Satiety role of the small intestine examined in sham-feeding rhesus monkeys.

Gibbs, James; Maddison, S.; Rolls, Edmund T.

doi:10.1037/h0077845

Cited by 62 publications

(17 citation statements)

References 32 publications

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“…Intestinal nutrient infusions reduce food intake in many species, including humans (14) - an effect that commences within seconds of nutrient infusion, indicating that at least some of the associated satiation signals emanate from the gut, rather than from postabsorptive sources (22). These, and other, findings demonstrate that the intestines play a dominant role in satiation.…”

Section: Intestinal Satiationmentioning

confidence: 78%

Gastrointestinal regulation of food intake

Cummings¹,

Overduin²

2007

J. Clin. Invest.

999

827

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Despite substantial fluctuations in daily food intake, animals maintain a remarkably stable body weight, because overall caloric ingestion and expenditure are exquisitely matched over long periods of time, through the process of energy homeostasis. The brain receives hormonal, neural, and metabolic signals pertaining to body-energy status and, in response to these inputs, coordinates adaptive alterations of energy intake and expenditure. To regulate food consumption, the brain must modulate appetite, and the core of appetite regulation lies in the gut-brain axis. This Review summarizes current knowledge regarding the neuroendocrine regulation of food intake by the gastrointestinal system, focusing on gastric distention, intestinal and pancreatic satiation peptides, and the orexigenic gastric hormone ghrelin. We highlight mechanisms governing nutrient sensing and peptide secretion by enteroendocrine cells, including novel taste-like pathways. The increasingly nuanced understanding of the mechanisms mediating gut-peptide regulation and action provides promising targets for new strategies to combat obesity and diabetes.

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Section: Intestinal Satiationmentioning

confidence: 78%

Gastrointestinal regulation of food intake

Cummings¹,

Overduin²

2007

J. Clin. Invest.

999

827

View full text Add to dashboard Cite

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“…5). It has been shown that free drinking behavior in water-deprived monkeys is controlled by many factors acting on different time scales, such as cellular dehydration, intestinal stimulation by water, gastric distension, and oropharyngeal metering (Gibbs et al 1981;Maddison et al 1980;Rolls and Rolls 1982;). The quality of the sigmoid function fit to our data shows that the collective effects of all these factors on the behavior can be described with a simple phenomenological model.…”

Section: Role Of the Internal Statementioning

confidence: 99%

Measuring and Modeling the Interaction Among Reward Size, Delay to Reward, and Satiation Level on Motivation in Monkeys

Minamimoto

Camera²,

Richmond³

2009

Journal of Neurophysiology

150

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Minamimoto T, La Camera G, Richmond BJ. Measuring and modeling the interaction among reward size, delay to reward and satiation level on motivation in monkeys. J Neurophysiol 101: 437-447, 2009. First published November 5, 2008 doi:10.1152/jn.90959.2008. Motivation is usually inferred from the likelihood or the intensity with which behavior is carried out. It is sensitive to external factors (e.g., the identity, amount, and timing of a rewarding outcome) and internal factors (e.g., hunger or thirst). We trained macaque monkeys to perform a nonchoice instrumental task (a sequential red-green color discrimination) while manipulating two external factors: reward size and delay-to-reward. We also inferred the state of one internal factor, level of satiation, by monitoring the accumulated reward. A visual cue indicated the forthcoming reward size and delay-to-reward in each trial. The fraction of trials completed correctly by the monkeys increased linearly with reward size and was hyperbolically discounted by delay-to-reward duration, relations that are similar to those found in free operant and choice tasks. The fraction of correct trials also decreased progressively as a function of the satiation level. Similar (albeit noiser) relations were obtained for reaction times. The combined effect of reward size, delay-to-reward, and satiation level on the proportion of correct trials is well described as a multiplication of the effects of the single factors when each factor is examined alone. These results provide a quantitative account of the interaction of external and internal factors on instrumental behavior, and allow us to extend the concept of subjective value of a rewarding outcome, usually confined to external factors, to account also for slow changes in the internal drive of the subject.

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“…Considerable advances have been made in understanding the mechanisms by which nutrients in the intestine suppress intake in a number of species (30,33), including rats (42,51,53) and humans (74). For example, it is well documented that intestinal carbohydrates reduce food intake in a dose-responsive manner (53,76) by preabsorptive (63,78) as well as postabsorptive (71) factors, largely through vagal afferent pathways (78,79).…”

mentioning

confidence: 99%

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

Savastano¹,

Carelle²,

Covașă³

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Savastano, David M., Melissa Carelle, and Mihai Covasa. Serotonin-type 3 receptors mediate intestinal Polycose-and glucoseinduced suppression of intake. Am J Physiol Regul Integr Comp Physiol 288: R1499 -R1508, 2005. First published February 17, 2005 doi:10.1152/ajpregu.00745.2004.-Ondansetron, a selective serotonin-type 3 (5-HT3) receptor antagonist, was used to test the hypothesis that duodenal infusion of isosmotic solutions of Polycose or its hydrolytic product glucose suppressed intake through 5-HT3 receptors. Polycose suppressed sucrose intake across both concentrations infused (132 mM, 7.6 Ϯ 0.6 ml; 263 mM, 2.3 Ϯ 0.5 ml), compared with intake under control conditions (12.6 Ϯ 0.3 ml, P Ͻ0.001). Pretreatment with 1.0 mg/kg ondansetron attenuated reduction of sucrose intake induced only by the highest concentration of Polycose (4.6 Ϯ 0.8 ml, P ϭ 0.004). Dose-response testing revealed that suppression of food intake by 263 mM Polycose was equally attenuated by ondansetron administered at 1.0, 2.0, and 5.0 mg/kg but not when given at 0.125, 0.25, and 0.5 mg/kg. Acarbose, an ␣-glucosidase inhibitor, attenuated Polycose-induced suppression of food intake, and pretreatment with 1.0 mg/kg ondansetron had no further effect. Suppression of intake after 990 mM glucose but not mannitol infusion was attenuated by pretreatment with 1.0 mg/kg ondansetron. The competitive SGLT1 inhibitor, phloridzin, had no effect on 60-min 990 mM glucose-induced suppression of intake or the ability of ondansetron to attenuate this suppression of intake. Conversely, glucoseinduced suppression of intake was attenuated by phloridzin at earlier time points and further attenuated when rats were pretreated with 1.0 mg/kg ondansetron. Ondansetron administration alone had no effect on intake at any dose tested. We conclude that 5-HT 3 receptors participate in the inhibition of food intake by intraduodenal infusion of carbohydrate solutions through a posthydrolytic, preabsorptive mechanism. nutrient absorption; food intake; satiation THE PRESENCE OF NUTRIENTS in the intestine elicits signals essential to feedback control of ingestion. Considerable advances have been made in understanding the mechanisms by which nutrients in the intestine suppress intake in a number of species (30, 33), including rats (42, 51, 53) and humans (74). For example, it is well documented that intestinal carbohydrates reduce food intake in a dose-responsive manner (53, 76) by preabsorptive (63, 78) as well as postabsorptive (71) factors, largely through vagal afferent pathways (78, 79). However, the complete mechanism(s) by which intestinal oligosaccharides or monosaccharides is perceived to elicit negative feedback control of intake is not known. Administration of the ␣-glucosidase inhibitor, acarbose, attenuates reduction of food intake and c-Fos-immunoreactivity by maltotriose (62, 63). Moreover, inhibition of sodium-dependent glucose transporter 1 (SGLT 1 ) by intestinal phloridzin infusion fails to attenuate suppression of food intake and vagal afferent activation...

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Satiety role of the small intestine examined in sham-feeding rhesus monkeys.

Cited by 62 publications

References 32 publications

Gastrointestinal regulation of food intake

Gastrointestinal regulation of food intake

Measuring and Modeling the Interaction Among Reward Size, Delay to Reward, and Satiation Level on Motivation in Monkeys

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

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