Serotonin-type 3 receptors mediate intestinal lipid-induced satiation and Fos-like immunoreactivity in the dorsal hindbrain

Savastano, David M.; Hayes, Matthew R.; Covașă, Mihai

doi:10.1152/ajpregu.00699.2006

Cited by 31 publications

(24 citation statements)

References 52 publications

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“…Interestingly, the paper from Savastano et al (9) in this issue as well as a previous paper from the same group (6) strongly supports the hypothesis of cooperation between CCK and 5-HT in these processes. The concept of cooperation between neuroactive modulators including 5-HT and CCK could represent a key mechanism in the understanding of the interplay between gut mechanosensitivity, gut chemosensitivity, and specific nutrient sensing, transduction, central encoding, and perception.…”

supporting

confidence: 75%

“…Altogether they exert feedback control of both gastrointestinal muscle contraction and intestinal secretion and also participate to the central feeling of satiation and satiety and to the control of food intake. Savastano et al (9) show that cooperation between CCK and 5-HT in luminal lipid-related information represents an interesting contribution to the understanding of these complex mechanisms.…”

mentioning

confidence: 99%

“…As a consequence, the physiological stimuli for the release of 5-HT from enteroendocrine cells may be both chemical and mechanical. The paper from Savastano et al (9) extends the release of 5-HT and 5-HT 3 receptor activation to lipid, but whether apolipoprotein A-IV or another lipid-associated signal is involved in the transduction mechanism remains to be determined. The central encoding of the 5-HT 3 and CCK1 receptors vagus-mediated mechanical and chemicalrelated sensory informations also represents an exciting area for future research.…”

mentioning

confidence: 99%

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From gut nutrient sensing to nutrient perception: a cooperative role involving CCK and 5-HT?

Tomé¹

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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GUT-BRAIN AXIS INTERPLAY REMAINS a major question in physiology. The release of 5-HT by endocrine cells was previously demonstrated to respond to different stimuli including pressure sensors and sodium-glucose cotransporter, whereas CCK release responds to apolipoprotein A-IV and Pept1 activation. The paper from Savastano, Hayes, and Covasa in this issue of Integrative and Comparative Physiology (9) extends the release of 5-HT and 5-HT 3 receptor activation to lipid and shows cooperation between CCK and 5-HT in luminal lipid-related informations. This concept could represent a key mechanism in the understanding of the interplay between gut mechanosensitivity, gut chemosensitivity, and specific nutrient sensing, transduction, central encoding, and perception. Whether apolipoprotein A-IV or another lipid-associated signal is involved in the transduction mechanism remains to be determined. The central encoding of the 5-HT 3 and CCK1 receptors vagus-mediated mechanical and chemical-related sensory informations also represents an exciting area for future research.Understanding the mechanisms involved in gut-brain axis interplay remains a major question in physiology. It is established that intrinsic and extrinsic afferent fibers from nerves of the gastrointestinal tract continuously receive informations related to a number of mechanical and chemical stimuli applied to the mucosa of the small intestine. They transmit these informations to the enteric nervous system (ENS) and to the central nervous system (CNS), respectively. Altogether they exert feedback control of both gastrointestinal muscle contraction and intestinal secretion and also participate to the central feeling of satiation and satiety and to the control of food intake. Savastano et al. (9) show that cooperation between CCK and 5-HT in luminal lipid-related information represents an interesting contribution to the understanding of these complex mechanisms.The regulatory mechanisms involving mechanosensitivity and chemosensitivity of intrinsic and extrinsic gut afferent fibers are of particular importance since they participate, during meals, in the overall control and concomitant adaptation of food intake, meal digestion, and nutrient assimilation. They adapt food ingestion to stomach distension, regulate intestinal processes according to the entry of nutrients from the stomach, and participate in the regulation of the supply of nutrients and energy to the body. The extent of the gut mechanosensitivity and chemosensitivity has been inferred from in vivo physiological experiments in a variety of animal models and in humans. These experiments demonstrated that gastric and intestinal distension triggers the peristaltic reflex, affect gastric secretion, and induce satiation and meal termination. Similarly, luminal perfusion of the intestine with acid, carbohydrate, lipid, protein, amino acids, or high-osmolarity solutions is known to decrease gastric motility, delay gastric emptying, decrease gastric acid secretion, induce satiation or satiety, and produc...

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confidence: 75%

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confidence: 99%

mentioning

confidence: 99%

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From gut nutrient sensing to nutrient perception: a cooperative role involving CCK and 5-HT?

Tomé¹

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Van der Hoek and Cooper [104] revealed a behaviourally specific reduction of palatable food consumption in non-deprived rats following peripheral administration of the selective 5-HT3 antagonist odansetron. However, odansetron did not alter sucrose or chow intake in food deprived rats in a later study, but blunted the anorectic response to a duodenal lipid infusion [105]. The findings of both studies are not necessarily contradictory, as one could assume in both situations a disinhibition of satiety, rather than a satiating effect per se.…”

Section: Brain 5-ht and Satietymentioning

confidence: 73%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

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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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“…Scientific RepoRts | 6:25145 | DOI: 10.1038/srep25145 receptor mediates the acute hypophagic effects of dietary carbohydrate in rats [29][30][31] . We extend these findings and demonstrate that ondansetron, a selective 5HT3 receptor antagonist, increased energy intake in rats that were fed isocaloric diets containing 0%, 5% and 10% protein with 67%, 62% and 57% carbohydrate calories, respectively.…”

Section: Discussionmentioning

confidence: 99%

0476 Low protein diets produce divergent effects on energy balance

Zapata

Pezeshki

Singh

et al. 2016

Journal of Animal Science

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Diets deficient in protein often increase food consumption, body weight and fat mass; however, the underlying mechanisms remain poorly understood. We compared the effects of diets varying in protein concentrations on energy balance in obesity-prone rats. We demonstrate that protein-free (0% protein calories) diets decreased energy intake and increased energy expenditure, very low protein (5% protein) diets increased energy intake and expenditure, whereas moderately low protein (10% protein) diets increased energy intake without altering expenditure, relative to control diet (15% protein). These diet-induced alterations in energy expenditure are in part mediated through enhanced serotonergic and β-adrenergic signaling coupled with upregulation of key thermogenic markers in brown fat and skeletal muscle. The protein-free and very low protein diets decreased plasma concentrations of multiple essential amino acids, anorexigenic and metabolic hormones, but these diets increased the tissue expression and plasma concentrations of fibroblast growth factor-21. Protein-free and very low protein diets induced fatty liver, reduced energy digestibility, and decreased lean mass and body weight that persisted beyond the restriction period. In contrast, moderately low protein diets promoted gain in body weight and adiposity following the period of protein restriction. Together, our findings demonstrate that low protein diets produce divergent effects on energy balance.The consumption of protein triggers adaptive responses in ingestive behavior, energy expenditure and metabolism that are under homeostatic controls. The 'protein leverage' hypothesis posits that protein intake is tightly regulated in several species including rats, mice and humans, which consume to acquire their required protein rather than meet requirements for fats and carbohydrates [1][2][3] . An increase in dietary protein density would decrease intake of carbohydrates and fats with consequent reduction in energy intake. There is substantial evidence that high protein diets promote satiety, weight loss and improve glycemic control 4,5 . A corollary to this hypothesis is that a reduction in the dietary protein concentration would increase total energy intake, due to overconsumption of carbohydrates and fat, in an effort to meet protein requirements. Consistent with this, moderately protein deficient diets were found to produce hyperphagia in rodents 6-9 and in some 1,10,11 but not all human studies 12,13 , whereas, severe protein restriction below a certain threshold leads to a reduction in food intake in rodents 9,14 . However, little is known of the underlying mechanisms by which moderate protein deficiency elicits such behavioural and metabolic adaptations and promotes positive energy balance with consequent predisposition to obesity and other metabolic disorders.The hyperphagic effects of moderately low protein diets are purported to be through multiple mechanisms. These include imbalances in plasma and brain amino acid concentrations in rats [15][16][17] ,...

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Serotonin-type 3 receptors mediate intestinal lipid-induced satiation and Fos-like immunoreactivity in the dorsal hindbrain

Cited by 31 publications

References 52 publications

From gut nutrient sensing to nutrient perception: a cooperative role involving CCK and 5-HT?

From gut nutrient sensing to nutrient perception: a cooperative role involving CCK and 5-HT?

Serotonin controlling feeding and satiety

0476 Low protein diets produce divergent effects on energy balance

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