Serum leptin levels after central and systemic injection of a serotonin precursor, 5-hydroxytryptophan, in mice

Yamada, Jun; Ujikawa, Masanori; Sugimoto, Yukihiko

doi:10.1016/s0014-2999(00)00624-5

Cited by 14 publications

(14 citation statements)

References 17 publications

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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

View full text Add to dashboard Cite

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“…We found that hyperleptinemia induced by 5-HTP was caused by formation of 5-HT in the periphery. 16) We demonstrated that 5-HTP did not affect leptin mRNA levels of white adipose tissues nor leptin release from isolated fat pads. 19) This indicates that leptin secretion caused by 5-HTP are mediated by leptin secretary factors.…”

Section: Discussionmentioning

confidence: 69%

“…In previous reports, we showed that 5-HTP elevated serum leptin levels in non-fasted mice. 15,16) Thus, it indicates that 5-HTP can increase leptin secretion in both fasted and non-fasted mice. Serum leptin levels after administration of 5-HTP are similar to those after milk intake in mice.…”

Section: Discussionmentioning

confidence: 99%

“…15,16) We examined the mechanism of leptin secretion induced by 5-HTP. We found that hyperleptinemia induced by 5-HTP was caused by formation of 5-HT in the periphery.…”

Section: Discussionmentioning

confidence: 99%

“…10,13,14) We previously demonstrated that systemic injection of a 5-HT precursor, 5-HTP, increases serum leptin levels in mice. 15,16) We further reported that hyperleptinemia elicited by 5-HTP is mediated by insulin but not corticosterone. 17) Since both 5-HTP and leptin cause hypophagia, it is suggested that 5-HTP-induced anorexia may be related to its leptin-releasing effects.…”

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confidence: 82%

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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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Long‐term fluoxetine administration does not result in major changes in bone architecture and strength in growing rats

Westbroek

Waarsing

Leeuwen

et al. 2006

J of Cellular Biochemistry

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Many studies have indicated that serotonin and its transporter play a role in bone metabolism. In this study we investigated the effect of selective serotonin re-uptake inhibitor (SSRI), fluoxetine (Prozac) on bone architecture and quality in growing female rats. We therefore administrated rats with clinically relevant doses of fluoxetine for a period of 6 months. DXA scans were performed during the treatment period in order to follow parameters as body weight, fat percentage and BMD. After 6 months of treatment, femurs were used to analyze bone architecture and bone strength, by means of microCT scans and three-point bending assays, respectively. We found a slightly diminished bone quality, reflected in a lower bone tissue strength, which was compensated by changes in bone geometry. As leptin and adiponectin could be possible factors in the serotonergic regulation of bone metabolism, we also determined the levels of these factors in plasma samples of all animals. Leptin and adiponectin levels were not different between the control group and fluoxetine-treated group, indicating that these factors were not involved in the observed changes in bone geometry and quality.

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Serum leptin levels after central and systemic injection of a serotonin precursor, 5-hydroxytryptophan, in mice

Cited by 14 publications

References 17 publications

Serotonin controlling feeding and satiety

Serotonin controlling feeding and satiety

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

Long‐term fluoxetine administration does not result in major changes in bone architecture and strength in growing rats

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