Advances in Understanding Adipokines in Metabolic Perturbations

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (31 March 2020) | Viewed by 2981

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Guest Editor
Department of Translational Medical Sciences, University of Campania “L. Vanvitelli”, 80131 Naples, Italy
Interests: metabolic perturbation of respiratory diseases; lung cancer immune evasion (mechanisms and therapy); tumor microenvironment
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Special Issue Information

Dear Colleagues,

Cross-talk between adipose tissue and other organs has been attracting growing interest. Secretion of hormones by adipose tissue such as “adipokines” is involved in the homeostasis of many organs, including the lungs, influencing pathways of inflammatory processes, immunity, insulin resistance, lipid/glucose metabolisms, as well as cell proliferation.

Among adipokines, adiponectin is a protein hormone of 244 amino acids, abundantly produced and secreted by adipose tissue, which circulates in high concentrations (5–30 mg/mL), accounting for 0.01% of total serum proteins.

This Special Issue will focus on advances in understanding the relevance of adipokines as drivers of metabolic perturbations in cross-talk between organs.

Prof. Andrea Bianco
Guest Editor

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Keywords

  • Adipokines
  • Adiponectin
  • Metabolic perturbations
  • Inflammation
  • Cross talk between organs

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Published Papers (1 paper)

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Research

11 pages, 1422 KiB  
Article
Implications of the Adiponectin System in Non-Small Cell Lung Cancer Patients: A Case-Control Study
by Ersilia Nigro, Fabio Perrotta, Maria Ludovica Monaco, Rita Polito, Pia Clara Pafundi, Maria Gabriella Matera, Aurora Daniele and Andrea Bianco
Biomolecules 2020, 10(6), 926; https://doi.org/10.3390/biom10060926 - 18 Jun 2020
Cited by 17 | Viewed by 2630
Abstract
Alterations of adipose tissue occurring in obesity have been recognized as a major risk factor for several cancers. The relationship between adipose tissue and lung cancer, which is the main cancer-related cause of death worldwide, still requires investigation. Perturbations in the adipokine system [...] Read more.
Alterations of adipose tissue occurring in obesity have been recognized as a major risk factor for several cancers. The relationship between adipose tissue and lung cancer, which is the main cancer-related cause of death worldwide, still requires investigation. Perturbations in the adipokine system are likely to interfere with inter-organ crosstalk in lung cancer, which may influence the lung tumor microenvironment. Adiponectin (Acrp30) expression is deregulated in several cancer types. Acrp30 circulates as oligomers with a Low (LMW), Medium (MMW), and High Molecular Weight (HMW), with the latter mediating the main biological effects. Acrp30 acts through AdipoR1 and AdipoR2 receptors. T-cadherin has been described as a non-signaling receptor. This study’s aim was to investigate the regulation of serum Acrp30 and its receptors in sample tissue from non-small cell lung cancer (NSCLC) patients. We recruited 72 NSCLC patients and 60 healthy controls, whom we evaluated in terms of their Acpr30 levels and oligomeric profile. In addition, the expression of AdipoRs in tissues from lung cancer specimens was also measured and compared to coupled healthy lung samples. Our findings show a significant reduction of total Acrp30 levels in NSCLC patients compared to normal subjects, with a specific down-regulation of HMW oligomers. Acrp30 expression was lower in lung adenocarcinoma than other subtypes, regardless of other factors. A significantly higher expression of AdipoR1 was observed, while no differences in R2 and a lower expression of T-cadherin were found in lung cancer specimens compared to normal healthy lung tissues. Involvement of the Acrp30 system in lung cancer may provide new insight into the interaction between adipose tissue and lung and sheds light on its potential ability to influence the lung tumor microenvironment. Full article
(This article belongs to the Special Issue Advances in Understanding Adipokines in Metabolic Perturbations)
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