Adipose Tissue and Metabolic Health

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (21 December 2019) | Viewed by 33223

Special Issue Editor


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Guest Editor
Department of Cell Biology, Histology, and Embryology, Gottfried Schatz Research Center for Cell Signaling, Metabolism, and Aging, Medical University of Graz, Graz, Austria
Interests: metabolism; nutrient sensing; fasting; starvation; transcription factor networks
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Special Issue Information

Dear Colleagues,

The time when adipose tissue was regarded as mere passive fat storage and cushion is long gone. With an endocrine repertoire both responsive to systemic changes and communicating with many peripheral organs, as well as with satiety centers in the brain, adipose tissue is now recognized as the central hub of energy homeostasis. In vertebrates, adipose depots are dispersed over multiple anatomic locations, and can be classified as white or brown adipose tissue (WAT and BAT, respectively). While WAT depots mainly store lipid moieties to provide energy in times of nutrient scarcity, BAT is responsible for non-shivering thermogenesis in euthermic animals. Both WAT and BAT depots consist of fat storing parenchymal cells that share some molecular markers (e.g., PPARs) and are responsive to similar physiological cues (e.g., sympathetic signaling, metabolites, nutrients, and hormones). However, because of their distinct molecular functions, WAT and BAT differ in their cellular and molecular make up, degree of innervation and vascularization, and energy demand and output. Interestingly, certain adipose depots exhibit the capability for interconversion between a brown-like and a white cellular phenotype (browning or beiging). Understanding the tissue- and depot-specific molecular details could pave the way to novel therapeutics to curb metabolic diseases such as obesity and diabetes.

This Special Issue aims to feature insights in both WAT and BAT biology, as well as in the etiological mechanisms of adipose tissue-related metabolic syndrome. Explicitly, we welcome brief reports, communications, articles, reviews, mini reviews, and opinion pieces that include, but are not limited to, topics like adipose tissue crosstalk with other organs and the immune system, BAT activation, browning, WAT expandability, and endocrine function. In addition, we will consider articles addressing the association between obesity and cancer in the context of adipose tissue function.

Dr. Andreas Prokesch
Guest Editor

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Keywords

  • adipose tissue
  • metabolic syndrome
  • obesity
  • adipogenesis
  • metabolomics
  • Adipose tissue inflammation
  • adipokines
  • adipose crosstalk (with other organs)
  • adipose senescence
  • brown adipose tissue
  • browning/beiging
  • lipolysis
  • energy homeostasis
  • cancer
  • diabetes

Published Papers (7 papers)

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Research

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19 pages, 15696 KiB  
Article
TGF-ß1 Induces Changes in the Energy Metabolism of White Adipose Tissue-Derived Human Adult Mesenchymal Stem/Stromal Cells In Vitro
by Olga Hahn, Lena-Christin Ingwersen, Abdelrahman Soliman, Mohamed Hamed, Georg Fuellen, Markus Wolfien, Julia Scheel, Olaf Wolkenhauer, Dirk Koczan, Günter Kamp and Kirsten Peters
Metabolites 2020, 10(2), 59; https://doi.org/10.3390/metabo10020059 - 7 Feb 2020
Cited by 5 | Viewed by 3426
Abstract
Adipose tissue plays an active role in the regulation of the body’s energy balance. Mesenchymal stem/stromal cells from adipose tissue (adMSC) are the precursor cells for repair and adipogenesis. Since the balance of the differentiation state of adipose tissue-resident cells is associated with [...] Read more.
Adipose tissue plays an active role in the regulation of the body’s energy balance. Mesenchymal stem/stromal cells from adipose tissue (adMSC) are the precursor cells for repair and adipogenesis. Since the balance of the differentiation state of adipose tissue-resident cells is associated with the development of various diseases, the examination of the regulation of proliferation and differentiation of adMSC might provide new therapeutic targets. Transforming growth factor-β1 (TGF-ß1) is synthetized by many cell types and is involved in various biological processes. Here, we investigated the effects of different concentrations of TGF-ß1 (1–10 ng/mL) on adMSC proliferation, metabolic activity, and analyzed the gene expression data obtained from DNA microarrays by bioinformatics. TGF-ß1 induced the concentration- and time-dependent increase in the cell number of adMSC with simultaneously unchanged cell cycle distributions. The basal oxygen consumption rates did not change significantly after TGF-ß1 exposure. However, glycolytic activity was significantly increased. The gene expression analysis identified 3275 differentially expressed genes upon exposure to TGF-ß1. According to the pathway enrichment analyses, they also included genes associated with energy metabolism. Thus, it was shown that TGF-ß1 induces changes in the energy metabolism of adMSC. Whether these effects are of relevance in vivo and whether they contribute to pathogenesis should be addressed in further examinations. Full article
(This article belongs to the Special Issue Adipose Tissue and Metabolic Health)
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10 pages, 571 KiB  
Article
Serum Adipocyte Fatty Acid-Binding Protein Level is Negatively Associated with Vascular Reactivity Index Measured by Digital Thermal Monitoring in Kidney Transplant Patients
by Tai-Li Chen, Ming-Che Lee, Ching-Chung Ho, Bang-Gee Hsu and Jen-Pi Tsai
Metabolites 2019, 9(8), 159; https://doi.org/10.3390/metabo9080159 - 31 Jul 2019
Cited by 9 | Viewed by 2769
Abstract
Adipocyte fatty acid-binding protein (A-FABP) is abundantly found in mature adipocytes and is involved in cardiovascular disease. Our aim is to investigate the association between serum A-FABP levels and endothelial function among kidney transplant (KT) patients. Fasting blood samples were obtained from 80 [...] Read more.
Adipocyte fatty acid-binding protein (A-FABP) is abundantly found in mature adipocytes and is involved in cardiovascular disease. Our aim is to investigate the association between serum A-FABP levels and endothelial function among kidney transplant (KT) patients. Fasting blood samples were obtained from 80 KT patients. Serum A-FABP levels were measured using a commercially available enzyme immunoassay kit. Endothelial function and vascular reactivity index (VRI) were measured using digital thermal monitoring test. In this study, VRI < 1.0, VRI 1.0–1.9, and VRI ≥ 2.0 were defined as poor, intermediate, and good vascular reactivity, respectively. There were 12 (15.0%), 30 (37.5%), and 38 (47.5%) KT patients categorized as having poor, intermediate, and good vascular reactivity, respectively. Increased serum levels of alkaline phosphatase (p = 0.012), γ-glutamyltranspeptidase (GGT; p = 0.032), and A-FABP (p < 0.001) were associated with decreased vascular reactivity. Multivariable forward stepwise linear regression analysis revealed that age (β = −0.283, adjusted R2 change = 0.072; p = 0.003) and serum log-A-FABP level (β = −0.514, adjusted R2 change = 0.268; p < 0.001) were significantly associated with VRI values in KT patients. We concluded that serum fasting A-FABP level is negatively associated with VRI values and plays a role in endothelial dysfunction of KT patients. Full article
(This article belongs to the Special Issue Adipose Tissue and Metabolic Health)
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Review

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29 pages, 1056 KiB  
Review
The Role of Autophagy in White Adipose Tissue Function: Implications for Metabolic Health
by Mercedes Clemente-Postigo, Alberto Tinahones, Rajaa El Bekay, María M. Malagón and Francisco J. Tinahones
Metabolites 2020, 10(5), 179; https://doi.org/10.3390/metabo10050179 - 30 Apr 2020
Cited by 48 | Viewed by 4399
Abstract
White adipose tissue (WAT) is a highly adaptive endocrine organ that continuously remodels in response to nutritional cues. WAT expands to store excess energy by increasing adipocyte number and/or size. Failure in WAT expansion has serious consequences on metabolic health resulting in altered [...] Read more.
White adipose tissue (WAT) is a highly adaptive endocrine organ that continuously remodels in response to nutritional cues. WAT expands to store excess energy by increasing adipocyte number and/or size. Failure in WAT expansion has serious consequences on metabolic health resulting in altered lipid, glucose, and inflammatory profiles. Besides an impaired adipogenesis, fibrosis and low-grade inflammation also characterize dysfunctional WAT. Nevertheless, the precise mechanisms leading to impaired WAT expansibility are yet unresolved. Autophagy is a conserved and essential process for cellular homeostasis, which constitutively allows the recycling of damaged or long-lived proteins and organelles, but is also highly induced under stress conditions to provide nutrients and remove pathogens. By modulating protein and organelle content, autophagy is also essential for cell remodeling, maintenance, and survival. In this line, autophagy has been involved in many processes affected during WAT maladaptation, including adipogenesis, adipocyte, and macrophage function, inflammatory response, and fibrosis. WAT autophagy dysregulation is related to obesity and diabetes. However, it remains unclear whether WAT autophagy alteration in obese and diabetic patients are the cause or the consequence of WAT malfunction. In this review, current data regarding these issues are discussed, focusing on evidence from human studies. Full article
(This article belongs to the Special Issue Adipose Tissue and Metabolic Health)
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14 pages, 2630 KiB  
Review
Challenging a “Cushy” Life: Potential Roles of Thermogenesis and Adipose Tissue Adaptations in Delayed Aging of Ames and Snell Dwarf Mice
by Teresa G. Valencak, Tanja Spenlingwimmer, Ricarda Nimphy, Isabel Reinisch, Jessica M. Hoffman and Andreas Prokesch
Metabolites 2020, 10(5), 176; https://doi.org/10.3390/metabo10050176 - 29 Apr 2020
Cited by 4 | Viewed by 3570
Abstract
Laboratory mouse models with genetically altered growth hormone (GH) signaling and subsequent endocrine disruptions, have longer lifespans than control littermates. As such, these mice are commonly examined to determine the role of the somatotropic axis as it relates to healthspan and longevity in [...] Read more.
Laboratory mouse models with genetically altered growth hormone (GH) signaling and subsequent endocrine disruptions, have longer lifespans than control littermates. As such, these mice are commonly examined to determine the role of the somatotropic axis as it relates to healthspan and longevity in mammals. The two most prominent mouse mutants in this context are the genetically dwarf Ames and Snell models which have been studied extensively for over two decades. However, it has only been proposed recently that both white and brown adipose tissue depots may contribute to their delayed aging. Here we review the current state of the field and supplement it with recent data from our labs. Full article
(This article belongs to the Special Issue Adipose Tissue and Metabolic Health)
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27 pages, 1656 KiB  
Review
The Lipolysome—A Highly Complex and Dynamic Protein Network Orchestrating Cytoplasmic Triacylglycerol Degradation
by Peter Hofer, Ulrike Taschler, Renate Schreiber, Petra Kotzbeck and Gabriele Schoiswohl
Metabolites 2020, 10(4), 147; https://doi.org/10.3390/metabo10040147 - 10 Apr 2020
Cited by 15 | Viewed by 6961
Abstract
The catabolism of intracellular triacylglycerols (TAGs) involves the activity of cytoplasmic and lysosomal enzymes. Cytoplasmic TAG hydrolysis, commonly termed lipolysis, is catalyzed by the sequential action of three major hydrolases, namely adipose triglyceride lipase, hormone-sensitive lipase, and monoacylglycerol lipase. All three enzymes interact [...] Read more.
The catabolism of intracellular triacylglycerols (TAGs) involves the activity of cytoplasmic and lysosomal enzymes. Cytoplasmic TAG hydrolysis, commonly termed lipolysis, is catalyzed by the sequential action of three major hydrolases, namely adipose triglyceride lipase, hormone-sensitive lipase, and monoacylglycerol lipase. All three enzymes interact with numerous protein binding partners that modulate their activity, cellular localization, or stability. Deficiencies of these auxiliary proteins can lead to derangements in neutral lipid metabolism and energy homeostasis. In this review, we summarize the composition and the dynamics of the complex lipolytic machinery we like to call “lipolysome”. Full article
(This article belongs to the Special Issue Adipose Tissue and Metabolic Health)
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19 pages, 273 KiB  
Review
The Interrelations between Biological and Targeted Synthetic Agents Used in Inflammatory Joint Diseases, and Obesity or Body Composition
by Eric Toussirot
Metabolites 2020, 10(3), 107; https://doi.org/10.3390/metabo10030107 - 13 Mar 2020
Cited by 14 | Viewed by 3237
Abstract
Obesity is a comorbidity that plays a role in the development and severity of inflammatory joint diseases, including rheumatoid arthritis, psoriatic arthritis and axial spondyloarthritis. The relationships between obesity and adipose tissue and the treatments given for inflammatory joint diseases are bidirectional. In [...] Read more.
Obesity is a comorbidity that plays a role in the development and severity of inflammatory joint diseases, including rheumatoid arthritis, psoriatic arthritis and axial spondyloarthritis. The relationships between obesity and adipose tissue and the treatments given for inflammatory joint diseases are bidirectional. In fact, biological agents (bDMARDs) and targeted synthetic agents (tsDMARDs) may influence body weight and body composition of treated patients, while obesity in turn may influence clinical response to these agents. Obesity is a prevalent comorbidity mainly affecting patients with rheumatoid arthritis (RA) and psoriatic arthritis (PsA) with specific phenotypes. Tumour necrosis factor alpha (TNFα) inhibitors have been associated with changes in body composition by improving lean mass, but also by significantly increasing fat mass, which localized toward the abdominal/visceral region. The IL-6 inhibitor tocilizumab is associated with an increase in lean mass without change in fat mass. The clinical response to TNFα inhibitors is attenuated by obesity, an effect that is less pronounced with IL-6 inhibitors and the B-cell depletion agent rituximab. Conversely, body weight has no influence on the response to the costimulation inhibitor abatacept. These effects may be of help to the physician in personalized medicine, and may guide the therapeutic choice in obese/overweight patients. Full article
(This article belongs to the Special Issue Adipose Tissue and Metabolic Health)
29 pages, 1335 KiB  
Review
Metabolically Healthy Obesity—Heterogeneity in Definitions and Unconventional Factors
by Inês Brandão, Maria João Martins and Rosário Monteiro
Metabolites 2020, 10(2), 48; https://doi.org/10.3390/metabo10020048 - 27 Jan 2020
Cited by 60 | Viewed by 8004
Abstract
The concept of heterogeneity among obese individuals in their risk for developing metabolic dysfunction and associated complications has been recognized for decades. At the origin of the heterogeneity idea is the acknowledgement that individuals with central obesity are more prone to developing type [...] Read more.
The concept of heterogeneity among obese individuals in their risk for developing metabolic dysfunction and associated complications has been recognized for decades. At the origin of the heterogeneity idea is the acknowledgement that individuals with central obesity are more prone to developing type 2 diabetes and cardiovascular disease than those with peripheral obesity. There have been attempts to categorize subjects according to their metabolic health and degree of obesity giving rise to different obese and non-obese phenotypes that include metabolically unhealthy normal-weight (MUHNW), metabolically healthy obese (MHO), and metabolically unhealthy obese (MUO). Individuals belonging to the MHO phenotype are obese according to their body mass index although exhibiting fewer or none metabolic anomalies such as type 2 diabetes, dyslipidemia, hypertension, and/or unfavorable inflammatory and fribinolytic profiles. However, some authors claim that MHO is only transient in nature. Additionally, the phenotype categorization is controversial as it lacks standardized definitions possibly blurring the distinction between obesity phenotypes and confounding the associations with health outcomes. To add to the discussion, the factors underlying the origin or protection from metabolic deterioration and cardiometabolic risk for these subclasses are being intensely investigated and several hypotheses have been put forward. In the present review, we compare the different definitions of obesity phenotypes and present several possible factors underlying them (adipose tissue distribution and cellularity, contaminant accumulation on the adipose tissue, dysbiosis and metabolic endotoxemia imposing on to the endocannabinoid tone and inflammasome, and nutrient intake and dietary patterns) having inflammatory activation at the center. Full article
(This article belongs to the Special Issue Adipose Tissue and Metabolic Health)
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