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At least 595 records · Page 33Linked to original sources
PubMed2005

Integration of endocannabinoid and leptin signaling in an appetite-related neural circuit.

Recently developed therapeutics for obesity, targeted against cannabinoid receptors, result in decreased appetite and sustained weight loss. Prior studies have demonstrated CB1 receptors (CB1Rs) and leptin modulation of cannabinoid synthesis in hypothalamic neurons. Here, we show that depolarization of perifornical lateral hypothalamus (LH) neurons elicits a CB1R-mediated suppression of inhibition in local circuits thought to be involved in appetite and "natural reward." The depolarization-induced decrease in inhibitory tone to LH neurons is blocked by leptin. Leptin inhibits voltage-gated calcium channels in LH neurons via the activation of janus kinase 2 (JAK2) and of mitogen-activated protein kinase (MAPK). Leptin-deficient mice are characterized by both an increase in steady-state voltage-gated calcium currents in LH neurons and a CB1R-mediated depolarization-induced suppression of inhibition that is 6-fold longer than that in littermate controls. Our data provide direct electrophysiological support for the involvement of endocannabinoids and leptin as modulators of hypothalamic circuits underlying motivational aspects of feeding behavior.

Animals↗
PubMed2005

Complementary roles for the amygdala and hippocampus during different phases of appetitive information processing.

Evidence collected from rodent models of memory storage suggests that rapid forms of learning engage the involvement of multiple brain regions each of which may participate in a different component of information processing. The present study used temporary inactivation of the amygdala and hippocampus during different phases of information processing on a one-trial appetitive-conditioning task to examine how these two regions might participate in the storage of appetitive memories. Male Long Evans rats were chronically implanted into the amygdala or dorsal hippocampus and food deprived. Rats were trained on a radial maze conditioned cue preference task where training occurred in one 40-min session and testing took place 24 h later. The amygdala or hippocampus was inactivated separately with muscimol (50 ng/microl) injected immediately before or after training, or immediately before testing. Saline-injected rats displayed a conditioned preference by spending more time in the arm that previously contained food than in the arm that did not contain food. Muscimol injected into the amygdala before training or testing blocked the conditioned preference. Muscimol injected into the hippocampus immediately after training blocked the conditioned preference. These results suggest that the processing of memories may require multiple contributions from separate brain systems for at least short-term (24 h) storage. The resulting output from each system may converge on a similar downstream target to influence behavior.

Amygdala↗
PubMed2004

Reciprocal cross-sensitization between amphetamine and salt appetite.

Previous work in our laboratory has demonstrated a potentiation of the psychomotor effects of amphetamine in animals with a history of sodium depletion, a process referred to as cross-sensitization. The present studies were done to further develop this finding by assessing multiple effects of amphetamine in rats with and without a history of sodium depletion. For Experiments 1-3, rats were depleted of sodium twice then subjected to one of three experimental procedures [open-field activity, conditioned place preference (CPP) and conditioned taste aversion (CTA)]. A history of depletion produced an elevation in the psychomotor effects of amphetamine. CPP, used to assess the rewarding properties of amphetamine, developed in rats with a history of depletion but not in controls. The aversive component of amphetamine as measured by CTA was unaffected by previous experience with sodium depletion. Finally, acute salt appetite after depletion was assessed in rats exposed to a sensitizing regimen of amphetamine. Animals with a drug history demonstrated a significant elevation in NaCl solution intake after depletion in comparison to controls. Together, the data provide strong evidence for the reciprocal cross-sensitization of salt appetite and response to amphetamine.

Amphetamine↗
PubMed2004

Fat in the intestine as a regulator of appetite--role of CCK.

The present review summarizes the appetite-suppressing effects of intestinal fat in the regulation of food intake in humans, with a special focus on the role of cholecystokinin (CCK). Current evidence supports a role for intestinal fat (especially long-chain free fatty acids) acting via the peptide CCK as a physiological satiety pathway. The regulation of satiety is, however, complex and it is not surprising that multiple control systems exist. It is interesting to note that nutrients, such as hydrolysis products of fat in the small intestine, stimulate the release of satiety peptides, such as CCK or PYY, that serve as satiety signals. CCK, released from the gastrointestinal tract by the local action of digested food, exerts various functions: stimulation of gallbladder contraction and exocrine pancreatic secretion, inhibition of gastric emptying, and inhibition of appetite. CCK functions therefore (1) as a positive feedback signal to stimulate digestive processes and (2) as negative feedback signal to limit the amount of food consumed during an individual meal.

Appetite↗
PubMed2004

Test-meal palatability alters the effects of intragastric fat but not carbohydrate preloads on intake and rated appetite in healthy volunteers.

Manipulations of test meal palatability and nutritional need-state to examine feeding behaviour have, to date, been studied in isolation. Recent investigations have attempted to examine these influences in combination. In the present study, healthy young males received intragastric infusions of soup (265 or 1514 kJ) on four different occasions. The infusion was shortly followed by a meal varying in its palatability (PALATABLE or BLAND). The effect of macronutrient type (CHO or Fat) in the high-energy preloads was also examined in a between-subject manner. High CHO preloads significantly decreased test meal intake and this decrease was unaffected by meal palatability. High fat preloads did not significantly reduce test meal intake. Additionally, more food was consumed following high fat preloads when the test meal was PALATABLE. Within-meal ratings of appetite revealed that hunger was diminished to a greater extent by CHO than by Fat preloads. Appetite was stimulated by the PALATABLE meal to a greater extent in the group receiving Fat than in those receiving the CHO preload. Comparison with a similar oral preloading study revealed differences that suggest possible interactions between cognitive, oro-sensory and gastric controls of feeding when palatable foods are consumed.

Adult↗
PubMed2006

Oral, post-oral and genetic interactions in sweet appetite.

Inbred mouse strains differ in their preferences for sweeteners, due in part to variations in their T1R3 sweet taste receptor. Recent studies of sweet sensitive C57BL/6J (B6) and subsensitive 129P3/J (129) mice indicate that experiential and post-oral effects of sugar substantially modify sweetener preference. In fact, the strain difference in sucrose preference disappeared after the mice were given 23 h/day tests with sucrose at ascending concentrations (0.5-32%). Intragastric infusions of sucrose (16%) also conditioned increased preference for and absolute intake of flavored sweet solutions in B6 and 129 mice. An operant analysis of sweetener appetite revealed, unexpectedly, that sugar-experienced 129 mice respond more vigorously than B6 mice for 16% sucrose rewards. These findings indicate that experiential and nutritional factors can, to some degree, override genetic differences in peripheral taste sensitivity in determining food appetite.

Animals↗
PubMed2006

Characteristics of salt appetite in chronically sodium-depleted rats using a progressive ratio schedule of procurement.

Satiation of sodium appetite of rats was studied using a protocol of sodium loss induced by chronic diuretic treatment and daily salt consumption sessions. In the first experiment in which NaCl was freely available from a drinking spout, rats consumed substantially more hypertonic NaCl than their estimated physiological deficit. In the second and third experiments, a simulated foraging cost was imposed on obtaining NaCl. In these experiments, rats were required to perform a progressive ratio lever press task to procure aliquots of hypertonic NaCl, and under these conditions they showed a break point or satiation for NaCl when they had consumed an amount close to their estimated deficit. In the fourth experiment, we found that the chronic diuretic regimen produced hypovolemia along with large increases in plasma aldosterone concentration and renin activity, and that all of these parameters were reversed toward non-depleted control values at the time of behavioral satiation in the progressive ratio protocol. Examination of natriuresis revealed that excessive intake of NaCl had no lasting benefit in this protocol: NaCl consumed in excess of need on 1 day was completely lost at the subsequent diuretic treatment. In the final two experiments, we showed that oral preloads of NaCl had no significant effect on progressive ratio procurement of NaCl, but that oral preloads reduced subsequent oral drinking. The data are discussed in terms of definitions of satiation of appetite in regard to the tightly regulated domain of body fluid homeostasis, and by extension, their relevance to systems such as energy homeostasis where set points appear to be less tightly regulated.

Aldosterone↗
PubMed2004

Gut hormones and the control of appetite.

Obesity is the main cause of premature death in the UK. Worldwide its prevalence is accelerating. It has been hypothesized that a gut nutriment sensor signals to appetite centres in the brain to reduce food intake after meals. Gut hormones have been identified as an important mechanism for this. Ghrelin stimulates, and glucagon like peptide-1, oxyntomodulin, peptide YY (PYY), cholecystokinin and pancreatic polypeptide inhibit, appetite. At physiological postprandial concentrations they can alter food intake markedly in humans and rodents. In addition, in obese humans fasting levels of PYY are suppressed and postprandial release is reduced. Administration of gut hormones might provide a novel and physiological approach in anti-obesity therapy. Here, we summarize some of the recent advances in this field.

Animals↗
PubMed2002

Appetite suppressants and valvular heart disease in a population-based sample: the HyperGEN study.

PURPOSE: Previous studies of the association between the use of appetite suppressants and valvular heart disease have not accounted for the effects of valvular structure and aortic root diameter, which are associated with obesity. We assessed whether the use of the appetite suppressants fenfluramine/dexfenfluramine, either alone or with phentermine, was associated with aortic regurgitation while adjusting for these variables. SUBJECTS AND METHODS: The sample included 2524 adult participants in the population-based Hypertension Genetic Epidemiology Network study. Information regarding current drug use was assessed during a clinical examination. Medication use was continued at the time of echocardiographic study. Expert readers blinded to current therapy read echocardiograms centrally at Cornell Medical Center. Analyses of the associations between use of fenfluramine/dexfenfluramine (alone or with phentermine) and aortic regurgitation adjusted for potential confounders, including aortic root dilatation and valve fibrocalcification. RESULTS: Nineteen participants, all of whom had hypertension, were being treated with fenfluramine or dexfenfluramine (5 on these agents alone, 14 also with phentermine). Aortic regurgitation was present in 32% (n = 6) of those taking fenfluramine or dexfenfluramine versus 6% (162/2505) of remaining subjects (P = 0.001). In multivariate-adjusted analyses, treatment with fenfluramine or dexfenfluramine was associated with aortic regurgitation (odds ratio [OR] = 4.9; 95% confidence interval [CI]: 1.7 to 14) and aortic fibrocalcification (OR = 5.2; 95% CI: 1.9 to 15). CONCLUSION: In a population-based sample, use of fenfluramine or dexfenfluramine, alone or in combination with phentermine, was associated with aortic regurgitation independent of aortic dilatation or fibrocalcification.

Aortic Valve Insufficiency↗
PubMed1999

Valve replacement for appetite suppressant-induced valvular heart disease.

Valvular heart disease associated with the use of appetite-suppressant medication is a recently described clinical entity. Although the mechanism of valvular injury remains elusive pathologically, the valvular abnormalities resemble those observed in carcinoid syndrome. The incidence of clinically evident valvular heart disease is low with short-term (less than 3 months) exposure to appetite-suppressant drugs. Prolonged exposure to higher doses in addition to combination drug therapy confers an excess risk for valvular pathologic changes. We report the case of a patient with severe mitral regurgitation who had short-term exposure (3 weeks) to the combination of fenfluramine (20 mg) and phenteramine (15 mg).

Adult↗
PubMed1997

Appetitive operant behavior and free-feeding in rats exposed to acute stress.

This study investigated whether appetitive operant food reinforcement or free-feeding behavior in rats, food-restricted to 85% of body weight, was disrupted by exposures to 3 h of restraint stress or by 3 h of restraint plus water immersion stress (RWI). Rats were trained under a 3-cycle 10-min time-out-10-min time-in fixed-ratio 15 (FR15) schedule of food reinforcement. Free-feeding was measured in a 3-cycle 10-min food jar-out-10-min food jar-in test conducted in the operant chambers. Three hours of restraint stress did not significantly affect response rate or food reinforcement in the operant FR15 task or in the free-feeding condition. In contrast, 3 h of RWI completely abolished operant food reinforcement and suppressed response rate, whereas free-feeding was significantly reduced but not abolished in food-restricted, hungry rats. We conclude that acute restraint stress in food-restricted, hungry rats does not affect their appetite or motor ability to lever-press for food nor did it affect their ability to feed in a free-feeding situation. In contrast, RWI stress may have induced a motor impairment, or some other aspect of motivation independent of hunger, that disrupted their performance in the operant FR15 task.

Animals↗
PubMed2002

Orexins and appetite regulation.

Initial research on the functional significance of two novel hypothalamic neuropeptides, orexin-A and orexin-B, suggested an important role in appetite regulation. Since then, however, these peptides have also been shown to influence a wide range of other physiological and behavioural processes. In this paper, we review the now quite extensive literature on orexins and appetite control, and consider their additional effects within this context. Although the evidence for orexin (particularly orexin-A and the orexin-1 receptor) involvement in many aspects of ingestive physiology and behaviour is incontrovertible, central administration of orexins is also associated with increased EEG arousal and wakefulness, locomotor activity and grooming, sympathetic and HPA activity, and pain thresholds. Since the orexin system is selectively activated by signals indicating severe nutritional depletion, it would be highly adaptive for a hungry animal not only to seek sustenance but also to remain fully alert to dangers in the environment. Crucial evidence indicates that orexin-A increases food intake by delaying the onset of a behaviourally normal satiety sequence. In contrast, a selective orexin-1 receptor antagonist (SB-334867) suppresses food intake and advances the onset of a normal satiety sequence. These data suggest that orexin-1 receptors mediate the episodic signalling of satiety and appear to bridge the transition from eating to resting in the rats' feeding-sleep cycle. The argument is developed that the diverse physiological and behavioural effects of orexins can best be understood in terms of an integrated set of reactions which function to rectify nutritional status without compromising personal survival. Indeed, many of the non-ingestive effects of orexin administration are identical to the cluster of active defences mediated via the lateral and dorsolateral columns of the midbrain periaqueductal gray matter, i.e., somatomotor activation, vigilance, tachycardia, hypertension and non-opioid analgesia. In our view, therefore, the LH orexin system is very well placed to orchestrate the diverse subsystems involved in foraging under potentially dangerous circumstances, i.e., finding and ingesting food without oneself becoming a meal for someone else.

Animals↗
PubMed1987

Effects of gustatory deafferentation on Polycose and sucrose appetite in the rat.

Recent studies have revealed that rats are strongly attracted to the taste of starch-derived polysaccharides, and suggest that the taste receptors involved differ from those that respond to sucrose. The present study examined the possibility that different gustatory nerves mediate the rat's taste and appetite for polysaccharides and sucrose. This was accomplished by measuring the effects of selective gustatory nerve transection on the intake of Polycose and sucrose solutions in nondeprived female rats. Bilateral transection of the chorda tympani nerve produced comparable reductions in Polycose and sucrose intake, but bilateral transection of the glossopharyngeal nerve selectively reduced the intake of Polycose. Bilateral transection of the greater superficial petrosal nerve, and to a lesser degree, the pharyngeal branch of the vagus nerve, increased sucrose intake without affecting Polycose intake. These results indicate that while no single gustatory nerve mediates sucrose or polysaccharide taste, there is some specialization of function within the peripheral gustatory system. Combined bilateral transections of all four gustatory nerves produced the greatest reduction in solution intake, and reduced Polycose and sucrose consumption to the same degree. The suppressive effect was only partial, however, which indicates that relatively few intact taste receptors are required to maintain the rat's appetite for sugar and polysaccharide solutions.

Afferent Pathways↗
PubMed1985

Epinephrine facilitation of appetitive learning: attenuation with adrenergic receptor antagonists.

Previous studies using aversive training tasks have reported that retention is enhanced by post-training administration of epinephrine. This study investigated the effects of post-training administration of epinephrine on retention of an appetitive task. The results indicate that epinephrine can enhance retention performance in an appetitive task of both rats and mice. Pretraining injections of propranolol and phenoxybenzamine, alpha- and beta-adrenergic receptor antagonists, attenuate the memory-enhancing effects of epinephrine. These results are consistent with the view that release of peripheral epinephrine may regulate storage of new information and may mediate memory modulation produced by a variety of treatments.

Animals↗
PubMed2001

The hippocampus and motivation revisited: appetite and activity.

After reviewing the available data regarding the various effects of manipulating (e.g. lesions, chemical or electrical stimulation) the hippocampal formation, Jarrard concluded that this structure likely played a role in motivated behaviors, specifically in general behavioral activation and incentive motivation. Since that time there have been technical advances in lesion techniques and conceptual advances in theories of motivation and learning. Here, we present more recent data that demonstrates the effects of hippocampal lesions on general activity, the utilization of interoceptive state cues, ingestive behaviors, and appetitive responding. We critically evaluate several theories of hippocampal function that have been proposed to explain these data, including the hippocampus as an inhibitor of general activation, as a processor of energy state signals and as a mediator of reward valuation. Finally, we propose that these findings may also be accounted for based on a role for the hippocampus in the learned inhibition of appetitive behaviors. We conclude that, while the specific mechanism of hippocampal involvement may not yet be determined, it is clear that this structure is involved in food-related behaviors and we caution researchers to consider this as a possible confound in studies of learning and memory processes.

Animals↗
PubMed1987

Salivation and depression: a role for appetitive factors.

A decrease in salivary flow rate (SFR) is associated with depressive illness although the mechanisms underlying this association are unknown. Appetitive factors are known to influence SFR, but are not adequately considered in the studies of salivation and depression. Diminished SFR in depressive illness may be more closely related to the appetite disturbances commonly associated with depressive illness than to mood disorder or depressive illness per se. The implications for considering SFR as a physiological correlate of depressive illness are discussed in light of this possibility.

Appetite↗
PubMed1999

Effects of oral fructose and glucose on plasma GLP-1 and appetite in normal subjects.

Oral glucose is a potent stimulant of glucagon-like peptide-1 (GLP-1) secretion. The effect of oral fructose on GLP-1 secretion in humans is unknown. The aims of this study were to determine (i) whether oral fructose stimulates GLP-1 secretion and (ii) the comparative effects of oral glucose and fructose on appetite. On 3 separate days, 8 fasting healthy males received, in single-blind randomized order (i) 75 g glucose, (ii) 75 fructose, or (iii) 75 g glucose followed by 75 g fructose I h later. Venous glucose, insulin and GLP-1 were measured. Appetite was assessed by visual analog questionnaires and intake of a buffet meal. Whereas glucose and fructose both increased plasma glucose, insulin and GLP-1 (P < 0.000)] for all), the response to glucose was much greater (P < 0.005 for all). There was no increase in plasma GLP-1 when fructose was given after glucose. There was no difference in food intake after oral glucose or fructose. We conclude that oral fructose (75 g) stimulates GLP-1 (and insulin) secretion, but the response is less than that to 75 g glucose. These observations suggest that neither GLP-1 nor insulin play a major role in the regulation of satiation.

Adult↗
PubMed1998

Regulation of appetite and body weight in seasonal mammals.

As models of physiological regulation of body weight, adiposity and appetite, seasonal mammals offer unique opportunities for manipulating fundamental regulatory processes that may not be available in the more frequently-studied laboratory rodents. Seasonal weight and intake cycles are anticipatory rather than reactive in nature, being manifest despite the availability of adlibitum supplies of food. They are exhibited despite all other environmental variables being held constant, and are reversible. Appropriate body weight appears to be a sliding set point in many seasonal mammals, which can move in either direction, largely independently of age. While few data are available other than from rats and mice, there appears to be a strong commonality of central neuroendocrine and peripheral signalling systems between seasonal and non-seasonal mammals, although the conditions under which endogenous regulatory pathways are activated may differ significantly between species. Peripheral and central signalling systems implicated in the regulation of appetite and body weight may be modulated during seasonal transitions. Discussion will concentrate on hypothalamic neuropeptides, gastrointestinal satiety peptides, the recently-described peptide, leptin, that is secreted by adipose tissue, and the interactions between these regulatory components.

Animals↗