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Gut Hormone: Molecular Mechanism and Its Biological Functions

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

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 9216

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Prof. Dr. Bunzo Matsuura

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Department of Lifestyle-Related Medicine and Endocrinology, Graduate School of Medicine, Ehime University, Shitsukawa 454, Toon, Ehime 791-0295, Japan
Interests: gut hormone; thyroid disease; obesity; diabetes mellitus; nonalcoholic fatty liver disease
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Dear Colleagues,

Gut hormones are closely related to lifestyle and lifestyle-related disorders. Gut hormones affect appetite, gastrointestinal motility, digestion, absorption and metabolism, and hence abnormalities of gut hormones cause malnutrition, metabolic syndrome and GI disorders. Gastrin and insulin have cell proliferation activity, and therefore abnormality of these hormones or hormone receptors affects development or progression of several cancers, for example pancreatic cancer and colorectal cancer.

Understanding of the molecular basis of hormone binding and activation of receptors provides important insights into the active conformation of such receptors, providing critical information helpful for the design and refinement of receptor-active drugs. The family of guanine nucleotide-binding protein (G protein)-coupled receptors that includes receptors for many gut hormones are demonstrated as clinically useful pharmacological targets.

Papers related to any aspects of biochemistry, molecular biology, pharmacology, physiology, and pathology will be considered for this Special Issue. The pure clinical reports may not be accepted.

Prof. Dr. Bunzo Matsuura
Guest Editor

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Keywords

appetite
motility
digestion
absorption
metabolism
microbiome
immunity
cell proliferation
neuroendocrine tumor (NET)
cancer
functional dyspepsia
irritable bowel syndrome
metabolic/bariatric surgery

Published Papers (6 papers)

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Research

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13 pages, 6549 KiB

Open AccessArticle

Glucagon-like Peptide-2 Depresses Ileal Contractility in Preparations from Mice through Opposite Modulatory Effects on Nitrergic and Cholinergic Neurotransmission

by Eglantina Idrizaj, Cristina Biagioni, Chiara Traini, Maria Giuliana Vannucchi and Maria Caterina Baccari

Int. J. Mol. Sci. 2024, 25(3), 1855; https://doi.org/10.3390/ijms25031855 - 03 Feb 2024

Viewed by 583

Abstract

Glucagon-like peptide-2 (GLP-2) has been reported to influence gastrointestinal motor responses, exerting a modulatory role on enteric neurotransmission. To our knowledge, no data on GLP-2 effects on the motility of the isolated ileum are available; therefore, we investigated whether GLP-2 affects the contractile activity of mouse ileal preparations and the neurotransmitters engaged. Ileal preparations showed tetrodotoxin (TTX)- and atropine-insensitive spontaneous contractile activity, which was unaffected by the nitric oxide synthesis inhibitor, L-NNA. GLP-2 depressed the spontaneous contractility, an effect that was abolished by TTX or L-NNA and not influenced by atropine. Electrical field stimulation induced TTX- and atropine-sensitive contractile responses, which were reduced in amplitude by GLP-2 even in the presence of L-NNA. Immunohistochemical results showed a significant increase in nNOS-positive fibers in the ileal muscle wall and a significant decrease in ChAT-positive myenteric neurons in GLP-2-exposed preparations. The present results offer the first evidence that GLP-2 acts on ileal preparations. The hormone appears to depress ileal contractility through a dual opposite modulatory effect on inhibitory nitrergic and excitatory cholinergic neurotransmission. From a physiological point of view, it could be hypothesized that GLP-2 inhibitory actions on ileal contractility can increase transit time, facilitating nutrient absorption. Full article

(This article belongs to the Special Issue Gut Hormone: Molecular Mechanism and Its Biological Functions)

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12 pages, 961 KiB

Open AccessCommunication

Activation of TLRs Triggers GLP-1 Secretion in Mice

by Lorène J. Lebrun, Alois Dusuel, Marion Xolin, Naig Le Guern and Jacques Grober

Int. J. Mol. Sci. 2023, 24(6), 5333; https://doi.org/10.3390/ijms24065333 - 10 Mar 2023

Viewed by 1388

Abstract

The gastrointestinal tract constitutes a large interface with the inner body and is a crucial barrier against gut microbiota and other pathogens. As soon as this barrier is damaged, pathogen-associated molecular patterns (PAMPs) are recognized by immune system receptors, including toll-like receptors (TLRs). Glucagon-like peptide 1 (GLP-1) is an incretin that was originally involved in glucose metabolism and recently shown to be rapidly and strongly induced by luminal lipopolysaccharides (LPS) through TLR4 activation. In order to investigate whether the activation of TLRs other than TLR4 also increases GLP-1 secretion, we used a polymicrobial infection model through cecal ligation puncture (CLP) in wild-type and TLR4-deficient mice. TLR pathways were assessed by intraperitoneal injection of specific TLR agonists in mice. Our results show that CLP induces GLP-1 secretion both in wild-type and TLR4-deficient mice. CLP and TLR agonists increase gut and systemic inflammation. Thus, the activation of different TLRs increases GLP-1 secretion. This study highlights for the first time that, in addition to an increased inflammatory status, CLP and TLR agonists also strongly induce total GLP-1 secretion. Microbial-induced GLP-1 secretion is therefore not only a TLR4/LPS-cascade. Full article

(This article belongs to the Special Issue Gut Hormone: Molecular Mechanism and Its Biological Functions)

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15 pages, 2502 KiB

Open AccessArticle

Elevated Glucagon-like Peptide-1 Receptor Level in the Paraventricular Hypothalamic Nucleus of Type 2 Diabetes Mellitus Patients

by Éva Renner, Fanni Dóra, Erzsébet Oszwald, Árpád Dobolyi and Miklós Palkovits

Int. J. Mol. Sci. 2022, 23(24), 15945; https://doi.org/10.3390/ijms232415945 - 15 Dec 2022

Viewed by 1696

Abstract

Glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) agonists have been approved for the treatment of type 2 diabetes mellitus (T2DM); however, the brain actions of these drugs are not properly established. We used post mortem microdissected human hypothalamic samples for RT-qPCR and Western blotting. For in situ hybridization histochemistry and immunolabelling, parallel cryosections were prepared from the hypothalamus. We developed in situ hybridization probes for human GLP-1R and oxytocin. In addition, GLP-1 and oxytocin were visualized by immunohistochemistry. Radioactive in situ hybridization histochemistry revealed abundant GLP-1R labelling in the human paraventricular hypothalamic nucleus (PVN), particularly in its magnocellular subdivision (PVNmc). Quantitative analysis of the mRNA signal demonstrated increased GLP-1R expression in the PVNmc in post mortem hypothalamic samples from T2DM subjects as compared to controls, while there was no difference in the expression level of GLP-1R in the other subdivisions of the PVN, the hypothalamic dorsomedial and infundibular nuclei. Our results in the PVN were confirmed by RT-qPCR. Furthermore, we demonstrated by Western blot technique that the GLP-1R protein level was also elevated in the PVN of T2DM patients. GLP-1 fibre terminals were also observed in the PVNmc closely apposing oxytocin neurons using immunohistochemistry. The data suggest that GLP-1 activates GLP-1Rs in the PVNmc and that GLP-1R is elevated in T2DM patients, which may be related to the dysregulation of feeding behaviour and glucose homeostasis in T2DM. Full article

(This article belongs to the Special Issue Gut Hormone: Molecular Mechanism and Its Biological Functions)

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11 pages, 3093 KiB

Open AccessArticle

Impacts of Glucose-Dependent Insulinotropic Polypeptide on Orthodontic Tooth Movement-Induced Bone Remodeling

by Taisuke Yamauchi, Megumi Miyabe, Nobuhisa Nakamura, Mizuho Ito, Takeo Sekiya, Saki Kanada, Rina Hoshino, Tatsuaki Matsubara, Ken Miyazawa, Shigemi Goto and Keiko Naruse

Int. J. Mol. Sci. 2022, 23(16), 8922; https://doi.org/10.3390/ijms23168922 - 10 Aug 2022

Viewed by 1221

Abstract

Glucose-dependent insulinotropic polypeptide (GIP) exerts extra-pancreatic effects via the GIP receptor (GIPR). Herein, we investigated the effects of GIP on force-induced bone remodeling by orthodontic tooth movement using a closed-coil spring in GIPR-lacking mice (GIPRKO) and wild-type mice (WT). Orthodontic tooth movements were performed by attaching a 10-gf nickel titanium closed-coil spring between the maxillary incisors and the left first molar. Two weeks after orthodontic tooth movement, the distance of tooth movement by coil load was significantly increased in GIPRKO by 2.0-fold compared with that in the WT. The alveolar bone in the inter-root septum from the root bifurcation to the apex of M1 decreased in both the GIPRKO and WT following orthodontic tooth movement, which was significantly lower in the GIPRKO than in the WT. The GIPRKO exhibited a significantly decreased number of trabeculae and increased trabecular separation by orthodontic tooth movement compared with the corresponding changes in the WT. Histological analyses revealed a decreased number of steady-state osteoblasts in the GIPRKO. The orthodontic tooth movement induced bone remodeling, which was demonstrated by an increase in osteoblasts and osteoclasts around the forced tooth in the WT. The GIPRKO exhibited no increase in the number of osteoblasts; however, the number of osteoclasts on the coil-loaded side was significantly increased in the GIPRKO compared with in the WT. In conclusion, our results demonstrate the impacts of GIP on the dynamics of bone remodeling. We revealed that GIP exhibits the formation of osteoblasts and the suppression of osteoclasts in force-induced bone remodeling. Full article

(This article belongs to the Special Issue Gut Hormone: Molecular Mechanism and Its Biological Functions)

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Review

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44 pages, 1240 KiB

Open AccessReview

Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story

by Andreea-Ioana Inceu, Maria-Adriana Neag, Anca-Elena Craciun and Anca-Dana Buzoianu

Int. J. Mol. Sci. 2023, 24(4), 3385; https://doi.org/10.3390/ijms24043385 - 08 Feb 2023

Cited by 2 | Viewed by 2046

Abstract

Atherosclerotic cardiovascular disease is the most common cause of morbidity and mortality worldwide. Diabetes mellitus increases cardiovascular risk. Heart failure and atrial fibrillation are associated comorbidities that share the main cardiovascular risk factors. The use of incretin-based therapies promoted the idea that activation of alternative signaling pathways is effective in reducing the risk of atherosclerosis and heart failure. Gut-derived molecules, gut hormones, and gut microbiota metabolites showed both positive and detrimental effects in cardiometabolic disorders. Although inflammation plays a key role in cardiometabolic disorders, additional intracellular signaling pathways are involved and could explain the observed effects. Revealing the involved molecular mechanisms could provide novel therapeutic strategies and a better understanding of the relationship between the gut, metabolic syndrome, and cardiovascular diseases. Full article

(This article belongs to the Special Issue Gut Hormone: Molecular Mechanism and Its Biological Functions)

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Other

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11 pages, 13173 KiB

Open AccessCase Report

Duodenal Ampulla Neuroendocrine Tumor with GISTs of the Proximal Jejunum: A Case Report

by Georgiana Anca Nagy, Maria Adriana Neag, Radu Drasovean, Doinita Crisan and Romeo Ioan Chira

Int. J. Mol. Sci. 2022, 23(18), 10351; https://doi.org/10.3390/ijms231810351 - 08 Sep 2022

Cited by 1 | Viewed by 1535

Abstract

Neuroendocrine tumors (NEN) are a type of heterogenous, slow-growing tumors, that only in about half of the cases can be found in the gastrointestinal tract. Half of these is in the small intestine. The ampullary NENs are rare, accounting for less than 1% of gastroenteropancreatic NENs. Gastrointestinal stromal tumors (GIST) are a more common type of tumors of the gastrointestinal tract that consist of pacemaker cells. The occurrence of both tumors simultaneously is rare, but in patients with neurofibromatosis type 1, the co-existence of NEN and GIST is more often. Here we report a case of simultaneous occurrence of a well-differentiated NEN and a GIST in a patient without neurofibromatosis. Also, we provide a short review of the current knowledge and treatment strategies regarding these tumors. Full article

(This article belongs to the Special Issue Gut Hormone: Molecular Mechanism and Its Biological Functions)

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