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PubMed1994

Sodium appetite, thirst, and body fluid regulation in humans during rehydration without sodium replacement.

After a 7-h H2O and Na+ depletion period (DP), produced by intermittent light exercise (8 bouts) at 35 degrees C, we examined thirst and taste palatability responses to 10 different NaCl solutions during 23 h of rehydration (RH) at 25 degrees C. During DP, net H2O and Na+ loss were 27.2 +/- 2.9 ml/kg and 3.29 +/- 0.45 meq/kg, respectively. Plasma osmolality (POsm) and plasma Na+ concentration ([Na+]p) increased significantly during DP by 3.4 +/- 1.2 mosmol/kgH2O and 3.0 +/- 1.0 meq/kgH2O, respectively. Plasma volume (PV) decreased by 6.5 +/- 1.9%. Thirst rating, renal fractional reabsorption of H2O, and plasma arginine vasopressin concentration (PAVP) increased as POsm increased. This increased thirst was accompanied by increased palatability ratings to H2O. During RH, subjects drank deionized H2O ad libitum and ate a Na(+)-free diet for 23 h. POsm and [Na+]p returned to control levels within 1 h RH and remained at or below the control thereafter. PV remained reduced by approximately 5% throughout RH. The increased thirst and PAVP returned to their respective control levels within 1 h of RH as POsm decreased, but thirst rating increased against between 17 and 23 h of RH without increase in POsm or PAVP. Palatability ratings to a 1 M NaCl solution at and after 3 h RH and palatability ratings to 0.3 M at 17 and 23 h RH were significantly higher than control. Plasma aldosterone concentration (PAldo) increased after DP, decreased with drinking, and increased again between 6 and 23 h of RH, accompanied by a marked decrease in fractional Na+ excretion to < 0.07%. Thus both Na+ preference and thirst in humans are influenced by body fluid and electrolyte status. The increased Na+ palatability (Na+ appetite) was preceded by osmotically induced thirst, and accompanied by nonosmotically driven thirst [extracellular fluid (ECF) thirst] and increased PAldo. The "Na+ appetite" and "ECF thirst" along with increased renal Na+ retention could contribute to ECF volume regulation after thermally induced H2O and Na+ depletion.

Adult↗
PubMed1994

Effects of sinoaortic baroreceptor denervation on depletion-induced salt appetite.

This study examined the effects of denervation of the carotid sinus and aortic arch baroreceptors on sodium depletion-induced salt appetite in rats. Depletion of extracellular fluid began with two injections of furosemide (10 mg/kg sc), 30 min apart, and removal of all ambient sodium from the cages. Water and sodium-deficient chow were available overnight. The next morning, access to 0.3 M NaCl was provided, and intakes of water and saline were measured every 30 min for 2 h and again at 24 h. Three such tests were administered. Groups of sham and sinoaortic baroreceptor-denervated (SAD) rats had equivalently negative water and sodium balances before access to saline the next morning. Sham-denervated rats drank sufficient saline in 2 h to achieve positive sodium balance and subsequently ingested sodium in excess of need for another 22 h. SAD rats drank half as much saline as sham-denervated rats by 2 and 24 h and remained in negative balance at 2 h. Sham-denervated rats increased their intakes of saline solution with repeated tests, but SAD rats did not. These findings suggest that arterial baroreceptors provide critical neural input for the normal expression of salt appetite.

Animals↗
PubMed1994

Endocrine changes associated with a rapidly developing sodium appetite in rats.

Simultaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg) results in short-latency thirst and sodium appetite (i.e., the rapid ingestion of water and NaCl solution). To elucidate potential mechanisms for mediating this behavior, changes in plasma levels of key hormones involved in fluid intake and balance were characterized in rats subjected to this treatment protocol. Rats treated jointly with furosemide and low-dose captopril had exaggerated increases in plasma renin activity and angiotensin I but equivalent increases in plasma aldosterone compared with rats treated with either agent alone. Treatment with furosemide plus low-dose captopril increased plasma vasopressin but not plasma oxytocin. The administration of a higher dose of captopril (100 mg/kg) with furosemide, a combination of drugs that does not stimulate fluid intake (29), further increased plasma renin activity and angiotensin I but prevented the rise in plasma vasopressin. The results support the hypothesis that thirst and salt appetite generated by this protocol depend on angiotensin II formed within brain circumventricular organs rather than the systemic circulation.

Aldosterone↗
PubMed1997

Central infusion of the AT1 receptor antagonist losartan inhibits thirst but not sodium appetite in cattle.

Experiments in cattle compared the effects of intracerebroventricular (i.c.v.) infusions of losartan and PD-123319 on water intake caused by water restriction, i.c.v. infusion of hypertonic NaCl, or i.c.v. infusion of angiotensin II (ANG II). The effects of these receptor antagonists on sodium intake caused by sodium depletion were also examined. Losartan infusion caused dose-dependent inhibition of the high water intake caused by the physiological stimulus of water restriction or by ANG II infusion but did not affect salt appetite. PD-123319 infused at equimolar or greater (in ANG II experiments) doses did not affect water intake or salt intake due to sodium depletion. The results of these i.c.v. infusion experiments confirm our earlier proposal that the physiological regulation of water intake in cattle may be mediated by ANG II acting centrally via AT1 receptors. The dose of losartan that inhibited thirst in cattle did not inhibit sodium appetite, nor did an equimolar dose of PD-123319.

Angiotensin II↗
PubMed1997

Effects of small intestinal nutrient infusion on appetite and pyloric motility are modified by age.

The mechanisms responsible for the reduction in appetite and slowing of gastric emptying in older persons are unknown. The aims of this study were to evaluate the effects of aging on small intestinal regulation of appetite and pyloric motility. Eight healthy older (age 65-75 yr) and seven healthy young (age 20-34 yr) male subjects received isocaloric (2.9 kcal/min) intraduodenal infusions of lipid and glucose for 120 min, each on separate days. During the intraduodenal infusions, perceptions of hunger, desire to eat, and fullness were assessed by visual analog scales. Pyloric motility (isolated pyloric pressure waves and tonic pyloric pressure) was measured by manometry during the intraduodenal lipid infusion. On each day, after completion of the intraduodenal nutrient infusion the subject was offered a buffet meal and food intake was quantified. Before intraduodenal nutrient infusions, sensations of hunger (P < 0.01) and desire to eat (P < 0.05) were less in the older compared with the young subjects. In the young, intraduodenal lipid suppressed hunger to a greater extent than intraduodenal glucose (P < 0.05). In older persons, neither intraduodenal nutrient infusion suppressed hunger. Intraduodenal lipid and glucose increased fullness in both age groups (P < 0.05 for both), with no significant difference between the two nutrients. There was no significant difference in food intake from the buffet meal between the elderly and young subjects. Intraduodenal lipid infusion stimulated phasic pyloric pressure waves in both age groups (P < 0.01 for both), and this response was greater (P < 0.05) in older persons. There was an increase (P < 0.01) in tonic pyloric pressure during intraduodenal lipid infusion that was not significantly different between the two age groups. We conclude that the effect of small intestinal lipid infusion on hunger is attenuated, and the stimulation of phasic pyloric pressure waves increased in healthy older persons compared with healthy young males. Increased feedback from small intestinal nutrients does not appear to be responsible for the physiological anorexia of aging.

Adult↗
PubMed1998

Evidence that brain angiotensin II is involved in both thirst and sodium appetite in baboons.

The roles of ANG II in the brain mechanisms subserving thirst and Na appetite in baboons were investigated by chronic intracerebroventricular infusions of ANG II and AT1-receptor antagonists using subcutaneous miniosmotic pumps and by oral administration of captopril. ANG II at 3 or 5 micrograms/h for 7 days increased water intake from 2,455 +/- 107 to 7,052 +/- 562 ml/day by day 6 and 300 mM NaCl intake from 8.3 +/- 1.1 to 275 +/- 87 mmol/day by day 5. Concurrent intracerebroventricular losartan (300 micrograms/h) did not substantially reduce these responses, but they were abolished by intracerebroventricular ZD-7155 (50 micrograms/h). The increase of 300 mM NaCl intake when it was offered after intramuscular injection of furosemide, 2 mg . kg-1 . day-1 for 3 days, was unaltered by intracerebroventricular losartan (300 micrograms/h) but was reduced by intracerebroventricular ZD-7155 (50 micrograms/h) infused throughout Na depletion/repletion; oral captopril (1 g, 3 and 18 h before access to 300 mM NaCl) also reduced NaCl intake. Restriction of water intake to 25% of daily intake for 3 days caused a high intake of water on day 4, and this was reduced by intracerebroventricular losartan (300 micrograms/h) infused throughout the period of water restriction/rehydration. These novel results in a primate species suggest that brain ANG II is involved in both thirst and Na appetite, acting via AT1 receptors.

Administration, Oral↗
PubMed1999

Thirst and salt appetite elicited by hypovolemia in rats with chronic lesions of the nucleus of the solitary tract.

Cardiac vagal afferents terminating in the nucleus of the solitary tract (NTS) are believed to participate in stimulating neurohypophysial secretion of vasopressin as well as increased ingestion of water and NaCl solution in response to decreased blood volume. However, we recently reported that chronic lesions of NTS, which eliminate neural input from cardiac and arterial baroreceptors, do not impair hypovolemia-induced vasopressin secretion in rats. In the present investigation we sought to determine whether those sensory signals were necessary for hypovolemia-induced thirst and salt appetite. Rats with chronic lesions of the NTS increased consumption of water and NaCl solution normally when plasma volume was reduced isosmotically by subcutaneous injection of polyethylene glycol solution. These results were obtained whether rats were allowed to drink water or 0.15 M NaCl in one-bottle tests or water and 0.5 M NaCl in two-bottle tests. The induction of thirst and salt appetite by hypovolemia despite the apparent loss of neural input to the brain from cardiac volume-sensitive receptors indicates that other signals generated by plasma volume deficits can stimulate these behavioral responses in rats.

Animals↗
PubMed1991

Thirst and salt appetite in horses treated with furosemide.

When a preliminary experiment in sodium-replete ponies revealed an increase, but not a significant increase, in salt consumption after furosemide treatment, the experiment was repeated using sodium-deficient horses in which aldosterone levels might be expected to be elevated to test the hypothesis that a background of aldosterone is necessary for salt appetite. Ten Standardbred mares were injected intravenously with furosemide or an equivalent volume of 0.9% sodium chloride as a control to test the effect of furosemide on their salt appetite and blood constituents. Sodium intake and sodium loss in urine, as well as water intake and urine output, were measured and compared to determine accuracy of compensation for natriuresis and diuresis. Plasma protein and packed cell volume showed significant increases in response to furosemide treatment (F = 29.31, P less than 0.001 and F = 11.20, P less than 0.001, respectively). There were no significant changes in plasma sodium concentration or osmolality in response to the treatment (P greater than 0.05). The furosemide-treated horses consumed 126 +/- 14.8 g salt, significantly more than when they were given the control injection (94.5 +/- 9.8 g; t = 2.22, P = 0.05). In response to furosemide, horses lost 962 +/- 79.7 and consumed 2,170 +/- 5 meq sodium; however, compared with control, they lost 955 meq more sodium and ingested only 570 meq more sodium, so they were undercompensating for natriuresis. The furosemide-treated horses drank 9.6 +/- 0.8 kg of water, significantly more than when they received the control injection (6.4 +/- 0.8 kg; t = 6.9, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Metabolic and appetite responses to prolonged walking under three isoenergetic diets.

The effects of three isoenergetic diets on metabolic and appetite responses to prolonged intermittent walking were investigated. Eight men undertook three 450-min walks at intensities varying between 25-30 and 50-55% of maximal O2 uptake. In a balanced design, the subjects were given breakfast, snacks, and lunch containing total carbohydrate (CHO), protein (P), and fat (F) in the following amounts (g/70 kg body mass): mixed diet, 302 CHO, 50 P, 84 F; high-CHO diet, 438 CHO, 46 P, 35 F; high-fat diet, 63 CHO, 44 P, 196 F. Substrate balance was calculated by indirect calorimetry over the 450-min exercise period. Blood samples were taken before exercise and every 45 min during the exercise period. The high-fat diet resulted in a negative total CHO balance (-140 +/- 1 g) and a lower negative fat balance (-110 +/- 33 g) than the other two diets (P < 0.05). Plasma glucagon, nonesterified fatty acids, glycerol, and 3-hydroxybutyrate were higher with the high-fat diet (P < 0.05 vs. high CHO), whereas plasma insulin was lower after high fat (P < 0.05 vs. mixed and high CHO). Subjective ratings of fatigue and appetite showed no differences between the three trials. Although diet influenced the degree of total CHO and fat oxidation, fat was the main source of energy in all trials.

3-Hydroxybutyric Acid↗
PubMed2001

Selective expression of electrical correlates of differential appetitive classical conditioning in a feeding network.

Electrical correlates of differential appetitive classical conditioning were recorded in the neural network that underlies feeding in the snail Lymnaea stagnalis. In spaced training (15 trials over 3 days), the lips and the tentacle were used as CS+ (reinforced conditioned stimulus) or CS- (nonreinforced conditioned stimulus) sites for behavioral tactile conditioning. In one group of experimental animals, touch to the lips (the CS+ site) was followed by sucrose (the unconditioned stimulus, US), but touch to the tentacle (the CS- site) was not reinforced. In a second experimental group the CS+/CS- sites were reversed. Semi-intact lip-tentacle-CNS preparations were made from both experimental groups and a naive control group. Intracellular recordings were made from the B3 motor neuron of the feeding network, which allowed the monitoring of activity in the feeding central pattern generator (CPG) interneurons as well as early synaptic inputs evoked by the touch stimulus. Following successful behavioral conditioning, the touch stimulus evoked CPG-driven fictive feeding activity at the CS+ but not the CS- sites in both experimental groups. Naive snails/preparations showed no touch responses. A weak asymmetrical stimulus generalization of conditioned feeding was not retained at the electrophysiological level. An early excitatory postsynaptic potential (EPSP) response to touch was only enhanced following conditioning in the Lip CS+/tentacle CS- group but not in the Tentacle CS+/lip CS- group. The results show that the main features of differential appetitive classical conditioning can be recorded at the electrophysiological level, but some characteristics of the conditioned response are selectively expressed in the reduced preparation.

Animals↗
PubMed2002

Effects of lesions of nucleus taeniae on appetitive and consummatory aspects of male sexual behavior in Japanese quail.

Neurochemical, hodological and functional criteria suggest that the nucleus taeniae and parts of the adjacent archistriatum represent the avian homologue of parts of the mammalian amygdaloid complex. It has been proposed in particular that the nucleus taeniae is the homologue of the mammalian medial amygdala. In male quail, relatively large lesions to the posterior/medial archistriatum selectively decrease the expression of appetitive sexual behavior in a manner reminiscent of similar manipulations involving the medial amygdala in mammals. We investigated the effects of discrete lesions restricted to nucleus taeniae and of lesions to an adjacent part of the archistriatum (pars intermedium ventralis, AIv) on the expression of appetitive (ASB) and consummatory (CSB) aspects of male sexual behavior. ASB was measured by a learned social proximity response (after copulation a male quail stands in front of a window providing visual access to a female) and by the frequency of rhythmic cloacal sphincter movements. CSB was assessed by the frequency of mount attempts (MA) and cloacal contact movements (CCM). Lesions confined to nucleus taeniae and to AIv did not influence the acquisition or the maintenance of the two responses indicative of ASB. In contrast, lesions of nucleus taeniae significantly increased the occurrence frequencies of MA and CCM when administered before the beginning of behavior testing and increased the frequency of MA only when performed on sexually experienced subjects. No effect of AIv lesions could be detected. The discrepancy between these results and previous experiments in quail might reflect procedural differences, but more probably differences in locations of the lesions that were restricted in the current study to the anterior part of taeniae. Those in the Thompson study were in the posterior part of this nucleus. These findings indicate that there is a larger degree of functional heterogeneity in the nucleus taeniae than previously thought. The effects of taeniae lesions suggest that this nucleus, similar to the medial amygdala in mammals, might be implicated in the control of sexual satiety.

Amygdala↗
PubMed2006

Differences in the appetite-stimulating effect of orexin, neuropeptide Y and ghrelin among young, adult and old rats.

Aging is associated with a progressive decrease in appetite and food intake. The appetite-stimulating peptides orexin A, neuropeptide Y (NPY) and ghrelin are known to play a critical role in food intake. In this study, the stimulatory effect of intracerebroventricular administration of these peptides on food intake was compared among young (4 months old), adult (11 months old) and old (24-27 months old) male Wistar rats. A stainless steel cannula was implanted stereotactically into the left lateral ventricle. After a 7-day recovery period, different doses of orexin A (0.25-3 nmol), NPY and ghrelin (0.03-1 nmol) were injected into the left lateral ventricle without anesthesia. Food consumption was measured at 1, 2 and 4 h after injection. We also examined the plasma levels of acylated and desacyl ghrelin in young and old rats by ELISA. Intracerebroventricular administration of orexin A and NPY stimulated food intake in young and adult rats, but no effects were observed at any dose in old rats. Ghrelin increased food intake in a dose-dependent manner in all groups, and the effect of ghrelin was reduced with advancing age. Neither the acylated nor the desacyl plasma ghrelin level differed significantly between young and old rats. In conclusion, the orexigenic effect of the peptides orexin A, NPY and ghrelin decreased in old rats, and this reduction may have been responsible for the age-related decrease in food intake.

Aging↗
PubMed1996

Intracerebral administration of mineralocorticoid receptor antisense oligonucleotides attenuate adrenal steroid-induced salt appetite in rats.

The amygdala contains mineralocorticoid (MR) and glucocorticoid receptors (GR) involved in the arousal of salt appetite. In the present investigation, MR antisense oligonucleotides injected into the amygdala inhibited salt appetite induced by systemic desoxycorticosterone (DOCA) but not adrenalectomy (ADX). In contrast, GR antisense or scrambled oligonucleotides had no effect on stimulated salt intake. MR antisense oligomers also decreased MR but not GR in amygdala, whereas GR antisense oligomers decreased GR but not MR. Immunocytochemical labelling of the biotinylated MR antisense revealed that distribution of the oligomer was restricted to the injection site, with incorporation in neurons and neighboring glial cells. Together, these data demonstrate the utility of receptor antisense oligonucleotides for investigating the central actions of adrenal steroids and the role of amygdala in MR in DOCA-induced sodium intake.

Animals↗
PubMed1977

Effects of enteral and parenteral nutrition on appetite in monkeys.

Varied clinical observations of the presence of either hunger or anorexia during intragastric or intravenous alimentation have led to the current experiments. Nine rhesus monkeys (Macaca mulatta) were involved in studies of the long-term effects of enteral and parenteral nutrition on appetite as assessed by feeding behavior and gastric motility. The monkeys received either intragastric infusions of glucose or a complete liquid diet, or intravenous infusions of glucose or glucose/amino acid solutions. Oral intake was accurately adjusted to account for the calories administered by the intragastric route. Oral intake was also reduced in a calorically equivalent amount to account for the calories received during intravenous glucose. When glucose/amino acid solutions were administered parenterally, adjustments were less accurate, with resultant overeating and weight gain in some monkeys during parenteral nutrition, followed by prolonged suppression of appetite after cessation of the infusions. Further studies of the effects of varied compositions of parenteral nutrition, and varied methods of weaning from infusions, are indicated.

Animals↗
PubMed2004

Amphetamine decreases the expression and acquisition of appetitive conditioning but increases the acquisition of anticipatory responding over a trace interval.

The effects of amphetamine on selective learning were tested in a trace conditioning procedure, in which the informativeness of the conditioned stimulus (CS) (noise) was manipulated through the introduction of a time interval before the delivery of the unconditioned stimulus (UCS) (food). The results showed that d-amphetamine (0.5 and 1.5 mg/kg) impaired both the expression (Experiment 1b) and acquisition (Experiment 2) of appetitive conditioning. This was true for both trace and contiguously conditioned groups. The effects of the 0.5 mg/kg dose of d-amphetamine were not attributable to general motor (measured pre-CS) or motivational (measured post-UCS) effects of the drug. Moreover, the same pattern of effects (impaired appetitive conditioning, irrespective of the trace interval between CS and UCS) was confirmed in drug-free extinction tests. By contrast to the general depression in the acquisition and expression of associative learning observed under amphetamine, the 0.5 mg/kg dose promoted the acquisition of anticipatory responses made later in the trace interval (in Experiment 2 but, again, not the expression of previous conditioning in Experiment 1b). This suggests a dissociable effect of low-dose d-amphetamine on learning about the temporal relationship between CS and UCS.

Acoustic Stimulation↗
PubMed2004

Electrical signaling in central orexin/hypocretin circuits: tuning arousal and appetite to fit the environment.

In mammals, alertness and foraging are linked to the light-dark cycle and body energy levels. This link is crucially dependent on the novel peptide transmitters orexins/hypocretins. The firing of orexin neurons encodes the overall internal (body energy levels) and external (time of day) environment. In turn, orexins modulate arousal and appetite by innervating and electrically exciting wakeand appetite-promoting neurons. Electrical signaling in orexin circuits thereby couples arousal to the environment and synchronizes foraging with states of high alertness.

Animals↗
PubMed2006

Blood-brain leptin transport and appetite and reproductive neuroendocrine responses to intracerebroventricular leptin injection in sheep: influence of photoperiod.

Impaired anorectic actions of leptin may be due to intrahypothalamic insensitivity and/or reduced blood-brain transport. The influence of photoperiod on leptin responses and leptin transport from blood into cerebrospinal fluid (CSF) was examined in sheep. Sheep kept on ad libitum food for 15 wk in long days (LD) had higher voluntary food intake and lower GnRH/LH output than in short days (SD). Food intake was decreased approximately 30% after intracerebroventricular (icv) (and not iv) leptin injection, but only in SD. GnRH/LH secretion was decreased after icv (but not iv) leptin in both photoperiods. Leptin concentrations in CSF were higher in LD than SD but correlated with plasma leptin only in LD. Amounts of leptin entering CSF after iv leptin injection were greater in LD than SD. In a separate experiment, plasma (but not CSF) leptin was higher in fat than thin sheep in natural summer LD and after 5 wk in SD. CSF leptin correlated with plasma leptin in LD but not SD. CSF leptin after iv leptin injection was higher in thin than fat sheep but only in LD. Endogenous CSF to plasma concentration ratios correlated negatively with plasma concentrations, indicating decreased blood-brain transport with increased leptinemia. Therefore, icv (and not iv) leptin inhibited appetite only in SD and decreased GnRH/LH output in both photoperiods, and the proportion of circulating leptin entering CSF was higher in LD and thinner animals. Photoperiod apparently modulates intrahypothalamic leptin sensitivity of appetite, but not reproductive, regulatory pathways, whereas photoperiod and leptinemia influence leptin blood-brain transport.

Animals↗
PubMed2004

Somatostatin infusion lowers plasma ghrelin without reducing appetite in adults with Prader-Willi syndrome.

Prader-Willi syndrome (PWS) is characterized by life-threatening childhood-onset hyperphagia, obesity and, uniquely, high plasma levels of ghrelin, the orexigenic gastric hormone. Somatostatin suppresses ghrelin secretion in normal subjects. We therefore examined the effect of somatostatin on plasma ghrelin and appetite in four male PWS adults fasted overnight in a double-blind, placebo-controlled, randomized cross-over study. Subjects received an intravenous infusion of somatostatin (250 microg/hr) or saline for 300 min, and had blood samples taken every 30 min for measurement of plasma ghrelin and PYY3-36 (anorexigenic intestinal hormone) by radio-immunoassay, and glucose. Appetite was measured by counting sandwiches eaten over a 60 min free food access period from +120 min. Despite somatostatin lowering fasting plasma ghrelin by 60 +/- 2% (P = 0.04) to levels seen in non-PWS men, there was no associated reduction in food intake (105 +/- 9% of food intake during saline infusion, P = 0.6). Somatostatin also lowered plasma PYY levels by 45 +/- 16% (P = 0.04), and produced post-prandial hyperglycemia (P = 0.04). We conclude that either hyperghrelinemia may not contribute to hyperphagia in PWS adults, or perhaps concomitant reductions in anorexigenic gastrointestinal hormones by somatostatin counteracted any anorexigenic effect of lowering orexigenic ghrelin. Somatostatin analogues may therefore not be an effective therapy for obesity in PWS. Larger chronic studies with long-acting somatostatin analogues will be needed to determine their benefits and risks in treating PWS obesity.

Adult↗