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Inflammatory and Metabolic Dysregulations in Chronic Liver and Pancreas Disorders

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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 September 2022) | Viewed by 11570

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Special Issue Editors

Dr. Antonios Chatzigeorgiou

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Guest Editor

Department of Physiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece
Interests: obesity; NAFLD; insulin resistance; diabetes; inflammation; metabolic dysregulation

Dr. Ioannis Pateras

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Guest Editor

2nd Department of Pathology, “Attikon” University Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece
Interests: pathology; cancer pathology; colorectal cancer; lung cancer; pancreatic cancer; breast cancer; inflammation; infectious agents; cell cycle; metabolism
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Special Issue Information

Dear Colleagues,

Liver and pancreas are two major accessory organs of the digestive system. Chronic liver and pancreatic disorders comprise a heterogeneous group of usually progressive diseases that affect millions of people worldwide. They include non-neoplastic disorders, predominantly of viral or metabolic etiology, as well as neoplastic diseases. The dysregulation of metabolic and inflammatory processes during chronic liver and pancreas disorders is increasingly appreciated. Along this line, metabolic and inflammatory processes are interlinked at multiple levels. Metabolic reprogramming and cytokine responses shape liver and pancreatic tissue damage during infections and exposure to noxious agents. Besides, chronic tissue injury in liver and pancreas is linked with tumor development. Hence, it is important to understand the mechanisms implicated in aberrations in metabolic and inflammatory pathways.

In this Special Issue, we aim to assemble a collection of manuscripts that address the following issues:

How metabolic and inflammatory pathways are involved in the pathogenesis of chronic diseases of the pancreas and liver;
The impact of certain genetic traits and of nutrition in the interplay between metabolic and inflammatory processes in liver and pancreas;
The role of gut microbiome in metabolic and inflammatory reprogramming in the context of chronic disorders of the liver and pancreas;
Potential biomarkers for patient stratification with prognostic and therapeutic value in patients with chronic liver and pancreas disorders.

We encourage contributions in the form of original research articles and comprehensive reviews.

Dr. Antonios Chatzigeorgiou
Dr. Ioannis Pateras
Guest Editors

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

metabolism
inflammation
liver
pancreas
chronic disorders

Published Papers (3 papers)

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Research

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8 pages, 413 KiB

Open AccessArticle

Pancreatic Secretory Trypsin Inhibitor (SPINK1) Gene Mutation in Patients with Acute Alcohol Pancreatitis (AAP) Compared to Healthy Controls and Heavy Alcohol Users without Pancreatitis

by Anssi Nikkola, Kari Antero Mäkelä, Karl-Heinz Herzig, Shivaprakash Jagalur Mutt, Aishwarya Prasannan, Hanna Seppänen, Terho Lehtimäki, Mika Kähönen, Olli Raitakari, Ilkka Seppälä, Pihla Pakkanen, Isto Nordback, Juhani Sand and Johanna Laukkarinen

Int. J. Mol. Sci. 2022, 23(24), 15726; https://doi.org/10.3390/ijms232415726 - 11 Dec 2022

Cited by 2 | Viewed by 1295

Abstract

Only 3–5% of heavy alcohol users develop acute alcohol pancreatitis (AAP). This suggests that additional triggers are required to initiate the inflammatory process. Genetic susceptibility contributes to the development of AAP, and SPINK1 mutation is a documented risk factor. We investigated the prevalence of the SPINK1(N34S) mutation in patients with AAP compared to heavy alcohol users who had never suffered an episode of pancreatitis. Blood samples for the mutational analysis from patients with first episode (n = 60) and recurrent AAP (n = 43) and from heavy alcohol users without a history of AAP (n = 98) as well as from a control population (n = 1914) were obtained. SPINK1 mutation was found in 8.7% of the patients with AAP. The prevalence was significantly lower in healthy controls (3.4%, OR 2.72; 1.32–5.64) and very low in alcoholics without pancreatitis (1.0%, OR 9.29; 1.15–74.74). In a comparison adjusted for potential cofounders between AAP patients and alcoholics, SPINK1 was found to be an independent marker for AAP. The prevalence of the SPINK1 mutation is overrepresented in AAP patients and very low in alcoholics without pancreatitis. This finding may play a role in understanding the variable susceptibility to AAP found in heavy alcohol users. Full article

(This article belongs to the Special Issue Inflammatory and Metabolic Dysregulations in Chronic Liver and Pancreas Disorders)

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Review

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26 pages, 1677 KiB

Open AccessReview

The Effects of Probiotics, Prebiotics and Synbiotics in Non-Alcoholic Fat Liver Disease (NAFLD) and Non-Alcoholic Steatohepatitis (NASH): A Systematic Review

by Rodrigo Zamignan Carpi, Sandra M. Barbalho, Katia Portero Sloan, Lucas Fornari Laurindo, Heron Fernando Gonzaga, Paulo Cesar Grippa, Tereza L. Menegucci Zutin, Raul J. S. Girio, Cláudia Sampaio Fonseca Repetti, Cláudia Rucco Penteado Detregiachi, Patrícia C. Santos Bueno, Eliana de Souza Bastos Mazuqueli Pereira, Ricardo de Alvares Goulart and Jesselina Francisco dos Santos Haber

Int. J. Mol. Sci. 2022, 23(15), 8805; https://doi.org/10.3390/ijms23158805 - 08 Aug 2022

Cited by 40 | Viewed by 5333

Abstract

Modifications in the microbiota caused by environmental and genetic reasons can unbalance the intestinal homeostasis, deregulating the host’s metabolism and immune system, intensifying the risk factors for the development and aggravation of non-alcoholic fat liver disease (NAFLD). The use of probiotics, prebiotics and synbiotics have been considered a potential and promising strategy to regulate the gut microbiota and produce beneficial effects in patients with liver conditions. For this reason, this review aimed to evaluate the effectiveness of probiotics, prebiotics, and symbiotics in patients with NAFLD and NASH. Pubmed, Embase, and Cochrane databases were consulted, and PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analysis) guidelines were followed. The clinical trials used in this study demonstrated that gut microbiota interventions could improve a wide range of markers of inflammation, glycemia, insulin resistance, dyslipidemia, obesity, liver injury (decrease of hepatic enzymes and steatosis and fibrosis). Although microbiota modulators do not play a healing role, they can work as an important adjunct therapy in pathological processes involving NAFLD and its spectrums, either by improving the intestinal barrier or by preventing the formation of toxic metabolites for the liver or by acting on the immune system. Full article

(This article belongs to the Special Issue Inflammatory and Metabolic Dysregulations in Chronic Liver and Pancreas Disorders)

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11 pages, 890 KiB

Open AccessReview

Diagnostic Performance of Pancreatic Cytology with the Papanicolaou Society of Cytopathology System: A Systematic Review, before Shifting into the Upcoming WHO International System

by Ilias P. Nikas, Tanja Proctor, Svenja Seide, Stylianos S. Chatziioannou, Jordan P. Reynolds and Dimitrios Ntourakis

Int. J. Mol. Sci. 2022, 23(3), 1650; https://doi.org/10.3390/ijms23031650 - 31 Jan 2022

Cited by 9 | Viewed by 4274

Abstract

The Papanicolaou Society of Cytopathology (PSC) reporting system classifies pancreatobiliary samples into six categories (I–VI), providing guidance for personalized management. As the World Health Organization (WHO) has been preparing an updated reporting system for pancreatobiliary cytopathology, this systematic review aimed to evaluate the risk of malignancy (ROM) of each PSC category, also the sensitivity and specificity of pancreatic FNA cytology using the current PSC system. Five databases were investigated with a predefined search algorithm. Inclusion and exclusion criteria were applied to select the eligible studies for subsequent data extraction. A study quality assessment was also performed. Eight studies were included in the qualitative analysis. The ROM of the PSC categories I, II, III, IV, V, VI were in the ranges of 8–50%, 0–40%, 28–100%, 0–31%, 82–100%, and 97–100%, respectively. Notably, the ROM IVB (“neoplastic—benign”) subcategory showed a 0% ROM. Four of the included studies reported separately the ROMs for the IVO subcategory (“neoplastic—other”; its overall ROM ranged from 0 to 34%) with low (LGA) and high-grade atypia (HGA). ROM for LGA ranged from 4.3 to 19%, whereas ROM for HGA from 64 to 95.2%. When the subcategory IVO with HGA was considered as cytologically positive, together with the categories V and VI, there was a higher sensitivity of pancreatic cytology, at minimal expense of the specificity. Evidence suggests the proposed WHO international system changes—shifting the IVB entities into the “benign/negative for malignancy” category and establishing two new categories, the “pancreatic neoplasm, low-risk/grade” and “pancreatic neoplasm, high-risk/grade”—could stratify pancreatic neoplasms more effectively than the current PSC system. Full article

(This article belongs to the Special Issue Inflammatory and Metabolic Dysregulations in Chronic Liver and Pancreas Disorders)

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