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Cells
Special Issues
Adipose Tissue Functioning in Health and Diseases
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Adipose Tissue Functioning in Health and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 9132

Editor

Dr. Richard C Chang

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Guest Editor
Department of Developmental and Cell Biology, University of California, Irvine, CA 92697-2300, USA
Interests: obesogenic effects on metabolic health and transgenerational impacts; cellular and molecular mechanisms of adipogenesis; epigenetic regulation in metabolic diseases; role of microRNAs in inflammation and obesity; metabolic adaptation and programming in response to environmental exposures; endocrine and immune system interactions in metabolic regulation; high-fat diet-induced metabolic dysfunctions; chromatin dynamics in transgenerational epigenetic inheritance; preconception environmental exposures and their effects on offspring metabolism

Special Issue Information

Dear Colleagues,

Adipose tissue plays a critical role in maintaining metabolic homeostasis and energy balance. Beyond serving as a storage depot for lipids, it functions as an endocrine organ that regulates various physiological processes through the secretion of adipokines and cytokines. However, dysregulation in adipose tissue function is implicated in the pathogenesis of obesity, diabetes, cardiovascular diseases, and other metabolic disorders. This Special Issue, Adipose Tissue Functioning in Health and Diseases, highlights innovative research exploring the cellular and molecular mechanisms governing adipose tissue function, its interactions with other tissues, and its role in disease development. We invite contributions that examine adipose tissue remodeling, thermogenic regulation, metabolic crosstalk, and therapeutic approaches targeting adipose tissue. By assembling diverse perspectives and novel findings, this issue seeks to provide a comprehensive understanding of adipose tissue’s role in health and disease.

Dr. Richard C Chang
Guest Editor

Manuscript Submission Information

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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 biology
  • adipogenesis
  • lipolysis
  • adipose tissue inflammation
  • diet-induced obesity
  • non-coding RNA in metabolism
  • PPARγ signaling
  • metabolic health and disease
  • obesogens
  • epigenetics and chromatin regulation
  • transgenerational inheritance

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Published Papers (6 papers)

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Research

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21 pages, 9121 KB  
Article
Lim Homeobox 8 Is Essential for Beta Adrenergic Stimulation of Thermogenesis in Human Adipocytes
by Katalin Gyurina, Ádám Radványi, László Sasi-Szabó, Enikő Felszeghy, Emese Rácz, Gábor Méhes, Andrea Kádár, Csaba Fekete and Tamás Röszer
Cells 2026, 15(11), 1000; https://doi.org/10.3390/cells15111000 - 29 May 2026
Viewed by 306
Abstract
Catecholamines are crucial signaling molecules that initiate thermogenesis in adipocytes through beta-adrenergic receptors (ADRBs). Adipocyte catecholamine resistance is a common feature of pediatric obesity, often impeding weight loss and the maintenance of a healthy body fat percentage. Our aim was to identify possible [...] Read more.
Catecholamines are crucial signaling molecules that initiate thermogenesis in adipocytes through beta-adrenergic receptors (ADRBs). Adipocyte catecholamine resistance is a common feature of pediatric obesity, often impeding weight loss and the maintenance of a healthy body fat percentage. Our aim was to identify possible mechanisms that may be responsible for the development of catecholamine resistance in adipocytes. We demonstrate that Lim homeobox 8 (LHX8), a transcription factor previously known for its role in gametogenesis, is essential for catecholamine-induced thermogenesis in human adipocytes. LHX8 is expressed in developing human adipocytes throughout intrauterine and perinatal life, as well as in adulthood, and its expression levels positively correlate with the expression of key thermogenesis genes. Pediatric obesity diminished adipocyte expression of LHX8. Functionally, ADRB stimulation failed to induce thermogenesis in both mouse and human adipocytes when LHX8 was absent. Conversely, LHX8 overexpression enhanced thermogenesis in murine adipocytes. Mechanistically, LHX8 stimulated adipocyte interleukin-33 (IL-33) synthesis in response to ADRB activation, which subsequently increased thermogenic gene expression in both human and mouse adipocytes. In conclusion, adipocyte LHX8 is indispensable for catecholamine-responsive thermogenesis and represents a promising novel therapeutic target to overcome catecholamine resistance and promote effective weight management. Full article
(This article belongs to the Special Issue Adipose Tissue Functioning in Health and Diseases)
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20 pages, 3525 KB  
Article
Connexin-43-Mediated Gap Junction Coupling Between Adipocytes Regulates Norepinephrine-Induced Ca2+ Responses in Perivascular Adipose Tissue
by Ae Ra Kim, Julia Jamka, William F. Jackson, Emma D. Flood, Jonathon L. McClain and Brian D. Gulbransen
Cells 2026, 15(10), 906; https://doi.org/10.3390/cells15100906 - 15 May 2026
Viewed by 437
Abstract
Anticontractile factors secreted by perivascular adipose tissue (PVAT) play an important role in regulating vascular tone. This process is driven by the neurotransmitter norepinephrine (NE), but recent data show that adrenergic innervation in PVAT is sparse. How limited innervation might initiate broad responses [...] Read more.
Anticontractile factors secreted by perivascular adipose tissue (PVAT) play an important role in regulating vascular tone. This process is driven by the neurotransmitter norepinephrine (NE), but recent data show that adrenergic innervation in PVAT is sparse. How limited innervation might initiate broad responses through PVAT depots remains unknown. Here, we used Ca2+ imaging with genetically encoded sensors, selective drugs, immunolabeling and a conditional ablation model to test the hypothesis that gap junction coupling among PVAT adipocytes contributes to how signals initiated by NE are distributed through PVAT depots. Despite exhibiting differing sensitivities to NE, adipocytes in aortic and mesenteric PVAT and in white adipose tissue displayed robust expression of the gap junction protein connexin-43 (Cx43). Blocking gap junction coupling with the drug carbenoxolone (Cbx) limited NE-evoked Ca2+ responses among adipocytes, while blocking Cx43 hemichannels with the mimetic peptide 43Gap26 had no significant effect. Fluorescence recovery after photobleaching (FRAP) in mPVAT was decreased in the presence of Cbx, suggesting impaired gap junction communication. Wire myography recordings of mesenteric arteries showed that the EC50 for NE was higher in samples with intact PVAT than those without; however, this effect was not significantly different in samples from mice that lacked Cx43 in adipocytes. Analysis of multiple connexins showed that adipocytes upregulate Cx26 gene expression when Cx43 is deleted. These observations support the conclusion that Cx43-mediated gap junction coupling among PVAT adipocytes contributes to distributing signals initiated by NE; however, how this mechanism contributes to regulating vessel constriction remains unclear. This, and how potential compensatory mechanisms are enacted in adipocytes lacking Cx43, should be addressed in future work. Full article
(This article belongs to the Special Issue Adipose Tissue Functioning in Health and Diseases)
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15 pages, 3259 KB  
Article
Modulation of miRNA Signature in Human Adipose Tissue After 3 Months of ω-3PUFA Supplementation
by James Hernandez, Matthew Lee, Mary Cochran, Ting Li, Panwen Wang, Dawn K. Coletta, Cassandra Rau, Valentin Dinu and Eleanna De Filippis
Cells 2026, 15(7), 577; https://doi.org/10.3390/cells15070577 - 25 Mar 2026
Viewed by 734
Abstract
Obesity is a persistent public health issue, often resulting in metabolic complications such as insulin resistance (IR). The secretion of pro-inflammatory cytokines from adipose tissue (AT) is increased during obesity, contributing to the impairment of systemic insulin sensitivity. While interventions in animal models [...] Read more.
Obesity is a persistent public health issue, often resulting in metabolic complications such as insulin resistance (IR). The secretion of pro-inflammatory cytokines from adipose tissue (AT) is increased during obesity, contributing to the impairment of systemic insulin sensitivity. While interventions in animal models have shown that reducing inflammation restores insulin sensitivity, human studies reducing systemic inflammation have produced inconsistent results. We recently demonstrated that three months of high-dose (4 g/daily) ω-3PUFA (fish oil, FO) supplementation improved insulin sensitivity, and decreased systemic and AT inflammation in individuals with obesity (BMI  ≥  30 kg/m2). Given recent studies highlighting the involvement of microRNA (miRNA) in inflammatory cytokine production, we investigated the effect of ω-3PUFA supplementation on AT miRNA expression in this cohort. AT biopsies were collected before and after ω-3PUFA supplementation. miRNA was processed on the Affymetrix miRNA 4.0 GeneChip and analyzed using existing inflammatory gene sets sourced from MSigDB. Unbiased, differentially expressed miRNA analysis identified miR-4498 and miR-5689 as significantly increased after three months of ω-3PUFA supplementation. Real-time PCR confirmed bioinformatic analysis findings. Our study reports the modulation of miRNA in AT, reductions in systemic and AT markers of inflammation, and the improvement of IR post ω-3PUFA supplementation. Further research is needed to elucidate the link between miR-4498, miR-5689, and whole-body insulin sensitivity. Full article
(This article belongs to the Special Issue Adipose Tissue Functioning in Health and Diseases)
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29 pages, 9850 KB  
Article
Novel Hyperplastic Expansion of White Adipose Tissue Underlies the Metabolically Healthy Obese Phenotype of Male LFABP Null Mice
by Anastasia Diolintzi, Yinxiu Zhou, Angelina Fomina, Yifei Sun, Seema Husain, Labros S. Sidossis, Susan K. Fried and Judith Storch
Cells 2025, 14(11), 760; https://doi.org/10.3390/cells14110760 - 22 May 2025
Viewed by 3051
Abstract
Obesity is an important risk factor for the development of metabolic syndrome disorders. We previously showed that the liver fatty acid-binding protein null mouse (LFABP−/−) becomes obese upon high-fat diet (HFD) feeding but remains metabolically healthy. Here, we find that [...] Read more.
Obesity is an important risk factor for the development of metabolic syndrome disorders. We previously showed that the liver fatty acid-binding protein null mouse (LFABP−/−) becomes obese upon high-fat diet (HFD) feeding but remains metabolically healthy. Here, we find that the obese LFABP−/− mouse increases subcutaneous adipose tissue (SAT) mass by markedly increasing the number rather than the size of adipocytes, as is typical with HFD. Indeed, while HFD-fed LFABP−/− mice had almost double the fat mass of WT, SAT adipocyte size was >4-fold smaller and adipocyte number was 5-fold higher in the LFABP−/−. Transcriptomic analysis of SAT revealed that Lfabp deletion alters the expression of multiple pathways that modulate adipose expansion and function including cholesterol biosynthesis, adipogenesis, and extracellular matrix remodeling. LFABP is expressed in the liver and small intestine but not in adipose tissues; thus, its ablation may promote interorgan crosstalk that drives the hyperplastic expansion of metabolically beneficial SAT, contributing to the healthy obese phenotype of the LFABP−/− mouse. Full article
(This article belongs to the Special Issue Adipose Tissue Functioning in Health and Diseases)
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Review

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16 pages, 1290 KB  
Review
Platelet-Activating Factor-Induced Inflammation in Obesity: A Two-Sided Coin of Protection and Risk
by Smaragdi Antonopoulou
Cells 2025, 14(7), 471; https://doi.org/10.3390/cells14070471 - 21 Mar 2025
Cited by 2 | Viewed by 2259
Abstract
Obesity, marked by excessive fat accumulation, especially abdominal, is a global health concern with significant public impact. While obesity-associated chronic unresolved inflammation contributes to metabolic dysfunctions, acute inflammation supports healthy adipose tissue remodeling and expansion. Platelet-activating factor (PAF), a “primitive” signaling molecule, is [...] Read more.
Obesity, marked by excessive fat accumulation, especially abdominal, is a global health concern with significant public impact. While obesity-associated chronic unresolved inflammation contributes to metabolic dysfunctions, acute inflammation supports healthy adipose tissue remodeling and expansion. Platelet-activating factor (PAF), a “primitive” signaling molecule, is among the key mediators involved in the acute phase of inflammation and in various pathophysiological processes. This article explores the role of PAF in fat accumulation and obesity by reviewing experimental data from cell cultures, animals, and humans. It proposes an emerging biochemical mechanism in an attempt to explain its dual role in the healthy and obese adipose tissue, including also data on PAF’s potential involvement in epigenetic mechanisms that may be linked to the “obesity memory”. Finally, it highlights the potential of natural PAF modulators in promoting functional adipose tissue, thermogenesis, and obesity prevention through a healthy lifestyle, including a Mediterranean diet rich in PAF weak agonists/PAF receptor antagonists and regular exercise, which help maintain controlled PAF levels. Conversely, in cases of obesity-related systemic inflammation with excessive PAF levels, potent PAF inhibitors like ginkgolide B and rupatadine may help mitigate metabolic dysfunctions with PAFR antagonists potentially enhancing their effects synergistically. Full article
(This article belongs to the Special Issue Adipose Tissue Functioning in Health and Diseases)
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Other

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15 pages, 1446 KB  
Systematic Review
Histological and Immunohistochemical Characteristics of Mechanically Processed Adipose Tissue: A Systematic Review and Meta-Analysis
by Tom Schimanski, Rafael Loucas, Marios Loucas, Vanessa Brébant, Alexandra Anker, Silvan Klein, Sophia Theresa Diesch, Andrea Pagani and Lukas Prantl
Cells 2025, 14(21), 1664; https://doi.org/10.3390/cells14211664 - 23 Oct 2025
Cited by 1 | Viewed by 1508
Abstract
Background: Mechanical processing techniques are commonly employed to prepare adipose tissue for clinical applications in reconstructive and aesthetic procedures. However, their histological and immunohistochemical impact on adipose tissue remains incompletely characterized. Purpose: This systematic review aims to investigate the impact of mechanical processing [...] Read more.
Background: Mechanical processing techniques are commonly employed to prepare adipose tissue for clinical applications in reconstructive and aesthetic procedures. However, their histological and immunohistochemical impact on adipose tissue remains incompletely characterized. Purpose: This systematic review aims to investigate the impact of mechanical processing on the histological and immunohistochemical properties of adipose tissue. Methods: A systematic search was conducted using PubMed, Ovid, and Cochrane Library databases, with publications up to December 2024, employing Boolean operators (“mechanically processed” OR “lipoaspirate” OR “fat graft” OR “gauze rolling” OR “decantation” OR “coleman fat” OR “celt” OR “nanofat” OR “lipofilling” OR “human fat”) AND (“histol*”). Included were English-language studies or studies with a recognized English translation which had been subject to peer review and reported quantitative or qualitative markers of mechanically processed human adipose tissue with histology or immunohistochemistry. Risk of Bias was assessed with the OHAT score. Results: A total of 15 studies (n = 15) were included. In 13 of 15 studies (87%), mechanically processed adipose tissue demonstrated an increased stromal vascular fraction (SVF) cell density compared to unprocessed fat. Twelve studies (80%) reported improved preservation of the extracellular matrix (ECM), while 11 studies (73%) observed a reduction in mature adipocytes. Immunohistochemical analyses in 10 studies (67%) revealed elevated expression of vascular markers (CD31, CD34) and perilipin. Adverse histological features such as oil cysts, fibrosis, and inflammatory infiltrates were reduced in 9 studies (60%). Considerable heterogeneity in processing techniques and staining protocols precluded meta-analysis. Conclusions: Mechanical processing of adipose tissue is associated with favorable histological and immunohistochemical profiles, including increased SVF cell density, improved ECM preservation, and reduced inflammatory and fibrotic features. These findings support the potential of mechanical processing to enhance graft quality; however, standardization of techniques and evaluation protocols is needed to strengthen clinical translation. Full article
(This article belongs to the Special Issue Adipose Tissue Functioning in Health and Diseases)
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