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Serotonin Network and Energy Metabolism
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Serotonin Network and Energy Metabolism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 19054

Special Issue Editor

Prof. Dr. Katsunori Nonogaki

E-Mail Website
Guest Editor
Laboratory of Diabetes and Nutrition, Tohoku University, New Industry Creation Hatcher Center, Sendai, Japan
Interests: serotonin; serotonin receptor; Tph1; Tph2; tryptophan metabolism; GLP-1; GLP-1 receptor; FGF21; FGF15/19; neuropeptides; POMC; melanocortin receptor; orexin; gut-derived hormones; liver-derived hormones; stress; obesity; diabetes; appetite; food intake; hypothalamus; energy homeostasis; hepatosteatosis; glucose metabolism; lipid metabolism; organ network; milk protein; whey protein; casein; insulin resistance; adipose tissue; CNS; ghrelin; gene expression; sympathetic nervous system; blood pressure
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Serotonin (5-HT) is not only a neurotransmitter but also an endocrine hormone secreted by the gut and peripheral organs. Central and peripheral 5-HT systems contribute to the regulation of energy metabolism. Central 5-HT interacts with neuropeptides or other neurotransmitters, and orchestrates appetite and energy metabolism. In addition, peripheral 5-HT interacts with a variety of metabolic organs including liver, adipose tissues, pancreas and muscle, leading to alterations of hormones and energy metabolism. Nutrients could alter the 5-HT signals in the central nervous system and peripheral organs.

This Special Issue provides new insights into the 5-HT network and energy metabolism, which includes the network between nutrients and 5-HT synthesis, the network between 5-HT and other hormones, the network between 5-HT and metabolic signals, and the network between peripheral 5-HT and central molecules involved in energy homeostasis. Original papers and reviews are all welcome.

Prof. Dr. Katsunori Nonogaki
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • serotonin
  • serotonin receptor
  • energy metabolism
  • nutrients
  • hormones
  • central molecules
  • appetite
  • obesity
  • hepatosteatosis
  • diabetes

Published Papers (4 papers)

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Research

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20 pages, 6210 KiB  
Article
Ergotamine Stimulates Human 5-HT4-Serotonin Receptors and Human H2-Histamine Receptors in the Heart
by Hannes Jacob, Pauline Braekow, Rebecca Schwarz, Christian Höhm, Uwe Kirchhefer, Britt Hofmann, Joachim Neumann and Ulrich Gergs
Int. J. Mol. Sci. 2023, 24(5), 4749; https://doi.org/10.3390/ijms24054749 - 1 Mar 2023
Cited by 4 | Viewed by 2315
Abstract
Ergotamine (2′-methyl-5′α-benzyl-12′-hydroxy-3′,6′,18-trioxoergotaman) is a tryptamine-related alkaloid from the fungus Claviceps purpurea. Ergotamine is used to treat migraine. Ergotamine can bind to and activate several types of 5-HT1-serotonin receptors. Based on the structural formula of ergotamine, we hypothesized that ergotamine might [...] Read more.
Ergotamine (2′-methyl-5′α-benzyl-12′-hydroxy-3′,6′,18-trioxoergotaman) is a tryptamine-related alkaloid from the fungus Claviceps purpurea. Ergotamine is used to treat migraine. Ergotamine can bind to and activate several types of 5-HT1-serotonin receptors. Based on the structural formula of ergotamine, we hypothesized that ergotamine might stimulate 5-HT4-serotonin receptors or H2-histamine receptors in the human heart. We observed that ergotamine exerted concentration- and time-dependent positive inotropic effects in isolated left atrial preparations in H2-TG (mouse which exhibits cardiac-specific overexpression of the human H2-histamine receptor). Similarly, ergotamine increased force of contraction in left atrial preparations from 5-HT4-TG (mouse which exhibits cardiac-specific overexpression of the human 5-HT4-serotonin receptor). An amount of 10 µM ergotamine increased the left ventricular force of contraction in isolated retrogradely perfused spontaneously beating heart preparations of both 5-HT4-TG and H2-TG. In the presence of the phosphodiesterase inhibitor cilostamide (1 µM), ergotamine 10 µM exerted positive inotropic effects in isolated electrically stimulated human right atrial preparations, obtained during cardiac surgery, that were attenuated by 10 µM of the H2-histamine receptor antagonist cimetidine, but not by 10 µM of the 5-HT4-serotonin receptor antagonist tropisetron. These data suggest that ergotamine is in principle an agonist at human 5-HT4-serotonin receptors as well at human H2-histamine receptors. Ergotamine acts as an agonist on H2-histamine receptors in the human atrium. Full article
(This article belongs to the Special Issue Serotonin Network and Energy Metabolism)
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Review

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42 pages, 3144 KiB  
Review
Cardiac Roles of Serotonin (5-HT) and 5-HT-Receptors in Health and Disease
by Joachim Neumann, Britt Hofmann, Stefan Dhein and Ulrich Gergs
Int. J. Mol. Sci. 2023, 24(5), 4765; https://doi.org/10.3390/ijms24054765 - 1 Mar 2023
Cited by 17 | Viewed by 6037
Abstract
Serotonin acts solely via 5-HT4-receptors to control human cardiac contractile function. The effects of serotonin via 5-HT4-receptors lead to positive inotropic and chronotropic effects, as well as arrhythmias, in the human heart. In addition, 5-HT4-receptors may play [...] Read more.
Serotonin acts solely via 5-HT4-receptors to control human cardiac contractile function. The effects of serotonin via 5-HT4-receptors lead to positive inotropic and chronotropic effects, as well as arrhythmias, in the human heart. In addition, 5-HT4-receptors may play a role in sepsis, ischaemia, and reperfusion. These presumptive effects of 5-HT4-receptors are the focus of the present review. We also discuss the formation and inactivation of serotonin in the body, namely, in the heart. We identify cardiovascular diseases where serotonin might play a causative or additional role. We address the mechanisms which 5-HT4-receptors can use for cardiac signal transduction and their possible roles in cardiac diseases. We define areas where further research in this regard should be directed in the future, and identify animal models that might be generated to this end. Finally, we discuss in what regard 5-HT4-receptor agonists or antagonists might be useful drugs that could enter clinical practice. Serotonin has been the target of many studies for decades; thus, we found it timely to summarise our current knowledge here. Full article
(This article belongs to the Special Issue Serotonin Network and Energy Metabolism)
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16 pages, 590 KiB  
Review
The Regulatory Role of the Central and Peripheral Serotonin Network on Feeding Signals in Metabolic Diseases
by Katsunori Nonogaki
Int. J. Mol. Sci. 2022, 23(3), 1600; https://doi.org/10.3390/ijms23031600 - 29 Jan 2022
Cited by 10 | Viewed by 3943
Abstract
Central and peripheral serotonin (5-hydroxytryptamine, 5-HT) regulate feeding signals for energy metabolism. Disruption of central 5-HT signaling via 5-HT2C receptors (5-HT2CRs) induces leptin-independent hyperphagia in mice, leading to late-onset obesity, insulin resistance, and impaired glucose tolerance. 5-HT2CR mutant mice are more responsive than [...] Read more.
Central and peripheral serotonin (5-hydroxytryptamine, 5-HT) regulate feeding signals for energy metabolism. Disruption of central 5-HT signaling via 5-HT2C receptors (5-HT2CRs) induces leptin-independent hyperphagia in mice, leading to late-onset obesity, insulin resistance, and impaired glucose tolerance. 5-HT2CR mutant mice are more responsive than wild-type mice to a high-fat diet, exhibiting earlier-onset obesity and type 2 diabetes. High-fat and high-carbohydrate diets increase plasma 5-HT and fibroblast growth factor-21 (FGF21) levels. Plasma 5-HT and FGF21 levels are increased in rodents and humans with obesity, type 2 diabetes, and non-alcohol fatty liver diseases (NAFLD). The increases in plasma FGF21 and hepatic FGF21 expression precede hyperinsulinemia, insulin resistance, hyperglycemia, and weight gain in mice fed a high-fat diet. Nutritional, pharmacologic, or genetic inhibition of peripheral 5-HT synthesis via tryptophan hydroxylase 1 (Tph1) decreases hepatic FGF21 expression and plasma FGF21 levels in mice. Thus, perturbing central 5-HT signaling via 5-HT2CRs alters feeding behavior. Increased energy intake via a high-fat diet and/or high-carbohydrate diet can upregulate gut-derived 5-HT synthesis via Tph1. Peripheral 5-HT upregulates hepatic FGF21 expression and plasma FGF21 levels, leading to metabolic diseases such as obesity, insulin resistance, type 2 diabetes, and NAFLD. The 5-HT network in the brain–gut–liver axis regulates feeding signals and may be involved in the development and/or prevention of metabolic diseases. Full article
(This article belongs to the Special Issue Serotonin Network and Energy Metabolism)
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23 pages, 942 KiB  
Review
The Multifaceted Role of Serotonin in Intestinal Homeostasis
by Nienke Koopman, Drosos Katsavelis, Anne S. Ten Hove, Stanley Brul, Wouter J. de Jonge and Jurgen Seppen
Int. J. Mol. Sci. 2021, 22(17), 9487; https://doi.org/10.3390/ijms22179487 - 31 Aug 2021
Cited by 39 | Viewed by 5769
Abstract
The monoamine serotonin, 5-hydroxytryptamine (5-HT), is a remarkable molecule with conserved production in prokaryotes and eukaryotes and a wide range of functions. In the gastrointestinal tract, enterochromaffin cells are the most important source for 5-HT production. Some intestinal bacterial species are also able [...] Read more.
The monoamine serotonin, 5-hydroxytryptamine (5-HT), is a remarkable molecule with conserved production in prokaryotes and eukaryotes and a wide range of functions. In the gastrointestinal tract, enterochromaffin cells are the most important source for 5-HT production. Some intestinal bacterial species are also able to produce 5-HT. Besides its role as a neurotransmitter, 5-HT acts on immune cells to regulate their activation. Several lines of evidence indicate that intestinal 5-HT signaling is altered in patients with inflammatory bowel disease. In this review, we discuss the current knowledge on the production, secretion, and signaling of 5-HT in the intestine. We present an inventory of intestinal immune and epithelial cells that respond to 5-HT and describe the effects of these signaling processes on intestinal homeostasis. Further, we detail the mechanisms by which 5-HT could affect inflammatory bowel disease course and describe the effects of interventions that target intestinal 5-HT signaling. Full article
(This article belongs to the Special Issue Serotonin Network and Energy Metabolism)
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