Next Article in Journal
Injury to Cone Synapses by Retinal Detachment: Differences from Rod Synapses and Protection by ROCK Inhibition
Previous Article in Journal
Astrocytic CD44 Deficiency Reduces the Severity of Kainate-Induced Epilepsy
Previous Article in Special Issue
Expression of Steroid Receptor RNA Activator 1 (SRA1) in the Adipose Tissue Is Associated with TLRs and IRFs in Diabesity
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Editorial

Adipose Tissue Inflammation

by
Javier Gómez-Ambrosi
1,2,3
1
Metabolic Research Laboratory, Clínica Universidad de Navarra, 31008 Pamplona, Spain
2
Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, 31008 Pamplona, Spain
3
Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra (IdiSNA), 31008 Pamplona, Spain
Cells 2023, 12(11), 1484; https://doi.org/10.3390/cells12111484
Submission received: 22 May 2023 / Accepted: 24 May 2023 / Published: 26 May 2023
(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)
In recent decades, obesity has become one of the most common metabolic diseases. Excess adiposity increases the risk of developing type 2 diabetes (T2D), cardiometabolic diseases, dyslipidemia, fatty liver, and several types of cancer [1]. Much progress has been made in understanding the major regulatory pathways underlying adipose tissue inflammation, which represent one the main drivers of adipose tissue dysfunction and, consequently, of obesity-associated metabolic alterations [2].
This Special Issue presents recent advances in understanding the molecular processes that take place in adipose tissue inflammation; moreover, it discusses the impact of adipose tissue inflammation on systemic metabolic alterations associated with excess adiposity, as well as its repercussion in several pathological conditions.
Although obesity has traditionally been considered a single medical entity, in recent years, greater importance has been placed on phenotyping the different obesities in order to improve their clinical management [3,4]. In their cross-sectional and prospective study, Goldstein et al. analyze the usefulness of determining mast cell accumulation in human adipose tissue as a proxy of metabolic phenotyping [5]. They suggest that patients with obesity with high expression of mast cell genes exhibit a healthier metabolic phenotype than individuals with low expression. The authors also find that higher mast cell accumulation in adipose tissue in patients undergoing bariatric surgery is a predictor of greater weight loss after surgery. They conclude that a high number of mast cells defines a clinically favorable obesity phenotype [5].
Several studies discuss the molecular mechanisms that regulate the impact of adipose tissue inflammation. Lempesis et al. show that low physiological oxygen tension decreases the expression and secretion of proinflammatory adipokines in adipocytes obtained from patients with obesity, an effect that is not found in cells derived from donors of normal weight [6]. Kochumon and colleagues report that the adipose tissue expression of steroid receptor RNA activator 1 (SRA1) may represent a novel surrogate marker of metabolic inflammation through its association with Toll-like receptors (TLRs) [7].
Other studies provide interesting information regarding the regulation of inflammation in adipose tissue in mouse models. In one such study, Sandrini et al. study the effects of physical exercise on BDNF Val66Met mice, a model of increased adiposity associated with a proinflammatory and prothrombotic profile [8]. They find that four weeks of voluntary wheel running changes epididymal adipose tissue morphology and the expression of proinflammatory genes, inducing reversion of the prothrombotic phenotype; this suggests that a reduction in adipose tissue inflammation is important in promoting the positive effects of physical activity [8]. In another study, Mendes de Farias and colleagues find that daily melatonin supplementation for 10 weeks in mice on a high-fat diet reduces fat accumulation, adipocyte size, and the expression of proinflammatory adipokines in adipose tissue and the circulation; this suggests that melatonin could be considered as a therapeutic molecule for the treatment of obesity [9].
Adipokines and adipose tissue inflammation have been shown to play a role in several physiologic and pathophysiologic conditions [10,11], as stated in several studies included in this Special Issue. Morais et al. show that an adequate balance between adiponectin and leptin concentrations in human milk may regulate colostrum mononuclear cell activity, eliciting a more effective response against neonatal infection in breastfeeding infants [12]. Another adipokine, fatty acid-binding protein 4 (FABP4), implicated in the control of cellular lipid metabolism, is also involved in inflammation and the development of insulin resistance. In an exhaustive review, Trojnar et al. detail the different mechanisms by which FABP4 is involved in inflammation and insulin resistance and the potential role of this adipokine in T2D, gestational diabetes, and fatty liver, among other conditions [13]. Chang and Eibl describe the relevance of adipose tissue inflammation as an important driver of obesity-associated pancreatic ductal adenocarcinoma, and consider strategies aimed at reducing inflammation in this tissue as a weapon against this type of cancer [14]. In another interesting review, Cornide-Petronio and colleagues reinforce current knowledge regarding the interaction between the liver and adipose tissue during liver surgery. The scientific and clinical controversies in this area are reviewed, as are potential therapeutic approaches. The information provided could help to develop protective measures focused on manipulating the liver–visceral adipose tissue axis to enhance the postoperative results of hepatic surgery [15]. Finally, Demeulemeester et al. summarize scientific research on the link between obesity and COVID-19 severity, and analyze probable mechanisms that could help to understand why patients living with obesity exhibit an increased risk of serious consequences during COVID-19 [16].
In recent years, there have been significant advancements in the understanding of the cellular and molecular mechanisms involved in adipose tissue inflammation. Thanks to this progress, more tools and approaches are available for the treatment of obesity and T2D. However, in order to optimize the management of patients with obesity, more research needs to be conducted.

Funding

This paper was supported by ISCIII–FEDER (PI20/00080) and CIBEROBN, ISCIII, Spain, and by PC098-099 MEPERTROBE and the Department of Health 58/2021, Gobierno de Navarra-FEDER, Spain.

Conflicts of Interest

The author declares no conflict of interest.

References

  1. Catalán, V.; Avilés-Olmos, I.; Rodríguez, A.; Becerril, S.; Fernández-Formoso, J.A.; Kiortsis, D.; Portincasa, P.; Gómez-Ambrosi, J.; Frühbeck, G. Time to consider the “Exposome Hypothesis” in the development of the obesity pandemic. Nutrients 2022, 14, 1597. [Google Scholar] [CrossRef] [PubMed]
  2. Frühbeck, G.; Balaguer, I.; Méndez-Giménez, L.; Valentí, V.; Becerril, S.; Catalán, V.; Gómez-Ambrosi, J.; Silva, C.; Salvador, J.; Calamita, G.; et al. Aquaporin-11 contributes to TGF-b1-induced endoplasmic reticulum stress in human visceral adipocytes: Role in obesity-associated inflammation. Cells 2020, 9, 1403. [Google Scholar] [CrossRef] [PubMed]
  3. Salmón-Gómez, L.; Catalán, V.; Frühbeck, G.; Gómez-Ambrosi, J. Relevance of body composition in phenotyping the obesities. Rev. Endocr. Metab. Disord. 2023, 1–15. [Google Scholar] [CrossRef] [PubMed]
  4. Perdomo, C.M.; Avilés-Olmos, I.; Dicker, D.; Frühbeck, G. Towards an adiposity-related disease framework for the diagnosis and management of obesities. Rev. Endocr. Metab. Disord. 2023, 1–13. [Google Scholar] [CrossRef] [PubMed]
  5. Goldstein, N.; Kezerle, Y.; Gepner, Y.; Haim, Y.; Pecht, T.; Gazit, R.; Polischuk, V.; Liberty, I.F.; Kirshtein, B.; Shaco-Levy, R.; et al. Higher mast cell accumulation in human adipose tissues defines clinically favorable obesity sub-phenotypes. Cells 2020, 9, 1508. [Google Scholar] [CrossRef] [PubMed]
  6. Lempesis, I.G.; Hoebers, N.; Essers, Y.; Jocken, J.W.E.; Rouschop, K.M.A.; Blaak, E.E.; Manolopoulos, K.N.; Goossens, G.H. Physiological oxygen levels differentially regulate adipokine production in abdominal and femoral adipocytes from individuals with obesity versus normal weight. Cells 2022, 11, 3532. [Google Scholar] [CrossRef] [PubMed]
  7. Kochumon, S.; Arefanian, H.; Sindhu, S.; Thomas, R.; Jacob, T.; Al-Sayyar, A.; Shenouda, S.; Al-Rashed, F.; Koistinen, H.A.; Al-Mulla, F.; et al. Expression of steroid receptor RNA activator 1 (SRA1) in the adipose tissue is associated with TLRs and IRFs in diabesity. Cells 2022, 11, 4007. [Google Scholar] [CrossRef] [PubMed]
  8. Sandrini, L.; Ieraci, A.; Amadio, P.; Zara, M.; Mitro, N.; Lee, F.S.; Tremoli, E.; Barbieri, S.S. Physical exercise affects adipose tissue profile and prevents arterial thrombosis in BDNF Val66Met mice. Cells 2019, 8, 875. [Google Scholar] [CrossRef] [PubMed]
  9. Farias, T.; Paixao, R.I.D.; Cruz, M.M.; de Sa, R.; Simao, J.J.; Antraco, V.J.; Alonso-Vale, M.I.C. Melatonin supplementation attenuates the pro-inflammatory adipokines expression in visceral fat from obese mice induced by a high-fat diet. Cells 2019, 8, 1041. [Google Scholar] [CrossRef] [PubMed]
  10. Frühbeck, G.; Catalán, V.; Rodríguez, A.; Gómez-Ambrosi, J. Adiponectin-leptin ratio: A promising index to estimate adipose tissue dysfunction. Relation with obesity-associated cardiometabolic risk. Adipocyte 2018, 7, 57–62. [Google Scholar] [CrossRef] [PubMed]
  11. Frühbeck, G.; Catalán, V.; Rodríguez, A.; Ramírez, B.; Becerril, S.; Salvador, J.; Colina, I.; Gómez-Ambrosi, J. Adiponectin-leptin ratio is a functional biomarker of adipose tissue inflammation. Nutrients 2019, 11, 454. [Google Scholar] [CrossRef] [PubMed]
  12. Morais, T.C.; de Abreu, L.C.; de Quental, O.B.; Pessoa, R.S.; Fujimori, M.; Daboin, B.E.G.; Franca, E.L.; Honorio-Franca, A.C. Obesity as an inflammatory agent can cause cellular changes in human milk due to the actions of the adipokines leptin and adiponectin. Cells 2019, 8, 519. [Google Scholar] [CrossRef] [PubMed]
  13. Trojnar, M.; Patro-Malysza, J.; Kimber-Trojnar, Z.; Leszczynska-Gorzelak, B.; Mosiewicz, J. Associations between fatty acid-binding protein 4. A proinflammatory adipokine and insulin resistance, gestational and type 2 diabetes mellitus. Cells 2019, 8, 227. [Google Scholar] [CrossRef] [PubMed]
  14. Chang, H.H.; Eibl, G. Obesity-induced adipose tissue inflammation as a strong promotional factor for pancreatic ductal adenocarcinoma. Cells 2019, 8, 673. [Google Scholar] [CrossRef] [PubMed]
  15. Cornide-Petronio, M.E.; Jiménez-Castro, M.B.; Gracia-Sancho, J.; Peralta, C. New insights into the liver-visceral adipose axis during hepatic resection and liver transplantation. Cells 2019, 8, 1100. [Google Scholar] [CrossRef] [PubMed]
  16. Demeulemeester, F.; de Punder, K.; van Heijningen, M.; van Doesburg, F. Obesity as a risk factor for severe COVID-19 and complications: A review. Cells 2021, 10, 933. [Google Scholar] [CrossRef] [PubMed]
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Gómez-Ambrosi, J. Adipose Tissue Inflammation. Cells 2023, 12, 1484. https://doi.org/10.3390/cells12111484

AMA Style

Gómez-Ambrosi J. Adipose Tissue Inflammation. Cells. 2023; 12(11):1484. https://doi.org/10.3390/cells12111484

Chicago/Turabian Style

Gómez-Ambrosi, Javier. 2023. "Adipose Tissue Inflammation" Cells 12, no. 11: 1484. https://doi.org/10.3390/cells12111484

APA Style

Gómez-Ambrosi, J. (2023). Adipose Tissue Inflammation. Cells, 12(11), 1484. https://doi.org/10.3390/cells12111484

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop