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At least 613 records · Page 34Linked to original sources
PubMed2000

Effects of chronic kombucha ingestion on open-field behaviors, longevity, appetitive behaviors, and organs in c57-bl/6 mice: a pilot study.

Kombucha is a lightly fermented tea beverage popularly consumed as a self-prescribed folk-remedy for numerous ailments. Kombucha is claimed to enhance cognition, aid weight loss, and prolong life. This pilot study reports longevity, general health, and open-field exploratory behavioral outcomes from a 3-y longitudinal study of 64 C57-BL/6 mice (males and females), half of which chronically drank kombucha, and all of which experienced natural mortality. Compared by MANOVA to controls, mice that drank kombucha showed greater vertical exploration (P = 0.001) and a sex-interactive effect in novel object manipulation (P = 0.049). MANOVA of kombucha-drinking mice compared to controls detected differences in appetitive behaviors (food consumption, P < 0.001; beverage consumption, P = 0. 008), and gross body weight (P < 0.001). Appetitive behaviors changed with the addition of voluntary exercise on a running wheel, with differing patterns of change noted for males and females. Both male and female mice who drank kombucha lived longer than controls (P < 0.001), with the greatest variability among the male mice (sex interactive effect, P < 0.001). Comparable effects and mechanisms in humans remain uncertain, as do health safety issues, because serious health problems and fatalities have been reported and attributed to drinking kombucha.

Animals↗
PubMed1986

(S)-3-[(benzyloxy)methyl]morpholine hydrochloride: a nonstimulant appetite suppressant without conventional neurotransmitter releasing properties.

The synthesis and appetite-suppressant activity of (S)-3-[(benzyloxy)methyl]morpholine hydrochloride in dogs are reported. The oral ED50 for appetite suppression in dogs of 3 was 12 mg/kg, and it was tolerated up to 200 mg/kg. 3 had no inhibitory effect on the release or uptake of noradrenaline, dopamine, or serotonin at 10(-5) M. The (R) enantiomer of 3 was not anorexiant.

Animals↗
PubMed2001

Role of various types of serotonin receptors in regulation of drinking behavior and salt appetite in vasopressin-deficient brattleboro rats.

Serotonin 5-HT(1A)receptor agonist 8-OH DPAT suppressed drinking behavior in Brattleboro and Wistar rats. 5-HT(1B)agonist CGS-12066A and 5-HT(2A)antagonist ketanserin did not affect drinking behavior in Brattleboro rats; 5-HT(3)antagonist ondansetron suppressed water consumption and 5-HT(1A)agonist stimulated salt appetite in Brattleboro, but not in Wistar rats. Presumably, vasopressin regulates thirst and salt appetite by modulating sensitivity/density of various types of 5-HT receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

Enhanced sodium appetite in rats with lesions centered on nucleus medianus.

Recent experiments have demonstrated that rats with lesions of the ventral portion of nucleus medianus (vNM) frequently exhibit a chronic and robust hyperdipsia, which occurs only at night. This study indicates that the same brain damage may produce a nocturnal appetite for sodium that is similarly pronounced and persistent. Of 68 rats with vNM lesions, 33 were observed to drink at least 15 ml of 0.51 M NaCl solution per day, and 11 of them consumed more than 30 ml daily. The basis for this impressive consumption of saline is uncertain; the brain-damaged rats had normal sodium concentrations, renin activities, and aldosterone levels in plasma during basal maintenance conditions, and they conserved sodium in urine when maintained on a sodium-deficient diet. Nevertheless, the present results indicate that vNM and/or local fibers of passage may play an important role in the control of sodium appetite, as it does in the control of thirst.

Aldosterone↗
PubMed1988

Effects of "anorexia" on appetitive and consummatory behavior.

In order to assess the effects of anorexigenic agents on appetitive and consummatory behavior, rats were given sweetened milk either in a bottle or by infusion through an intraoral cannula. In the first experiment, amphetamine (AMP; 0, 0.25, 0.5, and 1 mg/kg) had no effect on the intake of cannula-fed rats but suppressed the intake of bottle-fed rats at the highest two doses. Although increased activity was observed at the highest dose, bottle-fed rats drank less than cannula-fed rats at each dose of the drug. Fenfluramine (FEN; 0, 2.5, 5, and 10 mg/kg) produced a dose-dependent decrease in intake with both methods of feeding, but the effect was greater in bottle-fed rats. Although FEN had marked sedative effects at the highest two doses, bottle-fed rats drank less than cannula-fed rats at each dose of the drug. In a second experiment, cannula- and bottle-fed rats were given milk adulterated with various concentrations of quinine hydrochloride (QHCl; 0, 0.0025, 0.005, 0.01, and 0.02%). QHCl had no effect on the intake of cannula-fed rats but decreased the intake of bottle-fed rats at the highest two concentrations. In a final experiment, the effect of AMP (1 mg/kg) was assessed in a conditioned aversion paradigm. Rats were given four conditioning trials in which access to a 0.1% sodium saccharin solution was followed by an injection of AMP. Again, bottle-fed rats showed greater suppression of intake than cannula-fed rats. Taken together, these results demonstrate that anorexigenic drugs affect appetitive behavior more than consummatory behavior. The implications of these findings for understanding the mechanism of behavioral tolerance are discussed.

Amphetamine↗
PubMed1988

Comparison of the effects of the dipeptidyl peptidase inhibitors captopril, ramipril, and enalapril on water intake and sodium appetite of Sprague-Dawley rats.

Two experiments were performed with Sprague-Dawley rats to study the effects of different inhibitors of angiotensin I converting enzyme (ACE) on water intake and sodium appetite. Subcutaneous administration of low doses of either enalapril (MK421) or ramipril (Hoe498), like captopril, was dipsogenic. Acute administration of ramipril also enhanced the drinking response to peripherally administered angiotensin I (Ang I). Higher doses inhibited the drinking response to Ang I, administered acutely either peripherally or centrally. These data provide behavioral evidence that the nonsulfhydryl inhibitors enalapril and ramipril inhibit brain converting enzyme activity and that they are considerably more potent than captopril. All three of these compounds, administered chronically in food, induced an appetite for sodium chloride (NaCl) solution. Enalapril and ramipril were more potent than captopril. Plasma renin activity was increased by each of these inhibitors, but the magnitude of the increase was not clearly related to the amount of NaCl consumed. The water intake in response to acute administration of either Ang I or isoproterenol was not reliably increased in rats treated chronically with these inhibitors.

Angiotensin I↗
PubMed1990

Effect of lithium chloride-induced aversion on appetitive and consummatory behavior.

The effect of lithium chloride-induced conditioned taste aversions on appetitive and consummatory behavior was determined. Rats were given access to a 0.1% saccharin solution for 15 min either in bottles or by infusion through an intraoral cannula. Bottle-fed rats given postprandial injections of lithium chloride showed greater aversion to saccharin than cannula-fed rats. During extinction, cannula-fed rats gradually recovered to control levels of intake, whereas bottle-fed rats continued to avoid the saccharin. These results suggest that lithium chloride affects appetitive behavior to a greater extent than it affects consummatory behavior.

Animals↗
PubMed1990

Sodium appetite in lactating rats.

Lactating rats that were given free access to sodium-deficient food, water, and 0.51 M NaCl solution showed no evidence of sodium appetite. The estimated daily loss of 1-2 mEq Na in milk was replaced by basal daily intake of 2-5 ml of saline. Sodium loss in urine was minimal, but milk sodium concentration was unchanged, and pups grew normally. Saline intake was enhanced when lactating rats that had been maintained on standard laboratory chow were injected with 30% polyethylene glycol solution to reduce plasma volume but no more so than when virgin female rats or male rats were similarly colloid-treated. Lactating rats markedly increased their intake of NaCl solution after simply depriving them of dietary sodium for 4 days, whereas male and virgin female rats did not. These findings indicate that pronounced sodium appetite does not invariably accompany lactation in rats, although it can occur whenever such animals become hypovolemic or sodium deficient.

Animals↗
PubMed1983

Self-administered intravenous infusion of hypertonic solutions and sodium appetite of sheep.

The effects of self-administered iv infusion of hypertonic NaCl, mannitol, glucose, urea, or isotonic NaCl on Na appetite were studied. Sodium-depleted sheep were trained to bar press in order to replace Na deficits of 300-500 mmol. During basal conditions, each delivery to a drinking cup was 15 ml of .6 M NaHCO3 (9 mmol). In the experimental situation, an iv infusion (10 ml) was given automatically with each delivery to the drinking cup. The ingestion of NaHCO3 solution was significantly reduced by all of the hypertonic solutions, the largest decrease being caused by hypertonic NaCl or mannitol. The decreased intake was observed within 10 (with infusion of hypertonic NaCl, mannitol, or glucose) or 20-40 (with urea infusion) min irrespective of whether water was concurrently available to drink. At 20 min, plasma Na concentration was increased by hypertonic NaCl, decreased by mannitol or glucose, and not changed by urea. Cerebrospinal fluid (CSF) Na concentration was increased by all of the hypertonic solutions. Isotonic NaCl had no effect on the ingestion of NaHCO3 solution, plasma, or CSF composition. In regard to the "turn-off" of Na appetite by systemic infusion, these data are consistent with the theory of neural cells within the blood-brain barrier responsive to changes of Na concentration or osmolality in their environment. In contrast, water intake was stimulated by hypertonic NaCl or mannitol but not by urea or glucose, results suggestive that the sensors involved in thirst (e.g., osmoreceptors) are in an area of the brain lacking the blood-brain barrier.

Animals↗
PubMed1983

Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: I. Relation to urinary sodium excretion.

Intracerebroventricular infusion of angiotensin II (Ang II) elicits a substantial sodium appetite in the rat. The present results demonstrate that this phenomenon consists of a small, early phase of sodium ingestion that is not the result of prior sodium loss but that thereafter urinary excretion of sodium exceeds intake and consequently the animals become hyponatremic and hypovolemic. The larger and more sustained bouts of sodium ingestion occurring 8-12 hr after the start of the Ang II infusion appear to represent a behavioral compensation for this incurred sodium deficit. These results confirm the arousal of a sodium appetite by action of Ang II on the brain but indicate the need for caution in assigning to it a direct and exclusive role in the neuroendocrine control of sodium intake.

Angiotensin II↗
PubMed1983

Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: II. Synergistic interaction with systemic mineralocorticoids.

Angiotensin and mineralocorticoids, the hormones of sodium conservation, acted together to arouse a sodium appetite with shorter latency and greater magnitude than is produced by larger amounts of each acting alone. This potentiation was selective for sodium ingestion and occurred in the absence of significant changes in sodium balance. Therefore, because endogenous angiotensin and mineralocorticoids are concurrently elevated during sodium deficiency, sodium appetite may be aroused by a synergy of the peptide and the steroid.

Angiotensin II↗
PubMed1984

Multiple factors in the satiation of salt appetite.

There is evidence in the literature that has been taken to show that, unlike hunger and thirst, salt appetite cannot be satiated in the absence of salt taste stimulation. The present study showed that repletion of body sodium in the absence of taste stimulation, that is, by gavage, can diminish subsequent saline intake. The satiating effects of gavage versus drinking of saline were studied at various intervals after repletion. For the first few hours, gastric loading was constantly less satiating than was drinking. But as the interval between gavage and testing was lengthened beyond 4-8 hr, the satiating effect began to increase until by 16 hr it was equal to that of drinking. The specificity of the satiating effect of saline gavage as a function of time between treatment and testing was also studied. There appeared to be a transient nonspecific blocking effect of solutes on solute intake which had a duration of less than 30 min. The satiating effect of saline gavage became specific after that time. The experiment suggests that there are multiple factors involved in the satiation of salt appetite--a taste factor, a short-latency post ingestional factor, and a long-latency postingestional factor.

Animals↗
PubMed1979

Modulation of behavioral inhibition in appetitive extinction following manipulation of adrenal steroids in rats: implications for involvement of the hippocampus.

Corticosterone, the principal glucocorticoid in the rat, binds selectively to the CA1 pyramidal neurons of the hippocampus where the hormone has been demonstrated to exert a moderate chronic suppression of spontaneous activity. In the first experiment of the current study, the functional behavioral significance of this hormone--brain interaction was investigated in the extinction of an appetitive runway response in normal rats and those with lesions of the hippocampus. During extinction, half of the animals in each group were given daily subcutaneous injections of corticosterone. Whie the classical retardation effect of hippocampal lesions on appetitive extinction was replicated, hormone treatment was without effect in normal or hippocampally damaged subjects. The absence of a hormone effect in normals was primarily attributed to a saturated limited-binding system operating in the normal animal. Experiment 2 tested this notion, repeating the first experiment, with adrenal-ectomized (ADX), ADX + corticosterone replacement, and normal groups of animals. Adrenalectomy produced a striking facilitation of extinction which was speculated to be the result of a hyperactive inhibitory neural organ free from an inhibitory endocrine feedback. Corticosterone treatment normalized the progress of extinction in ADX animals, providing support for the afore-mentioned speculation. In the normal animal, it appears that a stress-induced surge in hormone level interacts with a limited-capacity neural binding to produce a transient dynamic range of behavioral disinhibition, perhaps promoting persistence during initial stages of frustrative nonreward in moderate stress tasks.

Animals↗
PubMed1981

Disruption of appetite but not hunger or satiety following small lesions in the amygdala of rats.

Discretely localized lesions were made in the amygdala to examine how specifically they might alter various measures of feeding behavior in male rats. Behavioral tests included spontaneous intake and body weight regulation, reactivity to saccharin and quinine solutions, conditioned taste aversion, the feeding response to food deprivation, the response to glucose gavage, and teh response to dietary amino acid imbalance. Lesions in virtually all regions of the amygdala disrupted feeding behavior in some respect, but alterations in specific tasks were associated only with highly circumscribed brain damage. Body weight regulation, spontaneous food and water intake, and the responses to glucose gavage and long-term food deprivation were not altered by lesions in the amygdala. The results provide evidence that, in the rat, the amygdala may play a greater role in appetite than in hunger or safety. In particular, amygdaloid nuclei may participate in maintaining a negative bias in the reactivity to all appetitive stimuli.

Amygdala↗
PubMed1989

Forebrain sites of action for drinking and salt appetite to angiotensin or captopril.

Three-hour infusions of angiotensin II (ANG II) agonists and antagonists were used to determine the relative sites of action of ANG in producing water drinking and salt appetite. In the first experiment, lateral ventricular (LV) but not fourth ventricular (4V) ANG II elicited water and saline intake, and LV but not 4V sarile, a competitive ANG II receptor blocker, reduced saline intake aroused by ip injections of 10 mg/kg furosemide and 6 mg/kg captopril. In the second experiment, water, but not saline, intake to furosemide-captopril treatment was reduced by sarile infusions into the subfornical organ (SFO). It is concluded that (a) brain ANG receptors for water and saline intakes are more accessible from the forebrain than the hindbrain ventricles and (b) receptors for water drinking, but not saline intake, after captopril reside in part in the SFO. Salt appetite appears to be dependent on ANG II receptors somewhere in the forebrain other than in the SFO.

Angiotensin II↗
PubMed2005

Drug Insight: appetite suppressants.

The term 'appetite suppressant' is used to denote drugs that act primarily on the neurochemical transmitters of the central nervous system to reduce food intake. In addition to drugs that release or mimic the effect of norepinephrine (noradrenaline), this could include drugs that inhibit: reuptake of norepinephrine or 5-hydroxytryptamine (also known as serotonin); bind to the gamma-aminobutyric acid receptors or the cannabinoid receptors; and some peptides that reduce food intake. The sympathomimetic drugs phentermine, diethylpropion, benzphetamine, and phendimetrazine--so named because they mimic many effects of norepinephrine--are only approved in a few countries, and then only for short-term use. Sibutramine, a norepinephrine-5-hydroxytryptamine reuptake inhibitor, is approved for long-term use. Several new mechanisms for drug action are under investigation. Appetite suppressants should be viewed as useful adjuncts to diet and physical activity and might help selected patients to achieve and maintain weight loss.

Appetite Depressants↗
PubMed2004

Does perinatal omega-3 polyunsaturated fatty acid deficiency increase appetite signaling?

OBJECTIVE: To investigate the effect of maternal dietary omega-3 polyunsaturated fatty acid (PUFA) deficiency and repletion on food appetite signaling. RESEARCH METHODS AND PROCEDURES: Sprague-Dawley rat dams were maintained on diets either supplemented with (CON) or deficient in (DEF) omega-3 PUFA. All offspring were raised on the maternal diet until weaning. After weaning, two groups remained on the respective maternal diet (CON and DEF groups), whereas a third group, born of dams fed the DEF diet, were switched to the CON diet (REC). Experiments on food intake began when the male rats reached 16 weeks of age. Food intake was stimulated either by a period of food restriction, by blocking glucose utilization (by 2-deoxyglucose injection), or by blocking beta-oxidation of fatty acids (by beta-mercaptoacetate injection). RESULTS: DEF animals consumed more than CON animals in response to all stimuli, with the greatest difference (1.9-fold) demonstrated following administration of 2-deoxyglucose. REC animals also consumed more than CON animals in response to food restriction and 2-deoxyglucose but not to beta-mercaptoacetate. DISCUSSION: These findings indicate that supply of omega-3 PUFA, particularly during the perinatal period, plays a role in the normal development of mechanisms controlling food intake, especially glucoprivic (i.e. reduced glucose availability) appetite signaling. Dietary repletion of omega-3 PUFA from 3 weeks of age restored intake responses to fatty acid metabolite signaling but did not reverse those in response to food restriction or glucoprivic stimuli.

Animals↗
PubMed1998

Breakfasts high in monoglyceride or triglyceride: no differential effect on appetite or energy intake.

OBJECTIVE: To test whether isoenergetic isoenergetically-dense doses of dietary 1-monoglyceride or triglyceride differentially influence appetite and meal-to-meal energy intake in man. DESIGN: Six men and six women were each studied twice in a 2 d protocol. On day 1 (maintenance day) they were fed a medium fat (MF) maintenance diet (MF: 40% fat, 47% carbohydrate and 13% protein by energy) calculated at 1.6 x resting metabolic rate (RMR). On day 2 (manipulation day) at 08.30 h subjects consumed a high-fat breakfast designed to contain 80-85% of RMR, composition 10% protein, 56% fat and 34% carbohydrate by energy, with 65% of energy for fat derived as either 1-monoglyceride or triglyceride. Food and energy intake were monitored at lunch (given at 12.30pm) and throughout the remainder of the day. During this time subjects had ad libitum access to isoenergetic, isoenergetically dense MF (40:47:13) foods (550kJ/100g), until 22.30pm). Subjective hunger and satiety were tracked hourly, during waking hours. RESULTS: There was no significant effect of fat type on food or energy intake at lunch or during the ad libitum period. There was no diet effect on subjective hunger (F(1,10)0.00; P= 0.975) in the inter-meal periods of morning or afternoon, nor during the whole day. Subjects found both diets to be similarly pleasant (F(1,61)0.84;P= 0.364). Men and women responded similarly, except that men ate more on all occasions than women. CONCLUSIONS: This study suggests that when a large dose of l-monoglyceride or triglyceride is incorporated into a breakfast meal, it behaves in a manner that is very similar to triglyceride in terms of the effects on hunger, appetite or feeding behaviour.

Adult↗