Effects of peripheral 5-HT2 and 5-HT3 receptor agonists on food intake in food-deprived and 2-deoxy-d-glucose-treated rats

Sugimoto, Yukihiko; Yamada, Jun; Yoshikawa, Tomohiro; Noma, Toshiko; Horisaka, Kazuyoshi

doi:10.1016/s0014-2999(96)00660-7

Cited by 23 publications

(17 citation statements)

References 24 publications

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“…For example, administration of agonists activating postsynaptic 5-HT receptors produces marked reductions in food intake (4,64,68). Likewise, administration of 5-HT receptor antagonists has been shown to elicit food intake in rats (20,26).…”

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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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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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“…[8][9][10] We previously reported that the peripheral 5-HT 2 receptor agonist a-methyl-5-HT, reduces food intake in fasted rats and that it is mediated by the peripheral 5-HT 2A receptor. 11) We also found that the peripheral 5-HT 3 receptor agonist 2-methyl-5-hydroxytryptamine did not affect food intake in rats, which implying that the peripheral 5-HT 3 receptor is not associated with food intake. 11) It is known that 2-deoxy-D-glucose(2-DG) prevents utilization of intracellular glucose and elicits neuroglucopenia, leading to hyperphagia.…”

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confidence: 61%

“…11) We also found that the peripheral 5-HT 3 receptor agonist 2-methyl-5-hydroxytryptamine did not affect food intake in rats, which implying that the peripheral 5-HT 3 receptor is not associated with food intake. 11) It is known that 2-deoxy-D-glucose(2-DG) prevents utilization of intracellular glucose and elicits neuroglucopenia, leading to hyperphagia. 12,13) To date, 2-DG-induced feeding serves as an animal model of hyperphagia.…”

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confidence: 61%

Effects of Peripheral Administration of 5-Hydroxytryptamine (5-HT) on 2-Deoxy-D-glucose-Induced Hyperphagia in Rats.

Sugimoto

Yoshikawa

Yamada

2002

Biological & Pharmaceutical Bulletin

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Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter and regulates several physiological functions. It is well established that 5-HT is an important factor controlling food intake and that 5-HT depresses food intake in animals and humans mediated by 5-HT receptors.1-3) Activation of central 5-HT 1B , 5-HT 2A and 5-HT 2C receptors induces anorexia in rodents based on numerous results using 5-HT receptor agonists and antagonists.1,2,4-7) Direct administration of 5-HT into the brain also induces hypophagia in rodents and its effects may be elicited by these 5-HT receptors. 3)Peripherally administered 5-HT induces anorexia and this effect may be associated with peripheral 5-HT 2 receptors, since it was antagonized by the peripheral 5-HT 2 receptor antagonist xylamidine. [8][9][10] We previously reported that the peripheral 5-HT 2 receptor agonist a-methyl-5-HT, reduces food intake in fasted rats and that it is mediated by the peripheral 5-HT 2A receptor.11) We also found that the peripheral 5-HT 3 receptor agonist 2-methyl-5-hydroxytryptamine did not affect food intake in rats, which implying that the peripheral 5-HT 3 receptor is not associated with food intake. 11)It is known that 2-deoxy-D-glucose(2-DG) prevents utilization of intracellular glucose and elicits neuroglucopenia, leading to hyperphagia. 12,13) To date, 2-DG-induced feeding serves as an animal model of hyperphagia. However, the effects of 5-HT itself on 2-DG-induced hyperphagia remain unclear. In the present study, therefore, we investigated the effects of peripheral administration of 5-HT on hyperphagia elicited by 2-DG in rats.Since 2-DG induces glucoprivation by inhibition of glucose utilization of cells, it elevates plasma glucose levels to compensate it. 12,13) 2-DG-induced hyperphagia is elicited in response to low glucose levels in the brain. It suggests that facilitation of hyperglycemia may improve shortage of glucose in the brain by increasing glucose uptake to cells, which may lead to inhibition of hyperphagia. The peripheral 5-HT receptor participates in glucose regulation. [14][15][16][17] We reported that peripheral 5-HT elicits hyperglycemia in rats.16) Thus, 5-HT may affect food intake in 2-DG-treated rats through modifying glucose levels. We also examined effects of 5-HT on blood glucose levels in 2-DG-treated rats. MATERIALS AND METHODS AnimalsMale Sprague-Dawley rats (200-240 g) were obtained from SLC Japan. They were housed in individual cages and maintained under a controlled 12 h : 12 h light/dark cycle ( lights on at 07:00 h), with room temperature at 23Ϯ 1°C and humidity at 55Ϯ5% for at least 7 d prior to experiments. Rats were given free access to food and water.Drugs and Treatment 2-DG and 5-HT creatinine sulfate were purchased from Wako Pure Chemical Co. (Japan), Merck (Germany), respectively. Ketanserin tartrate were obtained from Research Biochemicals Inc. (U.S.A.). 2-DG, 5-HT and ketanserin were dissolved in saline. All drugs were injected i.p. 2-DG and 5-HT were injected i.p. simultaneously at opposite sites. Ket...

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“…[3][4][5] Anorectic effects of 5-HT may involve both the central and peripheral nervous system, since central and peripheral injection of 5-HT or the peripheral 5-HT receptor agonist can decrease food intake. 2,6,7) It has been reported that administration of the 5-HT precursor, 5-hydroxytryptophan (5-HTP) decreases food intake in rodents. 2,8) It is considered that the anorectic effects of 5-HTP are caused by 5-HT formation.…”

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Involvement of Leptin in Hypophagia Induced by the Serotonin Precursor 5-Hydroxytryptophan (5-HTP) in Mice

Yamada

Sugimoto

Ujikawa

2006

Biological & Pharmaceutical Bulletin

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We previously demonstrated that a serotonin (5-HT) precursor 5-hydroxytryptophan (5-HTP) increases serum leptin levels in mice. It was reported that administration of 5-HTP elicits hypophagia in rodents and humans. In the present study, we examined involvement of leptin in 5-HTP-elicited decreases in the milk intake of fasted mice. Serum leptin levels increased with increases in milk intake in mice, while 5-HTP strongly decreased milk intake in fasted mice compared to that in the control group. Serum leptin levels in fasted mice treated with 5-HTP were similar to those control mice after milk intake. As leptin is a powerful anorectic signal, 5-HTP-induced anorexia may be mediated by facilitation of leptin secretion.

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Effects of peripheral 5-HT2 and 5-HT3 receptor agonists on food intake in food-deprived and 2-deoxy-d-glucose-treated rats

Cited by 23 publications

References 24 publications

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

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

Effects of Peripheral Administration of 5-Hydroxytryptamine (5-HT) on 2-Deoxy-D-glucose-Induced Hyperphagia in Rats.

Involvement of Leptin in Hypophagia Induced by the Serotonin Precursor 5-Hydroxytryptophan (5-HTP) in Mice

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