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Obesity and Insulin Resistance: The Dark Sides of Adipose Organ Dysfunction in the Cardiometabolic Continuum

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 August 2024) | Viewed by 4700

Special Issue Editors

Dr. Giuseppe Murdolo

E-Mail Website
Guest Editor
Department of Internal Medicine, Endocrinology and Metabolism, Perugia University Hospital Santa Maria Misericordia, Ospedale di Perugia, 06081 Perugia, Italy
Interests: obesity; insulin resistance; adipose tissue; diabetes mellitus
Dr. Desirée Bartolini

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, University of Perugia, 06123 Perugia, Italy
Interests: adipose tissue; insulin resistance; type 2 diabetes; obesity; oxidative stress; lipidomics; vitamin E; stem cells; adipose precursor cells

Special Issue Information

Dear Colleagues,

Obesity represents a major contributor of the metabolic syndrome, a cluster of cardiovascular risk factors centered on abdominal adiposity and insulin resistance. Although the expansion of the adipose organ is, by definition, the hallmark of obesity, fat mass accrual per se is not sufficient for the development of a “cardiometabolically unhealthy” phenotype. A novel paradigm in adipose biology points to restricted adipogenesis in the abdominal subcutaneous fat as a missing link between “unhealthy” fat mass expansion and impairment of glucose and cardiovascular homeostasis. In this scenario, adipose oxidative stress, lypoxidation, inflammation, and cell senescence emerge as the alleged instigators of unhealthy fat. Nonetheless, the occurrence of cellular dysfunction in different under-explored fat microdepots (i.e., perivascular and epicardial fat) as well as the impairment of brown adipose tissue function, further circumstantiate the importance of adipose cell subpopulations in the continuum of the cardiometabolic risk.

This Special Issue of IJMS is calling for both original articles and reviews providing a comprehensive picture and elucidation of the complex relationships between adipose organ dysregulation, insulin resistance, and cardiovascular homeostasis. Suitable topics include but are not limited to impairment of adipose precursor cell differentiation and trans-differentiation, role of fat microdepots and brown adipose tissue, as well as the importance of oxidative stress and different adipose-derived mediators (i.e., fatty acids derivatives, lipokines, adipokines, batokines, etc.) in the impairment of cardiometabolic homeostasis. Finally, the potential effect of current and future therapeutic strategies tailored to curb adipose dysfunction and obesity-associated insulin resistance will be highlighted.

Dr. Giuseppe Murdolo
Dr. Desirée Bartolini
Guest Editors

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

  • obesity
  • insulin resistance
  • type 2 diabetes
  • atherosclerosis
  • adipose precursor cell
  • endothelial dysfunction
  • brown adipose tissue
  • fatty liver
  • lipokines
  • oxidative stress
  • senescence

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Published Papers (2 papers)

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Research

15 pages, 3013 KiB  
Article
Accumulation of 4-Hydroxynonenal Characterizes Diabetic Fat and Modulates Adipogenic Differentiation of Adipose Precursor Cells
by Giuseppe Murdolo, Desirée Bartolini, Cristina Tortoioli, Cristiana Vermigli, Marta Piroddi and Francesco Galli
Int. J. Mol. Sci. 2023, 24(23), 16645; https://doi.org/10.3390/ijms242316645 - 23 Nov 2023
Cited by 3 | Viewed by 2071
Abstract
Redox imbalance in fat tissue appears to be causative of impaired glucose homeostasis. This “proof-of-concept” study investigated whether the peroxidation by-product of polyunsaturated n-6 fatty acids, namely 4-hydroxynonenal (4-HNE), is formed by, and accumulates in, the adipose tissue (AT) of obese patients with [...] Read more.
Redox imbalance in fat tissue appears to be causative of impaired glucose homeostasis. This “proof-of-concept” study investigated whether the peroxidation by-product of polyunsaturated n-6 fatty acids, namely 4-hydroxynonenal (4-HNE), is formed by, and accumulates in, the adipose tissue (AT) of obese patients with type 2 diabetes (OBT2D) as compared with lean, nondiabetic control subjects (CTRL). Moreover, we studied the effects of 4-HNE on the cell viability and adipogenic differentiation of adipose-derived stem cells (ASCs). Protein–HNE adducts in subcutaneous abdominal AT (SCAAT) biopsies from seven OBT2D and seven CTRL subjects were assessed using Western blot. The effects of 4-HNE were then studied in primary cultures of ASCs, focusing on cell viability, adipogenic differentiation, and the “canonical” Wnt and MAPK signaling pathways. When compared with the controls, the OBT2D patients displayed increased HNE–protein adducts in the SCAAT. The exposure of ASCs to 4-HNE fostered ROS production and led to a time- and concentration-dependent decrease in cell viability. Notably, at concentrations that did not affect cell viability (1 μM), 4-HNE hampered adipogenic ASCs’ differentiation through a timely-regulated activation of the Wnt/β-catenin, p38MAPK, ERK1/2- and JNK-mediated pathways. These “hypothesis-generating” data suggest that the increased accumulation of 4-HNE in the SCAAT of obese patients with type 2 diabetes may detrimentally affect adipose precursor cell differentiation, possibly contributing to the obesity-associated derangement of glucose homeostasis. Full article
(This article belongs to the Special Issue Obesity and Insulin Resistance: The Dark Sides of Adipose Organ Dysfunction in the Cardiometabolic Continuum)
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13 pages, 452 KiB  
Article
Association of HDL Subfraction Profile with the Progression of Insulin Resistance
by Peter Piko, Tibor Jenei, Zsigmond Kosa, Janos Sandor, Nora Kovacs, Ildiko Seres, Gyorgy Paragh and Roza Adany
Int. J. Mol. Sci. 2023, 24(17), 13563; https://doi.org/10.3390/ijms241713563 - 1 Sep 2023
Cited by 6 | Viewed by 1914
Abstract
Type 2 diabetes mellitus (T2DM) is a major global public health problem, as it is associated with increased morbidity, mortality, and healthcare costs. Insulin resistance (IR) is a condition characterized by disturbances in carbohydrate and lipid metabolism that precedes T2DM. The aim of [...] Read more.
Type 2 diabetes mellitus (T2DM) is a major global public health problem, as it is associated with increased morbidity, mortality, and healthcare costs. Insulin resistance (IR) is a condition characterized by disturbances in carbohydrate and lipid metabolism that precedes T2DM. The aim of the present study was to investigate the association between HDL and its subfraction profile and the progression of IR, as assessed by the Homeostatic Model Assessment for IR (HOMA-IR) index, and to define cut-off values to identify an increased risk of IR. Individuals with a HOMA-IR greater than 3.63 were considered to have IR. The HDL subfractions were separated using the Lipoprint system, which identifies ten subfractions (HDL-1-10) in three subclasses as large (HDL-L), intermediate (HDL-I) and small (HDL-S). Analyses were performed on samples from 240 individuals without IR and 137 with IR from the Hungarian general and Roma populations. The HDL-1 to -6 subfractions and the HDL-L and -I classes showed a significant negative association with the progression and existence of IR. Among them, HDL-2 (B = −40.37, p = 2.08 × 10−11) and HDL-L (B = −14.85, p = 9.52 × 10−10) showed the strongest correlation. The optimal threshold was found to be 0.264 mmol/L for HDL-L and 0.102 mmol/L and above for HDL-2. Individuals with HDL-L levels below the reference value had a 5.1-fold higher risk of IR (p = 2.2 × 10−7), while those with HDL-2 levels had a 4.2-fold higher risk (p = 3.0 × 10−6). This study demonstrates that the HDL subfraction profile (especially the decrease in HDL-2 and -L) may be a useful marker for the early detection and intervention of atherogenic dyslipidemia in subjects with impaired glucose and insulin metabolism. Full article
(This article belongs to the Special Issue Obesity and Insulin Resistance: The Dark Sides of Adipose Organ Dysfunction in the Cardiometabolic Continuum)
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