Regulation of fluid intake in dogs following water deprivation

Whereas water loss in land living animals occurs continuously, water intake takes place discontinuously. At the normal operating set point of plasma osmolality, urine is more concentrated than plasma due to secretion of vasopressin. Thus animals operate around a state of mild dehydration. As water loss occurs, the severity of dehydration and thirst increase in intensity and at some point water intake occurs. Sufficient water is consumed to return plasma osmolality to the normal operating set point. Food intake and water balance are interdependent as food provides the osmoles which determine obligatory renal solute excretion. When dry food with the same osmotic content was substituted for canned food (water content 74%), dogs increased water intake from 24.2 +/- 4.3 to 62.2 +/- 8.8 ml/kg. Urine output and urine osmolality were unchanged, as under conditions of normal hydration, near maximal urine concentration is achieved. Changing water intake is the only available variable to maintain water balance. During water deprivation, the major renal mechanism appears to be natriuresis. In rehydration, satiety mechanisms ensure appropriate water intake and renal sodium conservation restores sodium balance.     

Baclofen Pretreatment Attenuates the Suppressant Effect of Intraperitoneal Administration of Cholecystokinin (CCK) on Food Intake in Rats

The aim of this study was to investigate whether pretreatment with the GABAB receptor agonist baclofen could prevent the inhibitory effect of systemically administered cholecystokinin (CCK) on food intake in rats. Baclofen (2 mg/kg, SC) administered 60 min prior to IP injection of CCK (5 μg/kg) significantly attenuated the suppressant effect of the peptide on feeding in nondeprived rats (Experiment 1) and rats that had been deprived of food for 22 h (Experiment 2). Baclofen had no significant effects on food intake when administered alone. The results suggest that the inhibitory effect of exogenous peripheral CCK on food intake may be dependent on an interaction with a GABAB-receptor mediated mechanism. Copyright © 1996 Elsevier Science Inc.     

Vagotomy fails to block the satiating effect of food in the stomach

Normal rats and rats with bilateral subdiaphragmatic vagotomy, each equipped with a pyloric noose, ate liquid food after 3-hr food deprivation. When the noose was open, ingested food accumulated in the stomach and entered the intestine in normal fashion. When the noose was closed, ingested food was trapped in the stomach and did not enter the intestine. Normal and vagotomized rats ate the same size meal with the noose closed as they ate with the noose open and all rats displayed a postprandial sequence of satiety behavior that culminated in resting. Thus, vagotomy failed to block the satiating effect of food in the stomach. This result suggests that gastric distension mediated by vagal afferents is not a necessary stimulus for satiety elicited by food in the stomach.     

Hypothalamic sensitivity to 2-deoxy-D-glucose and glucose: effects on feeding behavior

The effect on food intake of intrahypothalamic deposition of glucose or the glucose metabolic inhibitor 2-deoxy-D-glucose was studied to determine the function of the often hypothesized hypothalamic glucoreceptors in feeding behavior. Our results suggest that the lateral hypothalamic region, as well as the medial hypothalamus, contain glucoreceptive cells that form part of a feeding system.     

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.     

Behavioral patterns proceeding from liver thermoreceptors

Subdiaphragmatic denervated, liver heated rats eat as much and as long as subdiaphragmatic denervated, non-heated rats. This points to vagus and/or splanchnic nerve afferentation from hepatic thermoreceptors. Left abdomen heated rats eat and drink as much as left abdomen non-heated rats. Since however they show some different behavior patterns, the intervention of other nerve fibers other than vagal and/or splanchnic fibers should be acknowledged in order to account for the different behavior pattern.     

Behavioral correlates of oral and postingestive satiety in the rat

Hungry rats display the characteristic "satiety sequence" after drinking a glucose solution: The end of ingestion is accompanied by grooming and exploring, followed by resting. With saccharin solutions over a range of concentrations, however, ingestion is accompanied and followed by persistent grooming and exploring; resting rarely occurs. Gastric preloads of glucose solution promote resting to reinstate the "satiety sequence" after a bout of saccharin ingestion. Therefore, the systemic effects of glucose are sufficient to promote resting. In the absence of postingestive factors, the "satiety sequence" is incomplete following saccharin ingestion as it is after sham-feeding.     

Comparison of gastric, duodenal and jejunal contributions to the inhibition of food intake in the rat

Rats equipped with tubes leading to their stomach, duodenum or jejunum were infused with a liquid diet for 9 hr (4 ml/hr) and were allowed to eat during the last 8 hr of infusion. All rats ate significantly less on diet infusion days than on saline or no infusion days. A second study showed that a taste aversion could not be conditioned to flavored water associated with diet infusion. Apparently, intrajejunal injection of nutrients produces satiety and not discomfort. Infusion of the diet for 5 consecutive days into the stomach, duodenum or jejunum consistently and significantly lowered food intake by reducing meal size, not meal frequency. Results suggest that the small intestine below the infusion site contributes to normal satiety.     

Vagal mediation of the cholecystokinin satiety effect in rats

Central (intracerebroventricular) and peripheral (intraperitoneal) injections of the octapeptide of cholecystokinin (CCK-8) were compared to determine the most effective route of administration to elicit satiety for food intake in the rat. Subdiaphragmatic bilateral vagotomy and spinal cordotomy (T2-T3) were also performed to investigate the importance of visceral nerves for the satiety effect. CCK-8 suppressed feeding and elicited satiety resting behavior when injected peripherally but it was less effective when injected centrally. The satiety effect of CCK-8 or CCK-33 following peripheral injections was blocked by vagotomy whereas spinal cordotomy had no effect. The results indicate that some component of the vagus is required to mediate the peripherally induced cholecystokinin satiety effect, but the splanchnic nerves are not necessary. The weak effect of CCK-8 following ventricular administration is additional evidence suggesting that cholecystokinin of intestinal origin acts in the periphery rather than directly on the brain to elicit its typically rapid satiety effect in rats.     

Examining the effects of lipopolysaccharide and cholecystokinin on water ingestion: comparing intake and palatability

Lipopolysaccharide (LPS) and cholecystokinin (CCK) have been shown to have anorectic properties in a variety of species. The present study examined the effects of LPS and CCK, both alone and in combination, on two different aspects of water ingestion, water intake and palatability. On test days, animals were first injected intraperitoneally (i.p.) with either LPS (200 microg/kg) or NaCl vehicle, and 2 h later received a second injection of either CCK (8 microg/kg) or NaCl vehicle. In Experiment 1, water intake was monitored for 1 h on 3 separate test days 72 h apart; while in Experiment 2, water palatability was assessed using the taste reactivity test (TRT), on two separate test days 72 h apart. Both LPS and CCK significantly (p<0.05) reduced water intake, with the effects of combined LPS with CCK being more pronounced than either agent injected alone. Rats developed a rapid tolerance to the effects of LPS on water intake on subsequent exposures to LPS. Results from the TRT indicated that LPS enhanced water palatability (p<0.05), as evidenced by a high level of ingestive responding, whereas CCK produced a pattern of responding indicative of satiety. LPS plus CCK reduced ingestive responding on the first test day, but these responses were significantly increased on the second test day (p<0.05). These results demonstrate that although LPS reduces water intake, it enhances water palatability. The results further underscore the necessity for examining palatability changes in addition to intake measures when studying the regulation of feeding and drinking.