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

Yamada, Jun; Sugimoto, Yukihiko; Ujikawa, Masanori

doi:10.1248/bpb.29.557

Cited by 13 publications

(13 citation statements)

References 22 publications

(42 reference statements)

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“…Peripheral administration of the 5-HT precursor 5-HTP increases serum leptin in mice [260,261] although it needs to be determined if the involvement of 5-HT in leptin-induced hypophagia is a direct effect because a further study suggested that hyperleptinemia following systemic injection of 5-HTP is elicited by 5-HT formed in the peripheral system [262]. However, immunohistochemical evidence suggests an inverse relationship between 5-HT and leptin in the dorsal raphe and the hypothalamus.…”

Section: -Ht Interactions With Cck and Leptinmentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

259

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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Section: -Ht Interactions With Cck and Leptinmentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

259

167

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“…Serotonin in CNS is synthesized at the raphe nuclei. Administration of serotonin or its precursor 5-hydroxytryptophan into CNS causes a decrease in foot intake and increases the metabolic rate (Yamada et al 2006 ). At least 18 receptors of serotonin have been identifi ed (Marston et al 2011 ).…”

Section: Type 2 Diabetes and Serotoninmentioning

confidence: 99%

Diabetes and Tryptophan Metabolism

Ünlütürk

Erbaş

2015

Molecular and Integrative Toxicology

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Tryptophan, an essential amino acid, can be metabolized to several kinds of physiologically active metabolites. Accumulating data indicate that an altered metabolism of tryptophan and its active metabolites have important roles for the pathogenesis and development of complications of diabetes mellitus. Changes in tryptophan-kynurenine and tryptophan-methoxyindole pathways are related to several pathophysiological mechanisms of type 1 or type 2 diabetes. Particularly, serotonin, melatonin, and their receptors would be novel targets not only to better understand the pathogenesis of diabetes but also to develop new antidiabetic agents. Keywords IntroductionIn addition to the traditional knowledge, recent studies show that amino acids are also among the regulators of the phosphorylation cascade of proteins and expression of genes. Moreover, they are crucial precursors of hormones and nitrogenous substances with outstanding biological importance. Even though physiological concentrations of amino acids and their metabolites are necessary for physiological processes, their elevated levels might be pathogenic in several disorders. Several

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“…Conversely, central injections of serotonin or its precursor 5-hydroxytryptophan (5HTP) caused hypophagia (Blundell and Latham, 1979; Fletcher and Burton, 1986; Simansky, 1996; Yamada et al, 2006) as well as increased metabolic rate (Rothwell and Stock, 1987; Le Feuvre et al, 1991). Fenfluramine, a drug that increases synaptic serotonin concentrations by inducing vesicular release and inhibiting reuptake, also produced hypophagia, reducing meal size, and increasing inter-meal intervals in rats (Blundell et al, 1975; Grinker et al, 1980), effects which are mediated by central serotonin (Fletcher and Burton, 1986).…”

Section: Central Serotonin and Energy Balancementioning

confidence: 99%

Serotonin and the regulation of mammalian energy balance

Donovan¹,

Tecott²

2013

Front. Neurosci.

127

100

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Maintenance of energy balance requires regulation of the amount and timing of food intake. Decades of experiments utilizing pharmacological and later genetic manipulations have demonstrated the importance of serotonin signaling in this regulation. Much progress has been made in recent years in understanding how central nervous system (CNS) serotonin systems acting through a diverse array of serotonin receptors impact feeding behavior and metabolism. Particular attention has been paid to mechanisms through which serotonin impacts energy balance pathways within the hypothalamus. How upstream factors relevant to energy balance regulate the release of hypothalamic serotonin is less clear, but work addressing this issue is underway. Generally, investigation into the central serotonergic regulation of energy balance has had a predominantly “hypothalamocentric” focus, yet non-hypothalamic structures that have been implicated in energy balance regulation also receive serotonergic innervation and express multiple subtypes of serotonin receptors. Moreover, there is a growing appreciation of the diverse mechanisms through which peripheral serotonin impacts energy balance regulation. Clearly, the serotonergic regulation of energy balance is a field characterized by both rapid advances and by an extensive and diverse set of central and peripheral mechanisms yet to be delineated.

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

Cited by 13 publications

References 22 publications

Serotonin controlling feeding and satiety

Serotonin controlling feeding and satiety

Diabetes and Tryptophan Metabolism

Serotonin and the regulation of mammalian energy balance

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