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Special Issue "Role of Dysfunctional Adipose Tissue in the Pathogenesis of Multiple Organ Injuries"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 30 September 2022 | Viewed by 1087

Special Issue Editor

Prof. Sebastio Perrini
E-Mail Website
Guest Editor
Department of Emergency and Organ Transplantation, Section of Internal Medicine, Endocrinology, Andrology and Metabolic Diseases, University of Bari Aldo Moro, I-70124 Bari, Italy
Interests: insulin resistance; glucose transport, adipose stem cells, adipose tissue, adipogenesis, obesity and metabolic diseases

Special Issue Information

Dear Colleagues,

This Special Issue of the International Journal of Molecular Sciences (IJMS) aims to address all aspects of the most recent research on molecular mechanisms linking dysfunctional adipose tissue to an array of health problems, including insulin resistance, type 2 diabetes, dyslipidemia, fatty liver disease, neurodegenerative disorders, and cardiovascular diseases. Understanding the mechanisms linking dysfunction adipose tissue to unhealthy obesity could potentially lead to identifying novel therapeutic targets better able to manage the adverse cardiometabolic outcomes of obesity.

The scope of this Special Issue includes, but is not limited to, the following:

  • Dysfunctional adipose tissue and beta-cell wellness: an ineffective combination.
  • Impact of dysfunctional adipose tissue depots on the cardiovascular system.
  • Role of adipose tissue dysfunction in the onset of obesity-related hypogonadism.
  • Adipose tissue inflammation and pulmonary dysfunction in obesity.
  • Mechanisms linking excess of adipose tissue to increased risk of neurodegenerative diseases.
  • Dysfunctional adipose as risk factors for the development of dermatological diseases.

Prof. Sebastio Perrini
Guest Editor

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Dysfunctional adipose tissue
  • unhealthy obesity
  • beta-cell dysfunction
  • cardiovascular diseases
  • hypogonadism
  • pulmonary dysfunction
  • neurodegenerative diseases
  • dermatological diseases

Published Papers (2 papers)

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Review

Review
Adipose Tissue Secretion Pattern Influences β-Cell Wellness in the Transition from Obesity to Type 2 Diabetes
Int. J. Mol. Sci. 2022, 23(10), 5522; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105522 - 15 May 2022
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Abstract
The dysregulation of the β-cell functional mass, which is a reduction in the number of β-cells and their ability to secure adequate insulin secretion, represents a key mechanistic factor leading to the onset of type 2 diabetes (T2D). Obesity is recognised as a [...] Read more.
The dysregulation of the β-cell functional mass, which is a reduction in the number of β-cells and their ability to secure adequate insulin secretion, represents a key mechanistic factor leading to the onset of type 2 diabetes (T2D). Obesity is recognised as a leading cause of β-cell loss and dysfunction and a risk factor for T2D. The natural history of β-cell failure in obesity-induced T2D can be divided into three steps: (1) β-cell compensatory hyperplasia and insulin hypersecretion, (2) insulin secretory dysfunction, and (3) loss of β-cell mass. Adipose tissue (AT) secretes many hormones/cytokines (adipokines) and fatty acids that can directly influence β-cell function and viability. As this secretory pattern is altered in obese and diabetic patients, it is expected that the cross-talk between AT and pancreatic β-cells could drive the maintenance of the β-cell integrity under physiological conditions and contribute to the reduction in the β-cell functional mass in a dysmetabolic state. In the current review, we summarise the evidence of the ability of the AT secretome to influence each step of β-cell failure, and attempt to draw a timeline of the alterations in the adipokine secretion pattern in the transition from obesity to T2D that reflects the progressive deterioration of the β-cell functional mass. Full article
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Review
Adipose Tissue Plasticity in Response to Pathophysiological Cues: A Connecting Link between Obesity and Its Associated Comorbidities
Int. J. Mol. Sci. 2022, 23(10), 5511; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105511 - 14 May 2022
Viewed by 345
Abstract
Adipose tissue (AT) is a remarkably plastic and active organ with functional pleiotropism and high remodeling capacity. Although the expansion of fat mass, by definition, represents the hallmark of obesity, the dysregulation of the adipose organ emerges as the forefront of the link [...] Read more.
Adipose tissue (AT) is a remarkably plastic and active organ with functional pleiotropism and high remodeling capacity. Although the expansion of fat mass, by definition, represents the hallmark of obesity, the dysregulation of the adipose organ emerges as the forefront of the link between adiposity and its associated metabolic and cardiovascular complications. The dysfunctional fat displays distinct biological signatures, which include enlarged fat cells, low-grade inflammation, impaired redox homeostasis, and cellular senescence. While these events are orchestrated in a cell-type, context-dependent and temporal manner, the failure of the adipose precursor cells to form new adipocytes appears to be the main instigator of the adipose dysregulation, which, ultimately, poses a deleterious milieu either by promoting ectopic lipid overspill in non-adipose targets (i.e., lipotoxicity) or by inducing an altered secretion of different adipose-derived hormones (i.e., adipokines and lipokines). This “adipocentric view” extends the previous “expandability hypothesis”, which implies a reduced plasticity of the adipose organ at the nexus between unhealthy fat expansion and the development of obesity-associated comorbidities. In this review, we will briefly summarize the potential mechanisms by which adaptive changes to variations of energy balance may impair adipose plasticity and promote fat organ dysfunction. We will also highlight the conundrum with the perturbation of the adipose microenvironment and the development of cardio-metabolic complications by focusing on adipose lipoxidation, inflammation and cellular senescence as a novel triad orchestrating the conspiracy to adipose dysfunction. Finally, we discuss the scientific rationale for proposing adipose organ plasticity as a target to curb/prevent adiposity-linked cardio-metabolic complications. Full article
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