d-Fenf luramine Anorexia: Dissociation of Ingestion Rate, Meal Duration, and Meal Size Effects

Kaplan, Joel M.; Donahey, Jamie C. K.; Baird, John-Paul; Simansky, Kenny J.; Grill, Harvey J.

doi:10.1016/s0091-3057(96)00340-1

Cited by 20 publications

(13 citation statements)

References 22 publications

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“…Third, this nonvolumetric information does not affect the control of the volume ingested during the meals as measured by 3-min intakes or the size of the meal measured by 30-min intakes. The failure of changes in the rate of ingestion to affect total intake is consistent with the recent reports of Kaplan and coworkers (16,17). We interpret this failure to mean that the nonvolumetric information did not contribute to the negative feedback from the stomach that is integrated with the positive and negative feedbacks from the mouth to control ingestion during the meal under these conditions.…”

Section: Cluster Size and Numbersupporting

confidence: 90%

“…We compared the intakes and licking behavior of the rats with cuffs on the duodenum to that of rats that had cuffs on the pylorus during tests in which no infusion was given or 12 ml of milk was infused in the first 6 min. There was no significant difference among the five baseline tests in volume ingested for the rats with duodenal cuffs [F (4,16) During the first 6 min of the baseline tests, rats with the duodenal cuffs had significantly more licks than rats with pyloric cuffs [t(47) ϭ 2.52, P ϭ 0.02; Fig. 10A].…”

Section: Microstructure Of Lickingmentioning

confidence: 99%

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Gastric negative feedback produced by volume and nutrient during a meal in rats

Eisen

Davis

Rauhofer

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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To investigate the gastric negative-feedback control of eating during a meal, we implanted male rats with pyloric cuffs and gastric catheters and gave them access to sweet milk for 30 min after overnight deprivation. Ingested milk and infused milk or saline were confined to the stomach because the pyloric cuffs were closed in all tests. Rats received five consecutive tests with no gastric infusion or with infusions of 3, 6, or 12 ml of milk or saline during the first 6 min of the test meal. Only 12-ml infusions decreased intake significantly compared with no infusion. Because 12 ml of saline inhibited intake as much as 12 ml of milk, the decreased intake was due to volume or rate of infusion, not nutrient. Although infusions of 3 and 6 ml of milk did not decrease intake, they decreased the number of licks after the infusions significantly more than equal volumes of saline. Thus a large volume or rapid rate of gastric infusion decreases intake, and some other aspect of small milk infusions decreases the rate of licking.

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Section: Cluster Size and Numbersupporting

confidence: 90%

Section: Microstructure Of Lickingmentioning

confidence: 99%

Gastric negative feedback produced by volume and nutrient during a meal in rats

Eisen

Davis

Rauhofer

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The effects of hUcn II on the microstructure of feeding were similar to those of serotonin-related agents that reduce meal size and eating rate, without affecting meal initiation. These compounds, such as fenfluramine, are hypothesized to act by facilitating satiation, or the process of terminating feeding (Blundell, 1986;Kaplan et al, 1997). Likewise, peripheral cholecystokinin (Ritter et al, 1999) and intrahepatic-portal vein glucose infusions (Langhans et al, 2001) decrease meal size and increase satiety ratio, without affecting meal frequency.…”

Section: Discussionmentioning

confidence: 99%

Human Urocortin II, a Selective Agonist for the Type 2 Corticotropin-Releasing Factor Receptor, Decreases Feeding and Drinking in the Rat

Inoue¹,

Valdez²,

Reyes³

et al. 2003

J Pharmacol Exp Ther

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Corticotropin-releasing factor (CRF) has been hypothesized to modulate consummatory behavior through the Type 2 CRF (CRF 2 ) receptor. However, behavioral functions subserved by the CRF 2 receptor remain poorly understood. Recently, human urocortin II (hUcn II), a selective CRF 2 receptor agonist, was identified. To study the effects of this neuropeptide on ingestive behavior, we examined the effects of centrally infused hUcn II (i.c.v. 0, 0.01, 0.1, 1.0, 10.0 g) on the microstructure of nosepoke responding for food and water in nondeprived, male rats. Malaise-inducing properties of the peptide were monitored using conditioned taste aversion (CTA) testing. To identify potential sites of action, central induction of Fos protein expression was examined. hUcn II dose dependently reduced the quantity and duration of responding for food and water at doses lower (0.01-1.0 g) than that forming a CTA (10 g). Effects were most evident during hours 4 to 6 of the dark cycle. Meal pattern analysis showed that hUcn II potently (0.1 g) increased the satiating value of food. Rats ate and drank smaller and shorter meals without changing meal frequency. Rats also ate more slowly. hUcn II induced Fos in regions involved in visceral sensory processing and autonomic/neuroendocrine regulation and resembling those activated by appetite suppressants. hUcn II is a promising neuropeptide for investigating the role of the CRF 2 receptor in ingestive behavior.Corticotropin-releasing factor (CRF) is hypothesized to mediate behavioral, autonomic, endocrine, and immunological responses to stress (Koob and Heinrichs, 1999). Intracerebroventricular (i.c.v.) administration of CRF in rats mimics several behavioral effects of stress, including motor activation, anxiety-like behavior, anorexia, reduced sexual behavior, and altered cognitive performance (Koob et al., 1994). Two genes encoding separate families of G-protein coupled CRF receptors, each having distinct distributions and functional and pharmacological properties (Perrin and Vale, 1999), have been identified (CRF 1 and CRF 2 ). Whereas molecular and receptor antagonist studies point to activating and anxiogenic-like roles of the CRF 1 receptor (Koob and Heinrichs, 1999), behavioral functions mediated by the CRF 2 receptor have remained obscure.

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“…Afferent projections from the rostral NTS reach the parabrachial nucleus at the junction of the midbrain and pons and at the hypothalamus, whereas the caudal NTS projects to vagal efferent neurons control parasympathetic gastrointestinal responses including insulin secretion and gastric emptying [153]. Decerebrate rats which lack the direct connection between the hindbrain and forebrain show a reduced feeding response to intra-oral infusion of 12.5% glucose following systemic administration of fenfluramine or mCPP [201][202][203]. As Decerebrate rats can only show behavioural responses controlled by brain stem circuits, these results show that caudal brainstem receptors are sufficient to produce anorectic effects after systemic administration of mCPP or fenfluramine.…”

Section: Brain Mechanisms Of Serotonergic Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

167

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Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

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d-Fenf luramine Anorexia: Dissociation of Ingestion Rate, Meal Duration, and Meal Size Effects

Cited by 20 publications

References 22 publications

Gastric negative feedback produced by volume and nutrient during a meal in rats

Gastric negative feedback produced by volume and nutrient during a meal in rats

Human Urocortin II, a Selective Agonist for the Type 2 Corticotropin-Releasing Factor Receptor, Decreases Feeding and Drinking in the Rat

Serotonin controlling feeding and satiety

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