Peripheral serotonin is an incomplete signal for eliciting satiety in sham-feeding rats

Simansky, Kenny J.; Jakubow, James J.; Sisk, F.C.; Vaidya, Anil H.; Eberle-Wang, K.

doi:10.1016/0091-3057(92)90417-e

Cited by 14 publications

(7 citation statements)

References 29 publications

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“…Moreover, investigations of the serotonergic system have attempted to determine the percent contribution of 5-HT to food intake and whether 5-HT-induced suppression of food intake is directly or indirectly mediated. Original exploration of 5-HT's effect on sham feeding indicated that peripheral 5-HT inhibits sham intake (45,46) in the absence of a complete satiety sequence (56). Neill and Cooper (45) demonstrated that administration of a peripheral-acting 5-HT 2a/2c receptor antagonist, xylamidine, attenuated systemically administered 5-HT-induced inhibition of sham feeding.…”

Section: Discussionmentioning

confidence: 99%

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Hayes¹,

Moore²,

Shah³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Hayes, Matthew R., Rachael L. Moore, Samit M. Shah, and Mihai Covasa. 5-HT 3 receptors participate in CCK-induced suppression of food intake by delaying gastric emptying. Am J Physiol Regul Integr Comp Physiol 287: R817-R823, 2004. First published June 10, 2004 10.1152/ajpregu.00295.2004.-Serotonin type 3 (5-HT 3) receptors have been shown to participate in the negative-feedback control of food intake. We previously reported that cholecystokinin (CCK)-induced suppression of food intake is partly mediated through 5-HT 3 receptors when rats were tested on a preferred liquid diet, but whether such an effect occurs when they are tested on a solid maintenance diet is unknown. In the present study, we examined the effects of ondansetron, a selective 5-HT 3 antagonist, on CCK-induced suppression of solid chow intake. Intraperitoneal administration of ondansetron significantly attenuated 30-and 60-min CCK-induced reduction of food intake, with suppression being completely reversed by 120 min. It is not known whether 5-HT 3 receptors directly mediate CCK-induced satiation or whether their participation depends on CCK acting as part of a feedback cascade to inhibit ongoing intake. Because CCKinduced inhibition of sham feeding does not depend on additive gastric/postgastric-feedback signals, we examined the ability of ondansetron to reverse CCK-induced satiation in sham-feeding rats.Ondansetron did not attenuate reduction of sham feeding by CCK, suggesting that ondansetron does not directly antagonize CCK-satiation signals. CCK suppresses real feeding through a delay in gastric emptying. Ondansetron could attenuate CCK-induced reduction of food intake by reversing CCK-induced inhibition of gastric emptying. We found that blockade of 5-HT3 receptors attenuates CCK-induced inhibition of gastric emptying of a solid meal, as well as saline and glucose loads. We conclude that 5-HT 3 receptors mediate CCKinduced satiation through indirect mechanisms as part of a feedback cascade involving inhibition of gastric emptying. ondansetron; serotonin; osmotic; glucose; satiety GASTRIC EMPTYING IS ONE MECHANISM involved in the regulation of food intake (33, 43). A delay in gastric emptying limits the rate of absorption by reducing the rate of nutrient delivery to the small intestine (5, 15, 58) and is associated with suppression of food intake (43). Inhibition of gastric emptying is mediated by peripheral vagal and sympathetic nerves and by the release of a variety of peptides and neurotransmitters (43,54). Cholecystokinin (CCK) and serotonin [5-hydroxytryptamine (5-HT)] are two humoral signals thought to exert control on gastric emptying and are released in response to nutrients entering the duodenum (6,28,30,43,49,60). Both of these satiety signals bind to receptors on terminals of vagal afferent fibers, resulting in a delay in gastric emptying (4, 24, 49).Considerable evidence indicates that the serotonergic system participates in the negative-feedback control of food intake (for review see Ref. 25). Systemic serotonergic activity h...

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Section: Discussionmentioning

confidence: 99%

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Hayes¹,

Moore²,

Shah³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Peripherally injected 5-HT advanced the BSS, and rats approached satiation quicker and in a behaviourally specific manner [147,148]. Peripheral 5-HT requires the simultaneous action of gastrointestinal mechanism to elicit a complete behavioural profile of satiety as shown with sham feeding experiments [148].…”

Section: Peripheral 5-ht and Satietymentioning

confidence: 99%

“…Peripheral 5-HT requires the simultaneous action of gastrointestinal mechanism to elicit a complete behavioural profile of satiety as shown with sham feeding experiments [148]. Peripherally acting 5-HT1 agonists like 5-carboxamidotryptamine (5-CT) and the 5-HT2 agonist α-methyl-5-hydroxytryptamine (5-α-Me-5-HT) also induce hypophagia [149].…”

Section: Peripheral 5-ht and Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

266

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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“…Peripherally administered serotonin, which poorly penetrates the blood -brain barrier, reduces meal size and duration, and advances satiety ( Refs 89,90,91). However, the preponderance of evidence implicates brain serotonin circuitry as the critical mediator of the serotonergic regulation of energy balance.…”

Section: Central Mechanisms Of Serotonergic Regulation Of Food Intakementioning

confidence: 97%

Serotonin and energy balance: molecular mechanisms and implications for type 2 diabetes

Lam

Heisler

2007

Expert Rev. Mol. Med.

135

101

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The neurotransmitter serotonin is an important regulator of energy balance. In the brain, serotonergic fibres from midbrain raphe nuclei project to key feeding centres, where serotonin acts on specific receptors to modulate the activity of various downstream neuropeptide systems and autonomic pathways and thus affects ingestive behaviour and energy expenditure. Serotonin, released by intestinal enterochromaffin cells, also appears to regulate energy homeostasis through peripheral mechanisms. Serotonergic effects on energy balance lead to secondary effects on glucose homeostasis, based on a well-established link between obesity and insulin resistance. However, serotonergic pathways may also directly affect glucose homeostasis through regulation of autonomic efferents and/or action on peripheral tissues. Several serotonergic compounds have been evaluated for clinical use in the treatment of obesity and type 2 diabetes; results of these trials are discussed here. Finally, future directions in the elucidation of serotonergic metabolic regulation are discussed.

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Peripheral serotonin is an incomplete signal for eliciting satiety in sham-feeding rats

Cited by 14 publications

References 29 publications

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Serotonin controlling feeding and satiety

Serotonin and energy balance: molecular mechanisms and implications for type 2 diabetes

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Peripheral serotonin is an incomplete signal for eliciting satiety in sham-feeding rats

Cited by 14 publications

References 29 publications

5-HT3receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

5-HT3receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Serotonin controlling feeding and satiety

Serotonin and energy balance: molecular mechanisms and implications for type 2 diabetes

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5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying