2C receptor antagonist, nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite-suppressing effects of milnacipran. Milnacipran suppressed food intake and body weight in wild-type mice and in A(y) mice, which have ectopic expression of the agouti protein. Moreover, milnacipran significantly increased hypothalamic proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels, while having no effect on hypothalamic neuropeptide Y, ghrelin, corticotropin-releasing hormone (CRH), and suppressor of cytokine signaling-3 mRNA levels. Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. The appetite-suppressing effects of milnacipran had no effects on food intake in food-restricted, wild-type mice and A(y) mice. On the other hand, fenfluramine suppressed food intake in food-restricted wild-type mice, but it had no effects in food-restricted A(y) mice. These results suggest that inhibition of 5-HT and NA reuptake induces appetite-suppressing effects independent of 5-HT2C and 5-HT1B receptors, and increases hypothalamic POMC and CART gene expression without increasing plasma corticosterone and blood glucose levels in mice.

Adrenergic Uptake Inhibitors↗
PubMed1999

Neuropeptide Y restores appetite and alters concentrations of GH after central administration to endotoxic sheep.

The objective of this study was to determine whether neuropeptide Y (NPY) and recombinant human interleukin-1 receptor antagonist (IL-1ra) would: first, increase food intake; secondly, decrease concentrations of GH; thirdly, reduce GHRH-induced release of GH; and fourthly, reduce changes to concentrations of IGF-I in plasma during experimental endotoxemia in sheep. Six treatments were given to six castrated male sheep in a 6x6 Latin square treatment order. Osmotic mini-pumps were implanted at 0 h and a jugular vein was cannulated. Each sheep was continuously infused with saline (0.9%) or lipopolysaccharide (LPS) (20 micrograms/kg per 24 h, s.c.) at 10 microliters/h for 72 h via the osmotic mini-pumps. Blood samples (3 ml) were collected at 15-min intervals from 24 to 33 h. At 26 h, one of three treatments (artificial cerebrospinal fluid, NPY or IL-1ra) was injected i.c.v. within 30 s (0.3 microgram/kg), then infused i.c.v. from 26 to 33 h (600 microliters/h) at 0.3 microgram/kg per h. GHRH was injected i.v. (0.075 microgram/kg) at 32 h after which blood samples were collected at 5, 10, 15, 30, 45 and 60 min. Feed intake was reduced up to 50% for 48 h in LPS-treated compared with non-LPS-treated sheep. NPY restored feed intake in LPS-treated sheep and induced hyperphagia in non-LPS-treated sheep from 24 to 48 h. In contrast, IL-1ra did not affect appetite. Injection of NPY increased concentrations of GH from 26 to 27 h, while IL-1ra had no effect. Infusion of NPY suppressed GHRH-induced release of GH. However, no treatment altered pulse secretion parameters of GH. Concentrations of IGF-I were 20% higher at 72 h in LPS-treated sheep given NPY than in sheep treated with LPS alone, and this may reflect increased appetite from 24 to 48 h. We concluded that reduced appetite during endotoxemia is due to down-regulation of an NPY-mediated mechanism. Furthermore, NPY stimulates release of GH in healthy sheep, does not reduce pulse secretion parameters of GH, but does suppress GHRH-induced release of GH in endotoxic sheep. Therefore, NPY may be an important neurotransmitter linking appetite with regulation of GH during endotoxemic and healthy states in sheep.

Animals↗
PubMed1990

A controlled trial of megestrol acetate on appetite, caloric intake, nutritional status, and other symptoms in patients with advanced cancer.

This double-blind, cross-over trial was designed to assess the effects of megestrol acetate (MA) on cancer-induced cachexia. Forty consecutive malnourished patients with advanced non-hormone-responsive tumors receiving no antineoplastic treatment were randomized to receive MA 480 mg/day versus placebo for 7 days. During day 8, a cross-over was made until day 15. Appetite, pain, nausea, depression, energy, and well-being were assessed with a visual analog scale (0 to 100 mm) at 9:00 AM and 4:00 PM during days 6, 7, 13, and 14. Weight (W;kg), tricep skinfold (TS; mm), arm circumference (AC; cm), and calf circumference (CC; cm) were measured at days 1, 8, and 15. Caloric intake (CI; Kcal/day) was determined during days 6, 7, 13, and 14. In 31 evaluable patients, the percentual difference in appetite at 9:00 AM, appetite at 4:00 PM, energy, and well-being after MA was +15.1, +14, +3.2, and +5.2, versus -12 (P = 0.03), -5.1 (P = 0.015), -10 (P = 0.024), and -8.3 (not significant) after placebo. Percentual difference in W, TS, AC, and CC after MA was +0.2, +1, -0.1, and +0.4 versus -0.8 (P = 0.03), -0.8 (P = 0.001), -0.3 (not significant), and -0.5 (P = 0.04) after placebo. CI during MA was 3480 +/- 1574 (48-hour intake), versus 2793 +/- 1542 (P less than 0.001) during placebo. Patients and investigators blindly chose MA in 20 (66%, P = 0.023) and 28 cases (92%, P less than 0.001), placebo in eight and two cases, and made no choice in three and one cases, respectively. Toxicity consisted of mild edema and nausea in three and two cases, respectively. After mean follow-up of 27 +/- 13 days, on an open basis, an average increase in W and AC of 4.8 +/- 1.7 kg and 2.8 +/- 1.7 cm was observed, respectively. The authors conclude that MA is a powerful appetite stimulant with subjective and objective effects on nutritional status.

Appetite↗
PubMed1993

Salt appetite consequent on sodium depletion in the suckling rat pup.

The ontogeny of the behavioral ability to compensate for sodium deficit was studied in the rat. The experiments showed that: 1) Before weaning age, sodium-depleted pups will increase their avidity for 3% NaCl solution; 2) the ability to select and drink a salt solution in response to a sodium deficit continues to evolve between 17-24 days of age, and that pups at these ages will modify their intake of salt and water as do adult rats when rectifying plasma osmolality; 3) The increased appetite for sodium is evident even when depleted preweanlings are dehydrated and provided with solid NaCl tablets to lick, showing that sodium appetite and hydrational status are already dissociated at this age; and finally, 4) sodium depletion first induces an increase in intake of orally infused 3% NaCl solution in 12-day-old pups. The picture of the development of salt appetite in the suckling rat that these findings present is of a precocious competence to meet a challenge to sodium homeostasis. In this respect salt appetite emerges in parallel to the other ingestive behaviors.

Animals↗
PubMed1997

Absence of a salt (NaCl) preference or appetite in sodium-replete or depleted kittens.

Many omnivores and herbivores exhibit an appetite for sodium or salt (NaCl) solutions, but a similar sodium appetite has not been demonstrated in carnivores. The choice for or against sodium-adequate diets of sodium-replete and depleted kittens (confirmed by an elevated plasma aldosterone concentration) was examined using a two-bowl choice test. Both bowls contained purified diets, one bowl with one of various levels of sodium (as NaCl) and the other bowl a sodium-deficient diet (0.1 g Na/Kg). Neither sodium-replete nor depleted kittens showed a choice of the diet containing 2 g Na/kg over the deficient diet. Both groups of kittens showed significant aversion to a diet containing 10 g Na/kg diet, with no change in total food intake. Kittens previously exposed to a diet containing 10 g Na/kg diet appeared to have a learned aversion to sodium in subsequent choice tests. We conclude that kittens do not possess an innate sodium appetite and that a sodium appetite is not induced in sodium-depleted kittens.

Animals↗
PubMed2002

Posttraining glucocorticoid receptor agonist enhances memory in appetitive and aversive Pavlovian discrete-cue conditioning paradigms.

Glucocorticoid modulation of emotional memory has repeatedly been shown in aversive learning paradigms, but has received little attention in appetitive tasks. It has also been suggested that it may be selective for contextual cues. In order to investigate if glucocorticoids can modulate memory in discrete-cue conditioning of both appetitive and aversive tasks, two experiments were carried out. Male Lister-Hooded rats received pairings of an auditory cue and either food-reward (experiment 1) or footshock (experiment 2), followed immediately by posttraining injections of the glucocorticoid receptor agonist dexamethasone (0.3, 0.6, and 1.2 mg/kg) or vehicle. Dexamethasone (1.2 mg/kg) led to significantly enhanced learning. These results give support to the notion that glucocorticoids play a role in the modulation of both appetitive and aversive emotional memories and show that their role in learning goes beyond the construction of context representations. The modulation of appetitive and aversive discrete-cue learning may be subserved by a common mechanism.

Animals↗
PubMed1990

[Central nervous appetite regulation: mechanisms and significance for the development of obesity].

This review focuses on neurotransmitter and neuropeptide actions on food ingestion, as well as on some of the mechanisms that may lead to the development and maintenance of obesity. In particular, the role of hypothalamic amines (catecholamines, serotonin) in appetite control is described. Thus, hypothalamic noradrenaline appears to stimulate food intake, while an enhanced brain serotonergic neurotransmission leads to a suppression of food ingestion, preferentially of carbohydrate intake. The involvement of brain serotonin neurons in appetite control is most attractive, since serotonin synthesis and release is readily affected by either precursor loading (i.e., 1-tryptophan) or pharmacological manipulation (e.g., drugs such as fenfluramine or fluoxetine). Recent data now suggest that at least a subgroup of obese patients is characterized by a disturbed serotonergic neurotransmission, thus exhibiting behaviors such as carbohydrate craving. Among neuropeptides involved in appetite control, the most attractive candidate appears to be corticotropin-releasing hormone which is released by neurons of the paraventricular nucleus and produces a stress-like activation of the organism, and has a strong appetite-suppressant effect.

Appetite↗
PubMedDate not supplied

The effects of uncontrollable, unpredictable aversive and appetitive events: similar effects warrant similar, but not identical, explanations?

Exposure to uncontrollable, unpredictable appetitive events produces a variety of cognitive debilitations and vegetative changes, as does exposure to uncontrollable, unpredictable aversive events. Similarities include impaired escape from aversive events, impaired discrimination, finicky consumption, analgesia, and body weight loss. However, in stark contrast, uncontrollable aversive stress causes reduced motor activity where as similar appetitive treatment does not; aversively induced debilitation is causally related to energy regulation, whereas the appetitively induced effects are not. Parallel mechanisms are suggested to explain these effects in terms of a revised anxiety account of the aversive effects, and a frustration account of the appetitive effects. Finally, factors likely to limit important research to resolve the many remaining issues are identified: negative presentation of animal research, political decision making, and ignorance and fear in committees which review the ethics of research.

Animals↗
PubMed2004

The cannabinoid CB1 receptor antagonist SR141716A reduces appetitive and consummatory responses for food.

RATIONALE: The CB1 receptor antagonist SR141716A reduces food intake in rats. This effect is likely to depend on modulation of reward related processes. OBJECTIVE: To investigate the effects of SR141716A on responding for food under a second order instrumental task in which responding and consumption of food can be separated, and on Pavlovian responding for a stimulus predictive of food reward. METHODS: Instrumental responding and pellet consumption following administration of SR141716A (0-3 mg/kg) were recorded under an FI5 min FR5(5:S) operant schedule that incorporates both a 5 min initial appetitive phase and a 25 min consummatory phase. We compared the drug-induced change in responding to that recorded following a reduction in motivational state induced by pre-feeding. In a second experiment we assessed the effects of SR141716A (0-3 mg/kg) on Pavlovian approach behaviour for a stimulus (lever) associated with food reward (CS+) and a neutral stimulus (lever) not associated with reward (CS-). RESULTS: SR141716A reduced pellet consumption and instrumental responding during both the appetitive and consummatory phases of the second order schedule. Pre-feeding had a similar effect on responding during the appetitive phase, suggesting an effect on incentive motivation. SR141716A also blocked an enhancement of responding that occurred during the consummatory phase in pre-fed animals. SR141716A and pre-feeding had no effect on responding in the Pavlovian autoshaping paradigm. CONCLUSIONS: SR141716A impacts on motivational processes in both the appetitive and consummatory phases of feeding behaviour.

Animals↗
PubMed2006

Assessing appetitive and consummatory phases of ethanol self-administration in C57BL/6J mice under operant conditions: regulation by mGlu5 receptor antagonism.

RATIONALE: The development of mouse models of ethanol consumption and ethanol-seeking behavior is of particular importance in understanding the underlying mechanisms of drug abuse because these models can enable an analysis of an effect of specific genotype on drug-seeking behavior and the interaction of potential therapeutics with genotype. However, there are some limitations with present models, notably the inability to examine appetitive and consummatory behavior separately. MATERIALS AND METHODS: In the present study, C57BL/6 mice were trained to self-administer 10% ethanol in a modified operant protocol that allowed a clear delineation of consummatory and appetitive phases. The utility of this procedure was confirmed with the use of the metabotropic glutamate 5 (mGlu5) receptor antagonist 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]-pyridine (MTEP). RESULTS: Limited-access consumption during the dark phase of the light-dark cycle with intermittent access (every second or third day) led to a high level of consumption by the mice. MTEP caused a dose-dependent decrease in both the consumption of ethanol and the appetitive response for ethanol. Furthermore, this effect was unrelated to any effect of MTEP on locomotor activity. CONCLUSIONS: The model provides a useful paradigm for examining both the appetitive and consummatory phases of ethanol consumption in mice; furthermore, the data indicate mGlu5 receptors are involved in both phases.

Alcohol Drinking↗
PubMed1999

Tonically active neurons in the monkey striatum do not preferentially respond to appetitive stimuli.

The tonically active neurons in the monkey striatum respond to stimuli presented during the performance of appetitively motivated behavior. To test whether these neurons are selectively responsive to the appetitive properties of stimuli, we studied their responsiveness to three different stimuli presented in an unsignalled manner to monkeys not performing any behavioral tasks: (1) an appetitive liquid, eliciting licking movements; (2) an aversive air puff directed towards the face, eliciting eyelid closure and facial movements; (3) a neutral sound, eliciting no overt behavioral reactions. The great majority of the tonic striatal neurons tested in two monkeys showed pronounced responses to the delivery of liquid (338 of 388 neurons, 87%) or the onset of the air puff stimulus (168 of 204, 82%). In contrast, few neurons (15 of 68, 22%) were modulated by the sound. The majority (80%) of the neurons tested with appetitive and aversive stimuli (n=189) responded to both types of stimulus. The characteristics of neuronal responses to the liquid were generally not similar to those described for the air puff in terms of response pattern and response duration. This suggests the existence of differences in the encoding of the affective significance of stimuli. It is concluded that tonic striatal neurons might function to differentiate stimuli that are important to the animal from those that are not, regardless of the specific motivational attributes of relevant stimuli.

Animals↗
PubMed1993

Forebrain lesions that disrupt water homeostasis do not eliminate the sodium appetite of sodium deficiency in sheep.

Brain structures located within the anterior wall of the third brain ventricle (subfornical organ, median preoptic nucleus and organum vasculosum of the lamina terminalis) are known to be involved in thirst as well as other aspects of body fluid and electrolyte balance. The present studies evaluated the role of these structures in the Na appetite of mildly or moderately Na-depleted sheep (sheep with a parotid fistula deprived of Na solution for 22 or 46 h). In addition, the role of these structures was tested in mildly Na-depleted sheep in which the Na appetite was enhanced by decreasing cerebrospinal fluid and brain extracellular fluid Na concentration (i.e., i.c.v. infusion of hypertonic saccharide solution) or was decreased by systemic infusion of hypertonic saline. The results indicated that sheep with lesions which reduced or eliminated daily water intake or water intake in response to hypertonicity of body fluids had, in all situations tested, appropriate changes in Na appetite (i.e., similar to their prelesion changes). Thus, the present experiments demonstrated that the brain areas involved in thirst as well as other aspects of body fluid and electrolyte balance are anatomically different from those involved in regulating Na appetite.

Animals↗
PubMed1986

Sex differences in appetitive learning of mice.

Learning abilities of male and female ddY mice were compared in two appetitive tasks (a lever-press task and an 8-arm radial maze task), and two avoidance tasks (a shuttle box task and a light-dark discrimination T-maze task). In the two types of appetitive learning, male mice were significantly superior to female mice. Sex differences were particularly apparent in the acquisition process. In contrast, there was no significant sex difference in learning of the two avoidance tasks. A sex difference in appetitive learning was not found in juvenile mice prior to sexual maturation, and the mice which had established a lever-press response as juveniles did not show any significant difference in the performance level when tested as adults. Thus, a sex difference appeared only in the acquisition stage of adult mice. These results suggest that there exists a sex difference in motivation level for hunting food but not for feeding, and that it causes a sex difference in appetitive learning.

Aging↗
PubMed1995

Sympathetic nervous system influences salt appetite in four strains of rats.

Sodium appetite and preference were examined in four rat strains using a social stressor and drugs to block sympathetic nervous system (SNS) activity. We have studied these strains for over 14 yr in our laboratory and the SHR strain has increased blood pressure and increased sympathetic nerve activity. The F1 crosses produce male offspring with the Y chromosome from a hypertensive or normotensive father, to examine its influence on sodium appetite. The pharmacological manipulation produces blockage of the SNS which may be partially responsible for stress induced sodium appetite. The objectives were to determine: (i) if the SNS was necessary for stress induced increased salt appetite; and (ii) if the Y chromosome from a hypertensive father increased salt intake or preference. Four strains (n = 6-8/group) of male rats were studied from 3-6 mo of age: normotensive Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHR) and hybrid crosses between a WKY mother and SHR father (WS) and the reciprocal cross (SW). Each group consumed Purina rat chow (0.3% Na) and was given a four-bottle choice of salt water ad lib (0.0%, 0.5%, 1.0%, and 1.5% NaCl). Social stress produced by intruder males significantly increased salt intake in all groups. SHR had higher salt intake than WKY both before and after exposure to intruder stress. In general, the SHR group preferred twice the concentration of saline (1.0%) as did the WKY (0.5%). Clonidine and reserpine both reduce SNS activity and consequently reduced salt intake after stress, from 20-44% depending on the genetic background of the rat strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Brief preoperative exposure to saline protects rats against behavioral impairments in salt appetite following central gustatory damage.

Adult rats who receive large electrolytic lesions at the level of the thalamic taste relay display impairments in taste related behavior, specifically the appetite for salt that results from changes in sodium balance. However, if the rats are given preoperative experience of ingesting a salty taste they are protected against these impairments in salt appetite that result from the lesion. In the present study we found that a brief (30 s) preoperative exposure to saline is sufficient to protect adult rats against expected deficits in salt appetite that normally result from central gustatory damage at the level of the thalamic taste relay. It is becoming increasingly clear that preoperative events can lessen the severity of the effects of brain damage. The results are discussed in the context of the appetite for salt, and preoperative immunization from behavioral deficits that result from brain damage.

Animals↗
PubMedDate not supplied

Comparing salt appetites: induction with intracranial hormones or dietary sodium restriction.

To raise a natural sodium appetite in the laboratory requires approximately 10 days on a very low sodium diet. Most other regimens induce sodium appetite more rapidly, but also result in behavioral or physiological changes not observed in the deprivation-induced state. We compared the characteristics of need-free sodium appetite induced either by systemic aldosterone combined with an intracerebroventricular (ICV) injection of angiotensin II or by a single ICV injection of renin with an appetite induced by 10 days of sodium deprivation. We measured the latency to drink water and 3% NaCl, as well as the amount of these fluids consumed at 30 min, 3 h, and 24 h. Angiotensin induced the shortest latency for both water and salt drinking, but the overall salt intake was lower. In 24 h, renin and sodium deprivation both induced about 14 ml of NaCl consumption, but the time course of the fluid intake differed for the two regimens.

Aldosterone↗
PubMed2006

A putative role for cytokines in the impaired appetite in depression.

Impaired appetite and weight changes are commonly seen in patients with depression, but the pathophysiology behind this imbalance between energy intake and energy expenditure remains largely unknown. The aim of this paper is to review the literature regarding a possible role for cytokines in the regulation of appetite and body weight, with special emphasis on depression. There now exists a substantial amount of evidence that depressed patients show signs of immune activation including increased levels of proinflammatory cytokines. Cytokines, which by themselves have anorectic properties, stimulate the release of the cytokine-like anorexogenic peptide leptin. In addition to their anorectic properties, both proinflammatory cytokines and leptin interact with the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic nervous system (SNS) and the immune system. In turn, these systems regulate energy balance as well as they are dysfunctional in depression. Furthermore, both proinflammatory cytokines and leptin can induce anhedonia, one of the cardinal symptoms of depression. In view of the different effects on appetite and/or body weight observed in melancholic versus atypical depression, we suggest that cytokines are differentially altered in these subtypes of depression, and that this may explain some of the inconsistency in the reported findings of cytokine as well as leptin levels in depressed patients. Finally, we propose that the immune system uses the interoceptive pathway projecting to the insular cortex, a brain region where cytokine-induced changes in appetite could be partly mediated, and that this pathway is activated in depression.

Animals↗