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PubMed1999

Effect of adrenocorticotrophic hormone on sodium appetite in mice.

A main vector of the effects of stress is secretion of corticotrophin releasing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Systemic administration of ACTH (2.8 microgram/day sc) for 7 days in BALB/c mice caused a very large increase of voluntary intake of 0.3 M NaCl equivalent to turnover of total body sodium content each day. Intracerebroventricular infusion of ACTH (20 ng/day) had no effect. Intracerebroventricular infusion of ovine CRF (10 ng/h for 7 days) caused an increase of sodium intake. The large sodium appetite-stimulating effect of systemic ACTH was not influenced by concurrent systemic infusion of captopril (2 mg/day). Induction of stress by immobilization of mice on a running wheel caused an increase in Na appetite associated with a 50% decrease of thymus weight, indicative of corticosteroid effects. The present data suggest that stress and the hormone cascade initiated by stress evoke a large sodium appetite in mice, which may be an important survival mechanism in environmental conditions causing stress.

Adrenocorticotropic Hormone↗

PubMed2000

Rapid induction of sodium appetite modifies taste-evoked activity in the rat nucleus of the solitary tract.

Sodium-deprived rats develop a salt appetite and show changes in gustatory responses to NaCl in the periphery and brain stem; salt-sensitive neurons respond less to hypertonic NaCl than do corresponding cells in replete controls. By administering DOCA and renin, we generated a need-free sodium appetite quickly enough to permit us to monitor the activity of individual neurons in the nucleus of the solitary tract before and after its creation, permitting a more powerful within-subjects design. Subjects received DOCA pretreatment followed by an intracerebroventricular infusion of renin. In animals that were tested behaviorally, this resulted in elevated intake of 0.5 M NaCl. In neural recordings, renin caused decreased responding to hypertonic NaCl across all neurons and in the salt-sensitive neurons that were most responsive to NaCl before infusion. Most sugar-sensitive cells, in contrast, gave increased phasic responses to NaCl. These results confirm that sodium appetite is accompanied by decreased responding to NaCl in salt-sensitive neurons, complemented by increased activity in sugar-sensitive cells, even when created rapidly and independently of need.

Acids↗

PubMed2001

Effects of glucose supplementation on gastric emptying, blood glucose homeostasis, and appetite in the elderly.

The aims of this study were to evaluate the effects of dietary glucose supplementation on gastric emptying (GE) of both glucose and fat, postprandial blood glucose homeostasis, and appetite in eight older subjects (4 males, 4 females, aged 65--84 yr). GE of a drink (15 ml olive oil and 33 g glucose dissolved in 185 ml water), blood glucose, insulin, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), and appetite (diet diaries, visual analog scales, and food intake at a buffet meal consumed after the GE study) were evaluated twice, after 10 days on a standard or a glucose-supplemented diet (70 g glucose 3 times a day). Glucose supplementation accelerated GE of glucose (P < 0.05), but not oil; there was a trend for an increase in GIP (at 15 min, P = 0.06), no change in GLP-1, an earlier insulin peak (P < 0.01), and a subsequent reduction in blood glucose (at 75 min, P < 0.01). Glucose supplementation had no effect on food intake during each diet so that energy intake was greater (P < 0.001) during the glucose-supplemented diet. Appetite ratings and energy intake at the buffet meal were not different. We conclude that, in older subjects, glucose supplementation 1) accelerates GE of glucose, but not fat; 2) modifies postprandial blood glucose homeostasis; and 3) increases energy intake.

Aged↗

PubMed2001

Cerebral Na concentration, Na appetite and thirst of sheep: influence of somatostatin and losartan.

Na and water intakes of Na-depleted sheep are influenced by changes in cerebral Na concentration. The effect of intracerebroventricular infusion of somatostatin or losartan, the ANG II type 1 receptor antagonist, on the Na appetite and thirst of Na-depleted sheep during infusions that decrease (intracerebroventricular hypertonic mannitol) or increase (intracerebroventricular or systemic hypertonic NaCl) cerebral Na concentration was investigated. Na intake was increased but water intake was unchanged during intracerebroventricular infusion of hypertonic mannitol. The increased Na appetite caused by intracerebroventricular infusion of hypertonic mannitol was decreased by concurrent intracerebroventricular infusion of either somatostatin or losartan, with somatostatin being most effective. Water intake was increased during intracerebroventricular infusion of hypertonic mannitol and somatostatin. Na intake was decreased and water intake was increased during systemic or intracerebroventricular infusion of hypertonic NaCl. Intracerebroventricular infusion of losartan blocked both (Na and water intake), whereas somatostatin did not influence either of these changes in intake. The results further consolidate a role for somatostatin and ANG II in the central mechanisms controlling Na appetite and thirst of sheep.

Angiotensin II↗

PubMed2001

Circulating angiotensin II mediates sodium appetite in adrenalectomized rats.

We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Adrenalectomized rats deprived of their main access to sodium (0.3 M NaCl) for 9 h drank 14.1 +/- 1.5 ml of the concentrated saline solution in 2 h of access. Intravenous infusion of captopril (2.5 mg/h) during the last 5 h of sodium restriction reduced sodium intake by 77 +/- 12% (n = 5) without affecting the degree of sodium depletion and hypovolemia incurred during deprivation. Functional evidence indicates that this dose of captopril blocked production of ANG II in the peripheral circulation, but not in the brain; that is, injection of ANG I into the lateral brain ventricle stimulated intake of both water and 0.3 M NaCl. Intravenous infusion of ANG II (starting 10-15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Longer (20 h) infusions of captopril in 22-h sodium-restricted rats also blocked sodium appetite, but reduced or prevented sodium depletion. Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II.

Adrenalectomy↗

PubMed1999

Appetite at "high altitude" [Operation Everest III (Comex-'97)]: a simulated ascent of Mount Everest.

We hypothesized that progressive loss of body mass during high-altitude sojourns is largely caused by decreased food intake, possibly due to hypobaric hypoxia. Therefore we assessed the effect of long-term hypobaric hypoxia per se on appetite in eight men who were exposed to a 31-day simulated stay at several altitudes up to the peak of Mt. Everest (8,848 m). Palatable food was provided ad libitum, and stresses such as cold exposure and exercise were avoided. At each altitude, body mass, energy, and macronutrient intake were measured; attitude toward eating and appetite profiles during and between meals were assessed by using questionnaires. Body mass reduction of an average of 5 +/- 2 kg was mainly due to a reduction in energy intake of 4.2 +/- 2 MJ/day (P < 0.01). At 5,000- and 6,000-m altitudes, subjects had hardly any acute mountain sickness symptoms and meal size reductions (P < 0.01) were related to a more rapid increase in satiety (P < 0.01). Meal frequency was increased from 4 +/- 1 to 7 +/- 1 eating occasions per day (P < 0. 01). At 7,000 m, when acute mountain sickness symptoms were present, uncoupling between hunger and desire to eat occurred and prevented a food intake necessary to meet energy balance requirements. On recovery, body mass was restored up to 63% after 4 days; this suggests physiological fluid retention with the return to sea level. We conclude that exposure to hypobaric hypoxia per se appears to be associated with a change in the attitude toward eating and with a decreased appetite and food intake.

Adult↗

PubMed1997

In vitro appetitive classical conditioning of the feeding response in the pond snail Lymnaea stagnalis.

In vitro appetitive classical conditioning of the feeding response in the pond snail Lymnaea stagnalis. J. Neurophysiol. 78: 2351-2362, 1997. An in vitro preparation was developed that allowed electrophysiological analysis of appetitive conditioning of feeding in the model molluscan system, Lymnaea. The network generating the feeding motor program (fictive feeding) is well characterized at the cellular level and consists of identified central pattern generator (CPG) interneurons, motor neurons, and modulatory interneurons. Activation of a modulatory interneuron, the slow oscillator (SO), evokes the three-phase fictive feeding rhythm in the same semi-intact preparations where tactile stimuli can be applied to the lips. By pairing touch as a conditioned stimulus (CS) with stimulation of the SO as an unconditioned stimulus (US), we established an effective in vitro paradigm for appetitive conditioning. Before training, touch to the lips evoked only brief and weak activity in the feeding interneurons and motor neurons. After 6-10 conditioning trials, there was a significant enhancement in the fictive feeding response to CS alone. This was not seen in controls (CS only, US only, random CS and US) and in preparations where there was no initial brief response to touch before conditioning. Direct recordings from the protraction phase N1M interneurons during in vitro conditioning indicated that the enhancement of the fictive feeding is due to an increased activation of these CPG cells by mechanosensory inputs from the lips. We also found that the conditioned response was not due to a facilitated activation of modulatory neurons in the feeding network, such as the SO or the cerebral giant cells (CGCs), because the activity of these cells remained unchanged after conditioning.

Animals↗

PubMed2001

Calcium: taste, intake, and appetite.

This review summarizes research on sensory and behavioral aspects of calcium homeostasis. These are fragmented fields, with essentially independent lines of research involving gustatory electrophysiology in amphibians, ethological studies in wild birds, nutritional studies in poultry, and experimental behavioral studies focused primarily on characterizing the specificity of the appetite in rats. Recently, investigators have begun to examine potential physiological mechanisms underlying calcium intake and appetite. These include changes in the taste perception of calcium, signals related to blood calcium concentrations, and actions of the primary hormones of calcium homeostasis: parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D. Other influences on calcium intake include reproductive and adrenal hormones and learning. The possibility that a calcium appetite exists in humans is discussed. The broad range of observations documenting the existence of a behavioral limb of calcium homeostasis provides a strong foundation for future genetic and physiological analyses of this behavior.

Animals↗

PubMedDate not supplied

Regulation of appetite in chronic renal failure.

Anorexia, nausea and vomiting in patients with severe renal failure may cause or contribute to development of protein-energy malnutrition, which is associated with increased morbidity and mortality. However, the specific mechanisms that cause appetite suppression in uremia are poorly understood. This review summarizes the general mechanisms by which appetite is regulated. Various factors are discussed that may potentially be involved in appetite suppression in chronic renal failure.

Amino Acids↗

PubMed1993

Mechanisms of appetite control and their abnormalities in obese patients.

Human appetite is a complex mixture of physiological and psychological phenomena which include feelings of hunger, total energy intake, ingestion of particular nutrients, distribution and sizes of meals and snacks, specific cravings and food preferences. These phenomena can be assembled into a profile of motivation and a pattern of eating which represents the way in which appetite fluctuates over time. The satiety cascade shows the processes through which nutrition exerts effects on the biological system and, therefore, on feelings and behaviour. Within the biological system, the control of appetite involves post-ingestive mechanisms, including signals arising from the gastrointestinal tract and the release of hormones when food is processed. Post-absorptive mechanisms include the detection of important products of digestion, such as glucose and amino acids, together with the nature of the fuel mix oxidized and other metabolic variables. In obese patients, evidence points to a defect in the control of fat intake. In these people, dietary fat exerts only a weak action on satiation and satiety; it fails to generate strong responses in the mechanisms of the satiety cascade. An imbalance between fat intake and oxidation favours weight gain. A consideration of the psychobiological system (interactions between behaviour, peripheral physiology and neurochemical profiles) suggests strategies for treating or preventing the development of weight gain in vulnerable individuals.

Appetite↗

PubMed2001

Field study of dairy cows with reduced appetite in early lactation: clinical examinations, blood and rumen fluid analyses.

The study included 125 cows with reduced appetite and with clinical signs interpreted by the owner as indicating bovine ketosis 6 to 75 days postpartum. Almost all of the cows were given concentrates 2 to 3 times daily. With a practitioners view to treatment and prophylaxis the cows were divided into 5 diagnostic groups on the basis of thorough clinical examination, milk ketotest, decreased protozoal activity and concentrations, increased methylene blue reduction time, and increased liver parameters: ketosis (n = 32), indigestion (n = 26), combined ketosis and indigestion (n = 29), liver disease combined with ketosis, indigestion, or both (n = 15), and no specific diagnosis (n = 17). Three cows with traumatic reticuloperitonitis and 3 with abomasal displacement were not grouped. Nonparametric methods were used when groups were compared. Aspartate aminotransferase, glutamate dehydrogenase, gamma-glutamyl transferase and total bilirubin were elevated in the group with liver disease. Free fatty acids were significantly elevated in cows with ketosis, compared with cows with indigestion. Activity and concentrations of large and small protozoas were reduced, and methylene blue reduction time was increased in cows with indigestion. The rumen fluid pH was the same for groups of cows with and without indigestion. Prolonged reduced appetite before examination could have led to misclassification. Without careful interpretation of the milk ketotest, many cases with additional diagnoses would have been reported as primary ketosis. Thorough clinical examination together with feasible rumen fluid examination and economically reasonable blood biochemistry did not uncover the reason(s) for reduced appetite in 14% of the cows. More powerful diagnostic methods are needed.

Animals↗

PubMed1986

Comparative effects of seven antidepressant regimes on appetite, weight and carbohydrate preference.

Appetite, weight, and preference for carbohydrate-containing food were followed in patients treated in double-blind trials of seven antidepressant regimes. Trimipramine and isocarboxazid combined had a significant effect in increasing appetite, carbohydrate preference, and weight; in patients who had lost appetite at presentation and were on this treatment, improvement in Hamilton score was linked to increase in weight--a finding not true of the other treatments.

Antidepressive Agents↗

PubMed2002

Long-term suppression of weight gain, adiposity, and serum insulin by central leptin gene therapy in prepubertal rats: effects on serum ghrelin and appetite-regulating genes.

Intracerebroventricular administration of recombinant adeno-associated virus (rAAV) encoding the rat leptin gene (rAAV-lep) to 24-d-old female and male rats suppressed postpubertal weight gain for extended periods by decreasing food consumption and adiposity, as reflected by lowered serum leptin, insulin, and FFA. Serum ghrelin levels were increased in young but not older rats. Central rAAV-lep therapy also increased energy expenditure through nonshivering thermogenesis in younger rats as shown by expression of uncoupling protein mRNA in brown adipose tissue. The sustained decrease in appetite seemingly resulted from attenuation of appetite-stimulating neuropeptide Y and enhancement of appetite-inhibiting melanocortin signalings in the hypothalamus. Neither the onset of pubertal sexual maturation nor reproductive cyclicity in adult female rats was affected by the sustained reduction in energy consumption and weight gain. These findings demonstrate that central leptin gene therapy in prepubertal rats is a novel therapy to control postpubertal weight gain, adiposity, and hyperinsulinemia for extended periods.

Adipose Tissue, Brown↗

PubMed2001

Ghrelin enhances appetite and increases food intake in humans.

Ghrelin is a recently identified endogenous ligand for the growth hormone secretagogue receptor. It is synthesized predominantly in the stomach and found in the circulation of healthy humans. Ghrelin has been shown to promote increased food intake, weight gain and adiposity in rodents. The effect of ghrelin on appetite and food intake in man has not been determined. We investigated the effects of intravenous ghrelin (5.0 pmol/kg/min) or saline infusion on appetite and food intake in a randomised double-blind cross-over study in nine healthy volunteers. There was a clear-cut increase in energy consumed by every individual from a free-choice buffet (mean increase 28 +/- 3.9%, p<0.001) during ghrelin compared with saline infusion. Visual analogue scores for appetite were greater during ghrelin compared to saline infusion. Ghrelin had no effect on gastric emptying as assessed by the paracetamol absorption test. Ghrelin is the first circulating hormone demonstrated to stimulate food intake in man. Endogenous ghrelin is a potentially important new regulator of the complex systems controlling food intake and body weight.

Adult↗

PubMed2026

Quantification of appetite-regulating hormones in children with hypothalamic and common obesity.

CONTEXT: The pathophysiology of hypothalamic obesity (HyOb) remains incompletely understood with no effective treatments. OBJECTIVE: We examined differences in appetite-regulating hormone concentrations between patients with HyOb, common obesity, and lean controls. DESIGN: Multiway cross-sectional case-control study of patients aged 2 through 19 years. SETTING: Two tertiary pediatric endocrinology centers. PATIENTS: Cases were obese (body mass index [BMI] > +2 SD score [SDS], "HyOb") and lean ("HyLean") patients with congenital (septo-optic dysplasia) or acquired (suprasellar brain tumor) hypothalamic disorders. Controls had common obesity ("Ob") or nonhypothalamic disorders and normal BMI ("Lean"). MAIN OUTCOME MEASURES: Relationships between the Dykens' Hyperphagia Questionnaire Score (DHQS), plasma or serum concentrations of leptin, insulin, α-melanocyte stimulating hormone (αMSH), brain-derived neurotrophic factor, oxytocin, acylated ghrelin, agouti-related peptide and copeptin, and BMI SDS. RESULTS: Dykens' Hyperphagia Questionnaire Score did not differ between HyOb and Ob patients (24 [17-34] vs 24 [18-31]) but correlated with BMI SDS in patients with hypothalamic disorders (P = 0.02). HyOb and Ob patients exhibited similarly increased anorexigens (insulin, leptin) and decreased orexigens (ghrelin, agouti-related peptide) compared to HyLean and Lean patients. The rate of BMI increase was independently associated with lower αMSH (β = -0.23 [-0.36 to -0.11], P = .0007) and ghrelin (β=-0.004 [-0.01 to 0.00], P = .001) concentrations, suggesting that αMSH replacement may be a therapeutic target for HyOb. HyLean patients demonstrated intermediate insulin responses to glucose compared to other subcohorts. CONCLUSION: In our cohort, patients with HyOb appeared indistinguishable from Ob in terms of their appetite and appetite-regulating neuroendocrine circuitry. Higher αMSH concentrations are associated with reduced weight gain and may be a target for therapeutic intervention.

alpha-MSH↗

PubMed2005

Appetite-suppressing effects of ammonia exposure in rainbow trout associated with regional and temporal activation of brain monoaminergic and CRF systems.

To assess whether the brain's monoaminergic and/or corticotropin-releasing factor (CRF) systems may be involved in mediating the appetite-suppressing effects of high environmental ammonia levels, we exposed rainbow trout to one of four NH4Cl treatments (0, 500, 750, 1000 micromol l(-1)) for 24 or 96 h and monitored changes in food intake, brain serotonin (5-HT) and dopamine (DA) activity, CRF and urotensin I (UI) mRNA levels, and plasma cortisol levels. Food intake decreased in a dose-dependent manner after 24 h of ammonia exposure and partially recovered in all groups after 96 h. Ammonia also elicited dose-dependent increases in serotonergic activity in the hypothalamus (HYP), telencephalon (TEL) and posterior brain (PB). Whereas the increase in serotonergic activity was timed with the 24 h food intake inhibition, TEL and PB serotonergic activity increased after 96 h. In the PB, exogenous ammonia also elicited dose-dependent increases in dopaminergic activity after both 24 and 96 h of exposure. Transient increases in TEL CRF and UI mRNA levels, HYP UI mRNA levels, and plasma cortisol concentrations were evidence that the hypothalamic-pituitary-interrenal (HPI) stress axis was primarily stimulated in the first 24 h of ammonia exposure when food intake was depressed. Overall, the transient nature of the appetite suppression during chronic ammonia exposure, and the time-dependent changes in brain monoaminergic and CRF systems, implicate 5-HT, DA, CRF and UI as potential mediators of the appetite-suppressing effects of ammonia. Among these anorexigenic signals, our results specifically identify hypothalamic 5-HT as a potentially key neurobiological substrate for the regulation of food intake during exposure to high external ammonia concentrations.

Ammonia↗

PubMed1989

A subpopulation of cerebral B cluster neurones of Aplysia californica is involved in defensive head withdrawal but not appetitive head movements.

The cerebral B cluster neurones of Aplysia californica were studied under experimental conditions designed to evoke head movements in a selective fashion: either to approach an appetitive stimulus, or to withdraw from an aversive one. Intracellular recordings indicated the presence of two types of B cluster neurones: Bn cells that had fast (narrow) spikes, and Bb cells that had slow (broad) spikes. Tactile stimulation of the tentacles, rhinophores and lips excited Bn neurones, but inhibited Bb neurones. Intracellular stimulation of Bn cells evoked contractions of body wall muscles. No contractions were observed when Bb cells were fired, indicating that it is unlikely that the Bb neurones are motor neurones. Several lines of evidence indicated that the Bn type neurones are involved in withdrawal responses but not in appetitive head turning. (1) Elimination of the descending axons of the Bn cells by lesioning the cerebropleural connectives (C-Pl connectives) did not affect the head-turning response. This lesion significantly altered the head-withdrawal response by selectively eliminating an initial fast component of the withdrawal movement. (2) In chronic recordings from the C-Pl connective, unit activity was obtained which was correlated with the presentation of an appetitive stimulus rather than with evoked or spontaneous turning movements. A substantial increase in activity also occurred during head withdrawal of the animal. On the basis of these data, we postulate that separate populations of motor neurones are responsible for the aversive withdrawal of the head, and for the directed turning response towards a stimulus.

Animals↗

PubMed1988

Acute effects of exercise intensity on appetite in young men.

This study investigated the acute effects of two exercise intensities on three measures of appetite. Fifteen, 12-h-fasted, college-age males completed three experimental sessions in counterbalanced orders: no-exercise control; cycle exercise performed at 35% VO2max; and cycle exercise performed at 68% VO2max. Both exercise conditions involved a total energy expenditure of 4.1 kcal.kg-1 body weight. Dependent measures were intermittent hunger and sucrose palatability ratings, and food intake at a test meal given approximately 1 h post-exercise. Hunger was briefly suppressed in the high-intensity exercise condition compared to low-intensity exercise and control, while intake of liquid-source kilocalories and carbohydrates was higher after the exercise sessions. Total caloric intake remained stable. Sucrose palatability did not vary across sessions. Intensity is inferred to be an important variable mediating exercise effects on appetite. Relations between appetite measures are discussed, and validity of sucrose palatability ratings and common methods of measuring food intake questioned. Exercise, while not decreasing food intake, does not appear to increase it, and the benefits of exercise for body fat reduction are not immediately offset by compensatory caloric intake.

Adult↗