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Unveiling Metabolic Regulation Networks and Mechanisms

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 (31 October 2024) | Viewed by 1290

Special Issue Editor


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Guest Editor
Division of Diabetes and Nutrition, RARiS, Tohoku University, Sendai 980-8579, Japan
Interests: bile acids; serotonin; serotonin receptor; Tph1; Tph2; tryptophan metabolites; GLP-1; GLP-1 receptor agonists; FGF21; FGF15/19; neuropeptides; gut-derived hormones; liver-derived hormones; obesity; diabetes; appetite; food intake; hypothalamus; energy homeostasis; hepatosteatosis; glucose metabolism; lipid metabolism; organ network; whey protein; soy protein; insulin, leptin, insulin resistance; adipose tissue; CNS; gene expression; sympathetic nervous system
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Special Issue Information

Dear Colleagues,

Metabolic regulation networks play a crucial role in understanding the pathophysiological mechanisms of human diseases and the actions of nutrients, hormones, and medical agents. As such, research based on these networks is also important to discover new diagnoses, as well as preventing and treating diseases.

This Special Issue aims to provide a comprehensive overview of metabolic regulation networks and their mechanisms by sharing contributions from academic research institutes and laboratories consolidating our understanding of this area. We welcome original research, reviews, and short communication articles that show novel findings related to metabolic regulation networks, including (but not limited to) topics such as metabolomics and the novel roles of genes, medical agents, nutrients, and hormones in metabolic regulation.

The topics of interest for this SI include the following:

  • Metabolomics
  • Role of genes in the regulation of the metabolism
  • Actions of medical agents on the metabolism
  • Actions of nutrients on the metabolism
  • Network of hormones
  • Regulators of bile acids
  • Regulators of tryptophan’s metabolites
  • Regulators of serotonin
  • Regulators of food intake
  • Regulators of body weight
  • Regulators of glucoregulatory hormones
  • Regulators of adipocyte-derived hormones
  • Regulators of gut-derived hormones
  • Regulators of liver-derived hormones
  • Metabolic networks and mechanisms in diabetes, obesity, fatty liver and/or MAFLD

Prof. Dr. Katsunori Nonogaki
Guest Editor

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Keywords

  • gut hormones
  • liver-derived hormones
  • pancreatic hormones
  • adipocyte-derived hormones
  • brain-derived hormones
  • feeding regulation
  • energy homeostasis
  • glucose homeostasis
  • lipid metabloims
  • fatty liver
  • MAFLD
  • hepatosteatosis
  • tryptophan’s metabolites
  • serotonin
  • bile acids
  • gene expression
  • GLP-1
  • GIP
  • GLP-1 receptor agonists
  • FGF21
  • FGF15/19
  • organs’ network
  • hormones’ network
  • neural network
  • neuropeptides
  • nutrients
  • protein intake
  • whey protein
  • soy protein

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Published Papers (1 paper)

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Research

9 pages, 563 KiB  
Communication
The GLP-1 Receptor Agonist Liraglutide Decreases Primary Bile Acids and Serotonin in the Colon Independently of Feeding in Mice
by Katsunori Nonogaki and Takao Kaji
Int. J. Mol. Sci. 2024, 25(14), 7784; https://doi.org/10.3390/ijms25147784 - 16 Jul 2024
Viewed by 1075
Abstract
Liraglutide, a glucagon-like peptide 1 analog used to treat type 2 diabetes and obesity, is a potential new treatment modality for bile acid (BA) diarrhea. Here, we show that administration of liraglutide significantly decreased total BAs, especially the primary BAs, including cholic acid, [...] Read more.
Liraglutide, a glucagon-like peptide 1 analog used to treat type 2 diabetes and obesity, is a potential new treatment modality for bile acid (BA) diarrhea. Here, we show that administration of liraglutide significantly decreased total BAs, especially the primary BAs, including cholic acid, chenodeoxycholic acid, taurocholic acid, taurochenodeoxycholic acid, glycocholic acid, and β-muricholic acid, in the liver and feces. In addition, liraglutide significantly decreased tryptophan metabolites, including L-tryptophan, serotonin, 5-hydroxy indole-3-acetic acid, L-kynurenine, and xanthurenic acid, in the colon, whereas it significantly increased indole-3-propionic acid. Moreover, the administration of liraglutide remarkably decreased the expression of apical sodium-dependent bile acid transporter, which mediates BA uptake across the apical brush border member in the ileum, ileal BA binding protein, and fibroblast growth factor 15 in association with decreased expression of the BA-activated nuclear receptor farnesoid X receptor and the heteromeric organic solute transporter Ostα/β, which induces BA excretion, in the ileum. Liraglutide acutely decreased body weight and blood glucose levels in association with decreases in plasma insulin and serotonin levels in food-deprived mice. These findings suggest the potential of liraglutide as a novel inhibitor of primary BAs and serotonin in the colon. Full article
(This article belongs to the Special Issue Unveiling Metabolic Regulation Networks and Mechanisms)
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