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Mechanisms of Adiponectin Action 3.0
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Mechanisms of Adiponectin Action 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 7144

Special Issue Editor

Dr. Tania Fiaschi

E-Mail Website
Guest Editor
Department of Experimental and Clinical Biomedical Sciences “M. Serio”, University of Florence, 50134 Florence, Italy
Interests: skeletal muscle; cancer cachexia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our 2020 Special Issue “Mechanisms of Adiponectin Action 2.0” and 2019 Special Issue “Mechanisms of Adiponectin Action”.

Adiponectin is an adipokine circulating in the blood stream and is locally produced by various tissues. The main effect of adiponectin concerns metabolism regulation, since it controls glucose and triglyceride homeostasis, thus helping insulin action in healthy tissues, such as liver and skeletal muscle. Obesity and metabolic syndrome lead to adiponectin decrease, thus predisposing diabetes onset. However, growing evidence suggests a more pleiotropic role of the hormone in different tissues. Adiponectin affects autophagy, cell differentiation, and stem cell behavior, while hypoadiponectinemia has been correlated with several types of cancers. The Special Issue on the topic of “Mechanisms of Adiponectin Action” in the International Journal of Molecular Sciences will include a selection of research papers and reviews about various aspects of the molecular and cellular biology of adiponectin. In addition, studies on molecules able to modulate adiponectin signaling, and their possible use in the treatment of pathologies in which adiponectin is involved, will also be considered.

Dr. Tania Fiaschi
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.

Keywords

  • Adiponectin
  • Metabolism
  • Cell signaling
  • Differentiation
  • Stem cells
  • Cancer

Published Papers (3 papers)

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Research

19 pages, 4713 KiB  
Article
Defining the Molecular Mechanisms of the Relaxant Action of Adiponectin on Murine Gastric Fundus Smooth Muscle: Potential Translational Perspectives on Eating Disorder Management
by Rachele Garella, Emanuele Cassioli, Flaminia Chellini, Alessia Tani, Eleonora Rossi, Eglantina Idrizaj, Daniele Guasti, Paolo Comeglio, Francesco Palmieri, Martina Parigi, Linda Vignozzi, Maria Caterina Baccari, Valdo Ricca, Chiara Sassoli, Giovanni Castellini and Roberta Squecco
Int. J. Mol. Sci. 2023, 24(2), 1082; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24021082 - 05 Jan 2023
Cited by 2 | Viewed by 1897
Abstract
Adiponectin (ADPN), a hormone produced by adipose tissue, facilitates gastric relaxation and can be a satiety signal in the network connecting peripheral organs and the central nervous system for feeding behavior control. Here, we performed preclinical research by morpho-functional analyses on murine gastric [...] Read more.
Adiponectin (ADPN), a hormone produced by adipose tissue, facilitates gastric relaxation and can be a satiety signal in the network connecting peripheral organs and the central nervous system for feeding behavior control. Here, we performed preclinical research by morpho-functional analyses on murine gastric fundus smooth muscle to add insights into the molecular mechanisms underpinning ADPN action. Moreover, we conducted a clinical study to evaluate the potential use of ADPN as a biomarker for eating disorders (ED) based on the demonstrated gastric alterations and hormone level fluctuations that are often associated with ED. The clinical study recruited patients with ED and healthy controls who underwent blood draws for ADPN dosage and psychopathology evaluation tests. The findings of this basic research support the ADPN relaxant action, as indicated by the smooth muscle cell membrane pro-relaxant effects, with mild modifications of contractile apparatus and slight inhibitory effects on gap junctions. All of these actions engaged the ADPN/nitric oxide/guanylate cyclase pathway. The clinical data failed to unravel a correlation between ADPN levels and the considered ED, thus negating the potential use of ADPN as a valid biomarker for ED management for the moment. Nevertheless, this adipokine can modulate physiological eating behavior, and its effects deserve further investigation. Full article
(This article belongs to the Special Issue Mechanisms of Adiponectin Action 3.0)
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22 pages, 5171 KiB  
Article
Aerobic Exercise Alleviates Abnormal Autophagy in Brain Cells of APP/PS1 Mice by Upregulating AdipoR1 Levels
by Ye Jian, Shunling Yuan, Jialun Yang, Yong Lei, Xuan Li and Wenfeng Liu
Int. J. Mol. Sci. 2022, 23(17), 9921; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23179921 - 31 Aug 2022
Cited by 12 | Viewed by 2160
Abstract
Abnormalities in autophagy are associated with Alzheimer’s disease (AD)-like lesions. Studies have shown that exercise can significantly improve AD autophagy abnormalities, but the mechanism underlying this phenomenon remains unclear. APN not only has an important regulatory effect on AD autophagy abnormalities, but also [...] Read more.
Abnormalities in autophagy are associated with Alzheimer’s disease (AD)-like lesions. Studies have shown that exercise can significantly improve AD autophagy abnormalities, but the mechanism underlying this phenomenon remains unclear. APN not only has an important regulatory effect on AD autophagy abnormalities, but also is affected by exercise. Therefore, this study aims to reveal the pathway by which exercise regulates abnormal autophagy in AD using the APN–AdipoR1 signaling pathway as an entry point. The results of the study showed that APP/PS1 double transgenic AD model mice (24 weeks) showed decreased AdipoR1 levels in the brain, abnormal autophagy, increased Aβ deposition, and increased cell apoptosis, and dendritic spines and cognitive function were reduced. Twelve weeks of aerobic exercise enhanced lysosomes and alleviated abnormal autophagy by activating the AdipoR1/AMPK/TFEB signaling pathway in the brains of AD mice, thereby alleviating Aβ deposition and its associated AD-like abnormalities. These findings suggest that the AdipoR1 plays an important role in aerobic exercise’s alleviation of abnormal autophagy in AD brain cells and alleviation of AD-like lesions. Full article
(This article belongs to the Special Issue Mechanisms of Adiponectin Action 3.0)
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13 pages, 1750 KiB  
Article
Adiponectin Deficiency Alters Placenta Function but Does Not Affect Fetal Growth in Mice
by Man Mohan Shrestha, Sanne Wermelin, Elisabet Stener-Victorin, Ingrid Wernstedt Asterholm and Anna Benrick
Int. J. Mol. Sci. 2022, 23(9), 4939; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094939 - 29 Apr 2022
Cited by 4 | Viewed by 2423
Abstract
Adiponectin administration to pregnant mice decreases nutrient transport and fetal growth. An adiponectin deficiency, on the other hand, as seen in obese women during pregnancy, alters fetal growth; however, the mechanism is unclear. To determine the role of adiponectin on placenta function and [...] Read more.
Adiponectin administration to pregnant mice decreases nutrient transport and fetal growth. An adiponectin deficiency, on the other hand, as seen in obese women during pregnancy, alters fetal growth; however, the mechanism is unclear. To determine the role of adiponectin on placenta function and fetal growth, we used adiponectin knockout, adiponectin heterozygote that displays reduced adiponectin levels, and wild-type mice on a control diet or high fat/high sucrose (HF/HS) diet. Triglycerides (TGs) in the serum, liver, and placenta were measured using colorimetric assays. Gene expression was measured using quantitative RT-PCR. Adiponectin levels did not affect fetal weight, but it reduced adiponectin levels, increased fetal serum and placenta TG content. Wildtype dams on a HF/HS diet protected the fetuses from fatty acid overload as judged by increased liver TGs in dams and normal serum and liver TG levels in fetuses, while low adiponectin was associated with increased fetal liver TGs. Low maternal adiponectin increased the expression of genes involved in fatty acid transport; Lpl and Cd36 in the placenta. Adiponectin deficiency does not affect fetal growth but induces placental dysfunction and increases fetal TG load, which is enhanced with obesity. This could lead to imprinting effects on the fetus and the development of metabolic dysfunction in the offspring. Full article
(This article belongs to the Special Issue Mechanisms of Adiponectin Action 3.0)
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