Can adiponectin have an additional effect on the regulation of food intake by inducing gastric motor changes?

The regulation of food intake is a complex mechanism, and the hypothalamus is the main central structure implicated. In particular, the arcuate nucleus appears to be the most critical area in the integration of multiple peripheral signals.Among these signals, those originating from the white adipose tissue and the gastrointestinal tract are known to be involved in the regulation of food intake.The present paper focuses on adiponectin, an adipokine secreted by white adipose tissue, which is reported to have a role in the control of feeding by acting centrally. The recent observation that adiponectin is also able to influence gastric motility raises the question of whether this action represents an additional peripheral mechanism that concurs with the central effects of the hormone on food intake. This possibility, which represents an emerging aspect correlating the central and peripheral effects of adiponectin in the hunger-satiety cycle, is discussed in the present paper.     

The kappa-opioid U-50,488H suppresses the initiation of nocturnal spontaneous drinking in normally hydrated rats

The effect of a systemic (IP) treatment with 1.0, 3.0 and 9.0 mg/kg U-50,488H (U50), a highly selective kappa-agonist, on spontaneous, nocturnal ingestive behavior of the rat was studied using a microcomputer controlled data acquisition system. The latency to initiate drinking was increased and drinking behavior was suppressed in the first hour after injection in a dose-dependent manner. The consummatory indices of drinking were not affected. After this period of adipsia, a phase of polydipsia, that was probably due to the diuretic effect of U50, was evident. The prophagic effect of U50 was evident only at the dose of 3 mg/kg and was accompanied by an increased duration of feeding episodes but not by a reduced latency to feed. These results suggest that kappa-receptors play a pivotal role in modulating spontaneous drinking in the normally hydrated rat and that this control is mainly exerted on the motivational aspect of drinking.     

Cholecystokinin and neuropeptide Y receptors on single rabbit vagal afferent ganglion neurons: site of prejunctional modulation of visceral sensory neurons

A [¹²⁵I]cholecystokinin (CCK) analog and [¹²⁵I]peptide YY (PYY) were used to localize and characterize CCK and neuropeptide Y (NPY) receptor binding sites in the rabbit vagal afferent (nodose) ganglion. High concentrations of CCK and NPY binding sites were observed in 10.6% and 9.2% of the nodose ganglion neurons, respectively. Pharmacological experiments using CCK or NPY analogs suggest that both subtypes of CCK (CCK-A and CCK-B) and NPY (Y1 and Y2) receptor binding sites are expressed by discrete populations of neurons in the nodose ganglion. These results suggest sites at which CCK or NPY, released in either the nucleus of the solitary tract or a peripheral tissue, may modulate the release of neurotransmitters from a select population of visceral primary afferent neurons. Possible functions mediated by these receptors include modulation of satiety, opiate analgesia, and the development of morphine tolerance.     

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.