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Processes
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Study on Metabolic Mechanism of Chronic Diseases
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Study on Metabolic Mechanism of Chronic Diseases

A special issue of Processes (ISSN 2227-9717). This special issue belongs to the section "Pharmaceutical Processes".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 18329

Special Issue Editors

Dr. Claudio Pirozzi

E-Mail Website
Guest Editor
Department of Pharmacy, University of Naples Federico II, Via Domenico Montesano 49, 80131 Naples, Italy
Interests: the main research interests of Dr Claudio Pirozzi lie in the pharmacological control of metabolic disorders, including obesity, nonalcoholic fatty liver disease (NAFLD), and metabolic syndrome
Dr. Adriano Lama

E-Mail Website
Guest Editor
Department of Pharmacy, University of Naples Federico II, Naples, Italy
Interests: mood disorders; obesity; neuroendocrinology; neuroinflammation; gut-brain axis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recently, many clinical studies have been performed to develop new therapeutic strategies for the treatment of metabolic disorders, including obesity, insulin resistance, diabetes, metabolic syndrome. Metabolic alterations related to incorrect dietary habits including fat overnutrition have become common, threatening public health, markedly enhancing the onset and the progression of metabolic diseases and associated immunological and inflammatory complications. However, many researchers have mainly focused on functional studies which attempt to discover metabolic mechanisms of these chronic pathologies.

This Special Issue welcomes papers on research characterized by in vitro and in vivo approaches aimed at identifying specific molecular mechanisms in controlling metabolic diseases caused by lipid overload or high-fat diets in addition to counteracting the associated disorders involving the induction of inflammatory process and immune response.

We welcome papers on the following topics:

  1. Study of metabolic mechanisms underlying chronic diseases
  2. Discovery of prophylactic and/or therapeutic approaches for the treatment of chronic diseases
  3. In vitro/in vivo models of fat overnutrition and/or lipid overload which mimic the alterations characterizing metabolic disorders, such as obesity and/or diabetes
  4. Metabolic analysis of various factors in vivo in animal disease models (chronic metabolic diseases, including obesity, diabetes, and insulin and/or leptin resistance)
  5. Immune-metabolic dysfunction induced by chronic diseases
  6. Low-grade inflammation and/or oxidative/mitochondrial damage associated with metabolic pathologies and their mechanisms
  7. Study of the gut–brain axis and its involvement in mental disorders
  8. The connection between metainflammation and neuroinflammation
  9. The influence of metabolic alterations in worsening neuropsychiatric disorders

Dr. Claudio Pirozzi
Dr. Adriano Lama
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. Processes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). 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

  • Chronic metabolic disorders
  • In vitro and in vivo mechanistic studies of metabolic diseases
  • Fat overnutrition or high-fat diets
  • Cell lipid overload which resembles the metabolic alterations characterizing obesity and insulin and leptin resistance
  • Understanding immunological involvement through cells and animal models
  • Metainflammation
  • Oxidative/mitochondrial damage as mechanisms of metabolic pathologies
  • Interconnection between metabolic alterations and mental disorders
  • Gut–brain axis

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Published Papers (3 papers)

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Research

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13 pages, 2371 KiB  
Article
Analysis of Gene Expression Microarray Data Reveals Androgen-Responsive Genes of Muscles in Polycystic Ovarian Syndrome Patients
by Seong-Beom Cho
Processes 2022, 10(2), 387; https://doi.org/10.3390/pr10020387 - 17 Feb 2022
Cited by 1 | Viewed by 2087
Abstract
Polycystic ovarian syndrome (PCOS) is an endocrine disorder that is characterized by hyperandrogenism. Therefore, information about androgen-induced molecular changes can be obtained using the tissues of patients with PCOS. We analyzed two microarray datasets of normal and PCOS muscle samples (GSE8157 and GSE6798) [...] Read more.
Polycystic ovarian syndrome (PCOS) is an endocrine disorder that is characterized by hyperandrogenism. Therefore, information about androgen-induced molecular changes can be obtained using the tissues of patients with PCOS. We analyzed two microarray datasets of normal and PCOS muscle samples (GSE8157 and GSE6798) to identify androgen-responsive genes (ARGs). Differentially expressed genes were determined using the t-test and a meta-analysis of the datasets. The overlap between significant results of the meta-analysis and ARGs predicted from an external database was determined, and differential coexpression analysis was then applied between these genes and the other genes. We found 313 significant genes in the meta-analysis using the Benjamini–Hochberg multiple testing correction. Of these genes, 61 were in the list of predicted ARGs. When the differential coexpression between these 61 genes and 13,545 genes filtered by variance was analyzed, 540 significant gene pairs were obtained using the Benjamini–Hochberg correction. While no significant results were obtained regarding the functional enrichment of the differentially expressed genes, top-level gene ontology terms were significantly enriched in the list of differentially coexpressed genes, which indicates that a broad range of cellular processes is affected by androgen administration. Our findings provide valuable information for the identification of ARGs. Full article
(This article belongs to the Special Issue Study on Metabolic Mechanism of Chronic Diseases)
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18 pages, 4715 KiB  
Article
Lipocalin, Resistin and Gut Microbiota-Derived Propionate Could Be Used to Predict Metabolic Bariatric Surgery Selected Outcomes
by Teresa Auguet, Miguel Lopez-Dupla, Jessica Ramos, Laia Bertran, David Riesco, Carmen Aguilar, Anna Ardévol, Montserrat Pinent, Fàtima Sabench, Daniel Del Castillo and Cristóbal Richart
Processes 2022, 10(1), 143; https://doi.org/10.3390/pr10010143 - 11 Jan 2022
Cited by 4 | Viewed by 2008
Abstract
Many patients with clinically severe obesity (CSO) need to undergo bariatric surgery, with possible side effects, so individualized predictive methods are required. Adipocytokines and gut/intestinal microbiota-derived metabolites could be predictive biomarkers of metabolic success post- surgery, but the knowledge in this field is [...] Read more.
Many patients with clinically severe obesity (CSO) need to undergo bariatric surgery, with possible side effects, so individualized predictive methods are required. Adipocytokines and gut/intestinal microbiota-derived metabolites could be predictive biomarkers of metabolic success post- surgery, but the knowledge in this field is undefined. The objective of this work was to determine whether adipocytokines and microbiota-derived metabolites can be used to predict the metabolic improvement post- surgery in women with CSO. We analyzed circulating levels of some cytokines and some microbiota-derived metabolites at baseline and 12 months post-surgery from 44 women with CSO and 21 women with normal weight. Results showed that glucose, insulin, glycosylated hemoglobin A1c (HbA1c), low-density lipoprotein (LDL-C), and triglycerides levels were decreased post-surgery, while high density lipoprotein increased. Twelve months later, leptin, resistin, lipocalin, PAI-1, TNF-α, and IL-1β levels were lower than baseline, meanwhile adiponectin, IL-8, and IL-10 levels were increased. Moreover, baseline lipocalin levels were associated with HbA1c reduction post-surgery; meanwhile baseline resistin was related to postoperative HOMA2 (insulin resistance) and baseline propionate was associated with LDL-C decrease. To conclude, the detection of lipocalin, resistin, and propionate levels may be used to predict the metabolic success following bariatric surgery, although new knowledge is needed. Full article
(This article belongs to the Special Issue Study on Metabolic Mechanism of Chronic Diseases)
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Review

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18 pages, 1413 KiB  
Review
Non-Alcoholic Fatty Liver Disease: From Pathogenesis to Clinical Impact
by Alfredo Caturano, Carlo Acierno, Riccardo Nevola, Pia Clara Pafundi, Raffaele Galiero, Luca Rinaldi, Teresa Salvatore, Luigi Elio Adinolfi and Ferdinando Carlo Sasso
Processes 2021, 9(1), 135; https://doi.org/10.3390/pr9010135 - 11 Jan 2021
Cited by 74 | Viewed by 12816
Abstract
Non-Alcoholic Fatty Liver Disease (NAFLD) is caused by the accumulation of fat in over 5% of hepatocytes in the absence of alcohol consumption. NAFLD is considered the hepatic manifestation of metabolic syndrome (MS). Recently, an expert consensus suggested as more appropriate the term [...] Read more.
Non-Alcoholic Fatty Liver Disease (NAFLD) is caused by the accumulation of fat in over 5% of hepatocytes in the absence of alcohol consumption. NAFLD is considered the hepatic manifestation of metabolic syndrome (MS). Recently, an expert consensus suggested as more appropriate the term MAFLD (metabolic-associated fatty liver disease). Insulin resistance (IR) plays a key role in the development of NAFLD, as it causes an increase in hepatic lipogenesis and an inhibition of adipose tissue lipolysis. Beyond the imbalance of adipokine levels, the increase in the mass of visceral adipose tissue also determines an increase in free fatty acid (FFA) levels. In turn, an excess of FFA is able to determine IR through the inhibition of the post-receptor insulin signal. Adipocytes secrete chemokines, which are able to enroll macrophages inside the adipose tissue, responsible, in turn, for the increased levels of TNF-α. The latter, as well as resistin and other pro-inflammatory cytokines such as IL-6, enhances insulin resistance and correlates with endothelial dysfunction and an increased cardiovascular (CV) risk. In this review, the role of diet, intestinal microbiota, genetic and epigenetic factors, low-degree chronic systemic inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress on NAFLD have been addressed. Finally, the clinical impact of NAFLD on cardiovascular and renal outcomes, and its direct link with type 2 diabetes have been discussed. Full article
(This article belongs to the Special Issue Study on Metabolic Mechanism of Chronic Diseases)
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