Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
6.0
Journals
Cells
Special Issues
The Adipose Tissue: From “Cinderella” to “Lion King” Organ
share announcement

The Adipose Tissue: From “Cinderella” to “Lion King” Organ

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 6440

Special Issue Editors

Dr. Valerio Costa

E-Mail Website
Guest Editor
Institute of Genetics and Biophysics "Adriano Buzzati-Traverso", IGB-CNR, 80131 Naples, Italy
Interests: PPARG; adipose tissue; obesity; gene expression; alternative splicing
Special Issues, Collections and Topics in MDPI journals
Dr. Marianna Aprile

E-Mail Website
Guest Editor
Institute of Genetics and Biophysics "Adriano Buzzati-Traverso", IGB-CNR, Via P. Castellino 111, 80131 Naples, Italy
Interests: adipose tissue dysfunction; hypertrophic obesity; PPARG; cell models of adipogenesis; alternative splicing
Dr. Jean-François Tanti

E-Mail Website
Guest Editor
Université Côte d’Azur, Inserm UMR1065, C3M, Team Cellular and Molecular Pathophysiology of Obesity, Nice, France
Interests: adipose tissue dysfunction; insulin resistance; insulin signaling; inflammation; senescence

Special Issue Information

Dear Colleagues,

Adipose tissue (AT) has often been considered as the “Cinderella” organ and a metabolically inert tissue, receiving less attention than other organs and tissues. However, the research interest on adipose tissue has gradually increased, compensating at least in part the scarcity of adipose-focused literature and leading to a reconsideration of the role of this understudied organ. To date, the research community has agreed to consider the adipose tissue a central hub in the regulation of whole-body energy homeostasis and insulin sensitivity.

The increasingly evident association between AT dysfunction and diseases has put adipose tissue biology under the spotlight of scientific interest. The functional failure of white adipose tissue depots to buffer postprandial lipids has been proposed as the link connecting AT and diseases. According to the “lipid overflow” hypothesis, the storage capacity is finite, and exceeding this limit leads to ectopic lipid accumulation, tissue fibrosis, lipotoxicity, insulin sensitivity reduction and systemic chronic inflammation. Thus, the risk of developing metabolic complications is strictly correlated to the individual adipose tissue storage capability, which affects the balance between adipocyte hypertrophy and hyperplasia.

In this context, elucidating the mechanisms governing adipose tissue expandability and the differentiation of new lipid-storing and insulin-sensitive adipocytes is crucial to define individual risk profiles.

This Special Issue aims to be a significant contribution to fill the gap in the knowledge of molecular mechanisms underlying the pathophysiology of adipose tissue in health and disease, with a focus on adipose tissue formation, expandability and the individual predisposition to metabolic disorders, functionally related to adipose tissue deficit.

This Special Issue will collect original articles, in-depth reviews and perspective opinions regarding:

  • Multifaceted roles of distinct adipose tissue subtypes;
  • Experimental approaches and/or cellular/animal models to study adipose tissue;
  • Therapeutic approaches to counteract adipose tissue dysfunction.

Dr. Valerio Costa
Dr. Marianna Aprile
Dr. Jean-François Tanti
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • adipose tissue subtypes
  • adipose tissue expandability
  • adipose tissue dysfunctions
  • pathophysiology of obesity
  • cellular models of adipocytes

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

17 pages, 4187 KiB  
Article
Stimulator of Interferon Genes (STING) Triggers Adipocyte Autophagy
by Kornél Z. Varga, Katalin Gyurina, Ádám Radványi, Tibor Pál, László Sasi-Szabó, Haidong Yu, Enikő Felszeghy, Tamás Szabó and Tamás Röszer
Cells 2023, 12(19), 2345; https://doi.org/10.3390/cells12192345 - 24 Sep 2023
Viewed by 1598
Abstract
Innate immune signaling in adipocytes affects systemic metabolism. Cytosolic nucleic acid sensing has been recently shown to stimulate thermogenic adipocyte differentiation and protect from obesity; however, DNA efflux from adipocyte mitochondria is a potential proinflammatory signal that causes adipose tissue dysfunction and insulin [...] Read more.
Innate immune signaling in adipocytes affects systemic metabolism. Cytosolic nucleic acid sensing has been recently shown to stimulate thermogenic adipocyte differentiation and protect from obesity; however, DNA efflux from adipocyte mitochondria is a potential proinflammatory signal that causes adipose tissue dysfunction and insulin resistance. Cytosolic DNA activates the stimulator of interferon response genes (STING), a key signal transducer which triggers type I interferon (IFN-I) expression; hence, STING activation is expected to induce IFN-I response and adipocyte dysfunction. However, we show herein that mouse adipocytes had a diminished IFN-I response to STING stimulation by 2′3′-cyclic-GMP-AMP (cGAMP). We also show that cGAMP triggered autophagy in murine and human adipocytes. In turn, STING inhibition reduced autophagosome number, compromised the mitochondrial network and caused inflammation and fat accumulation in adipocytes. STING hence stimulates a process that removes damaged mitochondria, thereby protecting adipocytes from an excessive IFN-I response to mitochondrial DNA efflux. In summary, STING appears to limit inflammation in adipocytes by promoting mitophagy under non-obesogenic conditions. Full article
(This article belongs to the Special Issue The Adipose Tissue: From “Cinderella” to “Lion King” Organ)
►▼ Show Figures

Graphical abstract

20 pages, 7512 KiB  
Article
Human Preadipocytes Differentiated under Hypoxia following PCB126 Exposure during Proliferation: Effects on Differentiation, Glucose Uptake and Adipokine Profile
by Zeinab El Amine, Jean-François Mauger and Pascal Imbeault
Cells 2023, 12(18), 2326; https://doi.org/10.3390/cells12182326 - 21 Sep 2023
Viewed by 942
Abstract
Persistent organic pollutants (POPs) accumulation and hypoxia are two factors proposed to adversely alter adipose tissue (AT) functions in the context of excess adiposity. Studies have shown that preadipocytes exposure to dioxin and dioxin-like POPs have the greatest deleterious impact on rodent and [...] Read more.
Persistent organic pollutants (POPs) accumulation and hypoxia are two factors proposed to adversely alter adipose tissue (AT) functions in the context of excess adiposity. Studies have shown that preadipocytes exposure to dioxin and dioxin-like POPs have the greatest deleterious impact on rodent and immortalized human preadipocyte differentiation, but evidence on human preadipocytes is lacking. Additionally, hypoxia is known to strongly interfere with the dioxin-response pathway. Therefore, we tested the effects of pre-differentiation polychlorinated biphenyl (PCB)126 exposure at 10 µM for 3 days and subsequent differentiation under hypoxia on human subcutaneous adipocytes (hSA) differentiation, glucose uptake and expression of selected metabolism- and inflammation-related genes. Pre-differentiation PCB126 exposure lowered the adenosine triphosphate (ATP) content, glucose uptake and leptin expression of mature adipocytes but had limited effects on differentiation under normoxia (21% O2). Under hypoxia (3% O2), preadipocytes ability to differentiate was significantly reduced as reflected by significant decreased lipid accumulation and downregulation of key adipocyte genes such as peroxisome proliferator-activated receptor gamma (PPARγ) and adiponectin. Hypoxia increased glucose uptake and glucose transporter 1 (GLUT1) expression but abolished the adipocytes insulin response and GLUT4 expression. The expression of pro-inflammatory adipokine interleukin-6 (IL-6) was slightly increased by both PCB126 and hypoxia, while IL-8 expression was significantly increased only following the PCB126-hypoxia sequence. These observations suggest that PCB126 does not affect human preadipocyte differentiation, but does affect the subsequent adipocytes population, as reflected by lower ATP levels and absolute glucose uptake. On the other hand, PCB126 and hypoxia exert additive effects on AT inflammation, an important player in the development of chronic diseases such as type 2 diabetes and cardiovascular diseases. Full article
(This article belongs to the Special Issue The Adipose Tissue: From “Cinderella” to “Lion King” Organ)
►▼ Show Figures

Graphical abstract

13 pages, 3258 KiB  
Article
CYP1A1, VEGFA and Adipokine Responses of Human Adipocytes Co-exposed to PCB126 and Hypoxia
by Zeinab El Amine, Jean-François Mauger and Pascal Imbeault
Cells 2022, 11(15), 2282; https://doi.org/10.3390/cells11152282 - 24 Jul 2022
Cited by 4 | Viewed by 1749
Abstract
It is increasingly recognized that hypoxia may develop in adipose tissue as its mass expands. Adipose tissue is also the main reservoir of lipophilic pollutants, including polychlorinated biphenyls (PCBs). Both hypoxia and PCBs have been shown to alter adipose tissue functions. The signaling [...] Read more.
It is increasingly recognized that hypoxia may develop in adipose tissue as its mass expands. Adipose tissue is also the main reservoir of lipophilic pollutants, including polychlorinated biphenyls (PCBs). Both hypoxia and PCBs have been shown to alter adipose tissue functions. The signaling pathways induced by hypoxia and pollutants may crosstalk, as they share a common transcription factor: aryl hydrocarbon receptor nuclear translocator (ARNT). Whether hypoxia and PCBs crosstalk and affect adipokine secretion in human adipocytes remains to be explored. Using primary human adipocytes acutely co-exposed to different levels of hypoxia (24 h) and PCB126 (48 h), we observed that hypoxia significantly inhibits the PCB126 induction of cytochrome P450 (CYP1A1) transcription in a dose-response manner, and that Acriflavine (ACF)—an HIF1α inhibitor—partially restores the PCB126 induction of CYP1A1 under hypoxia. On the other hand, exposure to PCB126 did not affect the transcription of the vascular endothelial growth factor-A (VEGFA) under hypoxia. Exposure to hypoxia increased leptin and interleukin-6 (IL-6), and decreased adiponectin levels dose-dependently, while PCB126 increased IL-6 and IL-8 secretion in a dose-dependent manner. Co-exposure to PCB126 and hypoxia did not alter the adipokine secretion pattern observed under hypoxia and PCB126 exposure alone. In conclusion, our results indicate that (1) hypoxia inhibits PCB126-induced CYP1A1 expression at least partly through ARNT-dependent means, suggesting that hypoxia could affect PCB metabolism and toxicity in adipose tissue, and (2) hypoxia and PCB126 affect leptin, adiponectin, IL-6 and IL-8 secretion differently, with no apparent crosstalk between the two factors. Full article
(This article belongs to the Special Issue The Adipose Tissue: From “Cinderella” to “Lion King” Organ)
►▼ Show Figures

Figure 1

Review

Jump to: Research

14 pages, 722 KiB  
Review
The Transcription Factor HOXA5: Novel Insights into Metabolic Diseases and Adipose Tissue Dysfunction
by Luca Parrillo, Rosa Spinelli, Michele Longo, Federica Zatterale, Gianluca Santamaria, Alessia Leone, Michele Campitelli, Gregory Alexander Raciti and Francesco Beguinot
Cells 2023, 12(16), 2090; https://doi.org/10.3390/cells12162090 - 18 Aug 2023
Viewed by 1234
Abstract
The transcription factor HOXA5, from the HOX gene family, has long been studied due to its critical role in physiological activities in normal cells, such as organ development and body patterning, and pathological activities in cancer cells. Nonetheless, recent evidence supports the [...] Read more.
The transcription factor HOXA5, from the HOX gene family, has long been studied due to its critical role in physiological activities in normal cells, such as organ development and body patterning, and pathological activities in cancer cells. Nonetheless, recent evidence supports the hypothesis of a role for HOXA5 in metabolic diseases, particularly in obesity and type 2 diabetes (T2D). In line with the current opinion that adipocyte and adipose tissue (AT) dysfunction belong to the group of primary defects in obesity, linking this condition to an increased risk of insulin resistance (IR) and T2D, the HOXA5 gene has been shown to regulate adipocyte function and AT remodeling both in humans and mice. Epigenetics adds complexity to HOXA5 gene regulation in metabolic diseases. Indeed, epigenetic mechanisms, specifically DNA methylation, influence the dynamic HOXA5 expression profile. In human AT, the DNA methylation profile at the HOXA5 gene is associated with hypertrophic obesity and an increased risk of developing T2D. Thus, an inappropriate HOXA5 gene expression may be a mechanism causing or maintaining an impaired AT function in obesity and potentially linking obesity to its associated disorders. In this review, we integrate the current evidence about the involvement of HOXA5 in regulating AT function, as well as its association with the pathogenesis of obesity and T2D. We also summarize the current knowledge on the role of DNA methylation in controlling HOXA5 expression. Moreover, considering the susceptibility of epigenetic changes to reversal through targeted interventions, we discuss the potential therapeutic value of targeting HOXA5 DNA methylation changes in the treatment of metabolic diseases. Full article
(This article belongs to the Special Issue The Adipose Tissue: From “Cinderella” to “Lion King” Organ)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop