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Molecular Mechanism Underlying the Endocrine Abnormalities Associated with Severe Illness
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Molecular Mechanism Underlying the Endocrine Abnormalities Associated with Severe Illness

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 May 2022) | Viewed by 13260

Special Issue Editor

Prof. Jose Joaquin Lado-Abeal

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Guest Editor
1. Professor of Medicine, Department of Internal Medicine, University of South Carolina School of Medicine, Columbia, SC, USA
2. Director, Division of Endocrinology, Diabetes and Metabolism Prisma Health Midlands, Columbia, SC, USA

Special Issue Information

Dear Colleagues,

The organism homeostasis and the endocrine system functions are closely related to each other. Although both are profoundly affected during a severe illness, a direct pathogenic role of changes in the endocrine system on the homeostasis of organisms during disease has not been established. The endocrine alterations observed during severe illness are considered adaptative. With the exception of glucocorticoids and insulin replacement, the prevalent idea in the clinical practice is that patients with hormonal abnormalities resulting from severe illness should not be given a hormonal replacement.  Due to the very high prevalence of endocrine abnormalities resulting from diseases, this clinical attitude implies that the most common endocrine problems occurring in the inpatient setting are neglected.

Nowadays, patients can be maintained on artificial life support for a prolonged period of time. Consequently, the hormonal abnormalities associated with the disease can be several weeks or even months. As such, the consequences of nonintervention with a hormonal replacement should be revisited and reviewed.

We will address the molecular changes and mechanisms underlying the multiple endocrine abnormalities observed in patients with severe illness in this Special Issue. We will review the mechanisms responsible for the differences in serum hormonal levels, in the action of hormones at cellular levels, and in the endocrine glands’ morphology during illnesses.  We hope that an accurate exposition of the knowledge acquired until today will lay the foundations for a rational scientific discussion about the current clinical practice regarding the endocrine system's function during illness.

Prof. Jose Joaquin Lado-Abeal
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.

Published Papers (5 papers)

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Research

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9 pages, 1007 KiB  
Communication
The Ubiquitin E3 Ligase Nedd4 Regulates the Expression and Amyloid-β Peptide Export Activity of P-Glycoprotein
by Amanda B. Chai, Richard Callaghan and Ingrid C. Gelissen
Int. J. Mol. Sci. 2022, 23(3), 1019; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031019 - 18 Jan 2022
Cited by 5 | Viewed by 1575
Abstract
The ATP-binding cassette transporter, P-glycoprotein (P-gp), has been demonstrated to facilitate the clearance of amyloid-beta (Aβ) peptides, exporting the neurotoxic entity out of neurons and out of the brain via the blood–brain barrier. However, its expression and function diminish with age and in [...] Read more.
The ATP-binding cassette transporter, P-glycoprotein (P-gp), has been demonstrated to facilitate the clearance of amyloid-beta (Aβ) peptides, exporting the neurotoxic entity out of neurons and out of the brain via the blood–brain barrier. However, its expression and function diminish with age and in Alzheimer’s disease. P-gp is known to undergo ubiquitination, a post-translational modification that results in internalisation and/or degradation of the protein. NEDD4-1 is a ubiquitin E3 ligase that has previously been shown to ubiquitinate P-gp and reduce its cell surface expression. However, whether this effect translates into altered P-gp activity remains to be determined. siRNA was used to knockdown the expression of Nedd4 in CHO-APP cells. Western blot analysis confirmed that absence of Nedd4 was associated with increased P-gp protein expression. This was accompanied by increased transport activity, as shown by export of the P-gp substrate calcein-AM, as well as enhanced secretion of Aβ peptides, as shown by ELISA. These results implicate Nedd4 in the regulation of P-gp, and highlight a potential approach for restoring or augmenting P-gp expression and function to facilitate Aβ clearance from the brain. Full article
(This article belongs to the Special Issue Molecular Mechanism Underlying the Endocrine Abnormalities Associated with Severe Illness)
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14 pages, 2994 KiB  
Article
MiR-320-3p Regulates the Proliferation and Differentiation of Myogenic Progenitor Cells by Modulating Actin Remodeling
by Mai Thi Nguyen and Wan Lee
Int. J. Mol. Sci. 2022, 23(2), 801; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020801 - 12 Jan 2022
Cited by 9 | Viewed by 1927
Abstract
Skeletal myogenesis is essential for the maintenance of muscle quality and quantity, and impaired myogenesis is intimately associated with muscle wasting diseases. Although microRNA (miRNA) plays a crucial role in myogenesis and relates to muscle wasting in obesity, the molecular targets and roles [...] Read more.
Skeletal myogenesis is essential for the maintenance of muscle quality and quantity, and impaired myogenesis is intimately associated with muscle wasting diseases. Although microRNA (miRNA) plays a crucial role in myogenesis and relates to muscle wasting in obesity, the molecular targets and roles of miRNAs modulated by saturated fatty acids (SFA) are largely unknown. In the present study, we investigated the role of miR-320-3p on the differentiation of myogenic progenitor cells. Palmitic acid (PA), the most abundant dietary SFA, suppressed myogenic factors expression and impaired differentiation in C2C12 myoblasts, and these effects were accompanied by CFL2 downregulation and miR-320-3p upregulation. In particular, miR-320-3p appeared to target CFL2 mRNA directly and suppress the expression of CFL2, an essential factor for filamentous actin (F-actin) depolymerization. Transfection of myoblasts with miR-320-3p mimic increased F-actin formation and nuclear translocation of Yes-associated protein 1 (YAP1), a key component of mechanotransduction. Furthermore, miR-320-3p mimic increased myoblast proliferation and markedly impeded the expression of MyoD and MyoG, consequently inhibiting myoblast differentiation. In conclusion, our current study highlights the role of miR-320-3p on CFL2 expression, YAP1 activation, and myoblast differentiation and suggests that PA-inducible miR-320-3p is a significant mediator of muscle wasting in obesity. Full article
(This article belongs to the Special Issue Molecular Mechanism Underlying the Endocrine Abnormalities Associated with Severe Illness)
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10 pages, 2697 KiB  
Article
Lactobacillus plantarum ATG-K2 and ATG-K6 Ameliorates High-Fat with High-Fructose Induced Intestinal Inflammation
by Miey Park, Eun-Jung Park, So-Hyeun Kim and Hae-Jeung Lee
Int. J. Mol. Sci. 2021, 22(9), 4444; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094444 - 24 Apr 2021
Cited by 9 | Viewed by 2710
Abstract
Obesity has become a worldwide health problem, and many significant inflammatory markers have been associated with the risk of side effects of obesity and obesity-related diseases. After a normal diet or high-fat diet with high-fructose water (HFHF) for 8 weeks, male Wistar rats [...] Read more.
Obesity has become a worldwide health problem, and many significant inflammatory markers have been associated with the risk of side effects of obesity and obesity-related diseases. After a normal diet or high-fat diet with high-fructose water (HFHF) for 8 weeks, male Wistar rats were divided randomly into four experimental groups according to body weight. Next, for 8 weeks, a normal diet, HFHF diet, and HFHF diet with L. plantarum strains ATG-K2 or ATG-K6 were administered orally. Compared to the control group, the HFHF diet group showed significantly increased visceral fat, epididymal fat, and liver weight. The mRNA and protein expression levels of FAS and SREBP-1c were higher in the HFHF diet group than in the HFHF diet with L. plantarum strains ATG-K2 and ATG-K6. The HFHF diet with L. plantarum strain ATG-K2 showed significantly decreased inflammatory cytokine expression in the serum and small intestine compared to the HFHF diet group. Furthermore, histological morphology showed minor cell injury, less severe infiltration, and longer villi height in the small intestine ileum of the HFHF diet with L. plantarum strains groups than in the HFHF diet group. These results suggest that L. plantarum strains K2 and K6 may help reduce intestinal inflammation and could be used as treatment alternatives for intestinal inflammatory reactions and obesity. Full article
(This article belongs to the Special Issue Molecular Mechanism Underlying the Endocrine Abnormalities Associated with Severe Illness)
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Review

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31 pages, 1388 KiB  
Review
The Intriguing Thyroid Hormones–Lung Cancer Association as Exemplification of the Thyroid Hormones–Cancer Association: Three Decades of Evolving Research
by Maria V. Deligiorgi and Dimitrios T. Trafalis
Int. J. Mol. Sci. 2022, 23(1), 436; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010436 - 31 Dec 2021
Cited by 7 | Viewed by 2234
Abstract
Exemplifying the long-pursued thyroid hormones (TH)–cancer association, the TH–lung cancer association is a compelling, yet elusive, issue. The present narrative review provides background knowledge on the molecular aspects of TH actions, with focus on the contribution of TH to hallmarks of cancer. Then, [...] Read more.
Exemplifying the long-pursued thyroid hormones (TH)–cancer association, the TH–lung cancer association is a compelling, yet elusive, issue. The present narrative review provides background knowledge on the molecular aspects of TH actions, with focus on the contribution of TH to hallmarks of cancer. Then, it provides a comprehensive overview of data pertinent to the TH–lung cancer association garnered over the last three decades and identifies obstacles that need to be overcome to enable harnessing this association in the clinical setting. TH contribute to all hallmarks of cancer through integration of diverse actions, currently classified according to molecular background. Despite the increasingly recognized implication of TH in lung cancer, three pending queries need to be resolved to empower a tailored approach: (1) How to stratify patients with TH-sensitive lung tumors? (2) How is determined whether TH promote or inhibit lung cancer progression? (3) How to mimic the antitumor and/or abrogate the tumor-promoting TH actions in lung cancer? To address these queries, research should prioritize the elucidation of the crosstalk between TH signaling and oncogenic signaling implicated in lung cancer initiation and progression, and the development of efficient, safe, and feasible strategies leveraging this crosstalk in therapeutics. Full article
(This article belongs to the Special Issue Molecular Mechanism Underlying the Endocrine Abnormalities Associated with Severe Illness)
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17 pages, 1621 KiB  
Review
Role of Adipose Tissue in Inflammatory Bowel Disease
by Eva Karaskova, Maria Velganova-Veghova, Milos Geryk, Hana Foltenova, Veronika Kucerova and David Karasek
Int. J. Mol. Sci. 2021, 22(8), 4226; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084226 - 19 Apr 2021
Cited by 35 | Viewed by 4237
Abstract
Inflammatory bowel diseases (IBDs), chronic inflammatory disorders affecting the gastrointestinal tract, include Crohn’s disease and ulcerative colitis. There are increasing clinical and experimental data showing that obesity, especially visceral adiposity, plays a substantial role in the pathogenesis of IBD. Obesity seems to be [...] Read more.
Inflammatory bowel diseases (IBDs), chronic inflammatory disorders affecting the gastrointestinal tract, include Crohn’s disease and ulcerative colitis. There are increasing clinical and experimental data showing that obesity, especially visceral adiposity, plays a substantial role in the pathogenesis of IBD. Obesity seems to be an important risk factor also for IBD disease severity and clinical outcomes. Visceral adipose tissue is an active multifunctional metabolic organ involved in lipid storage and immunological and endocrine activity. Bowel inflammation penetrates the surrounding adipose tissue along the mesentery. Mesenteric fat serves as a barrier to inflammation and controls immune responses to the translocation of gut bacteria. At the same time, mesenteric adipose tissue may be the principal source of cytokines and adipokines responsible for inflammatory processes associated with IBD. This review is particularly focusing on the potential role of adipokines in IBD pathogenesis and their possible use as promising therapeutic targets. Full article
(This article belongs to the Special Issue Molecular Mechanism Underlying the Endocrine Abnormalities Associated with Severe Illness)
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