Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Mechanisms of Insulin Resistance and Adipose Tissue Dysfunction 2.0

Special Issue Editors
Special Issue Information
Keywords
Related Special Issue
Published Papers

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: closed (30 December 2023) | Viewed by 4557

Share This Special Issue

Special Issue Editor

Prof. Dr. Jean-François Tanti

E-Mail Website
Guest Editor

Université Côte D'Azur, INSERM, C3M, Team “Cellular and Molecular Physiopathology of Obesity”, 06204 Nice, France
Interests: obesity, type 2 diabetes; metabolic syndrome; insulin resistance; adipose tissue; insulin signaling; adipose tissue inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

International Journal of Molecular Sciences (ISSN 1422-0067, IF 4.556) is currently running a Special Issue focused on "Mechanisms of Insulin Resistance and Adipose Tissue Dysfunction 2.0". Prof. Jean-François Tanti is serving as Guest Editor for this Issue. Based on your excellent expertise, we would be thrilled if you could submit a paper to this Issue.

Insulin resistance (IR) is defined as the impaired intracellular signaling of endogenous and exogenous insulin. IR is a major key player in those metabolic derangements that characterize pathological conditions (e.g., diabesity and metabolic syndrome). Adipocyte and adipose tissue dysfunction belong to the primary defects in obesity and may link obesity to several health problems, including increased risk of insulin resistance, type 2 diabetes, and fatty liver disease.

This Special Issue focuses on the study of the mechanisms of insulin resistance and adipose tissue dysfunction in obesity and type 2 diabetes. Potential topics include but are not limited to decipher the cellular and molecular mechanisms involved in insulin resistance, and the pathophysiological mechanisms connecting adipose tissue dysfunction to the development of insulin resistance, type 2 diabetes, or fatty liver. We warmly welcome original papers and reviews on this widely discussed topic.

Prof. Dr. Jean-François Tanti
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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

insulin resistance
obesity
type 2 diabetes
adipose tissue dysfunction
white adipose tissue (WAT)

Related Special Issue

Mechanisms of Insulin Resistance and Adipose Tissue Dysfunction in International Journal of Molecular Sciences (9 articles)

Published Papers (3 papers)

Download All Papers

Research

13 pages, 345 KiB

Open AccessArticle

Silymarin Reduced Insulin Resistance in Non-Diabetic Women with Obesity

by Karla MacDonald-Ramos, Adriana Monroy, Mariana Bobadilla-Bravo and Marco Cerbón

Int. J. Mol. Sci. 2024, 25(4), 2050; https://doi.org/10.3390/ijms25042050 - 8 Feb 2024

Viewed by 1050

Abstract

Silymarin has ameliorated obesity, type 2 diabetes (T2DM), and insulin resistance (IR) in combination with standard therapy, diet, or exercise in recent studies. Obesity and IR are the main risk factors for developing T2DM and other metabolic disorders. Today, there is a need for new strategies to target IR in patients with these metabolic diseases. In the present longitudinal study, a group of non-diabetic insulin-resistant women with type 1 and type 2 obesity were given silymarin for 12 weeks, with no change in habitual diet and physical activity. We used the Homeostatic Model Assessment for Insulin Resistance Index (HOMA-IR) to determine IR at baseline and after silymarin treatment (t = 12 weeks). We obtained five timepoint oral glucose tolerance tests, and other biochemical and clinical parameters were analyzed before and after treatment. Treatment with silymarin alone significantly reduced mean fasting plasma glucose (FPG) and HOMA-IR levels at 12 weeks compared to baseline values (p < 0.05). Mean fasting plasma insulin (FPI), total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (Tg), indirect bilirubin, and C-reactive protein (CRP) levels decreased compared to baseline values, although changes were non-significant. The overall results suggest that silymarin may offer a therapeutic alternative to improve IR in non-diabetic individuals with obesity. Further clinical trials are needed in this type of patient to strengthen the results of this study. Full article

(This article belongs to the Special Issue Mechanisms of Insulin Resistance and Adipose Tissue Dysfunction 2.0)

16 pages, 4618 KiB

Open AccessArticle

Chemerin as an Inducer of β Cell Proliferation Mediates Mitochondrial Homeostasis and Promotes β Cell Mass Expansion

by Min Li, Ruifan Zhang, Qian Ge, Lingzhi Yue, Dan Ma, Firas Khattab, Wenhua Xie, Yewei Cui, Patrick Gilon, Xueya Zhao, Xi Li and Rui Cheng

Int. J. Mol. Sci. 2023, 24(11), 9136; https://doi.org/10.3390/ijms24119136 - 23 May 2023

Cited by 2 | Viewed by 1252

Abstract

Loss of the β cell population is a crucial feature of type 2 diabetes. Restoring the β cell mass by stimulating β cell proliferation and preventing its apoptosis was proposed as a therapeutic approach to treating diabetes. Therefore, researchers have been increasingly interested in identifying exogenous factors that can stimulate β cell proliferation in situ and in vitro. Adipokine chemerin, which is secreted from adipose tissue and the liver, has been identified as a chemokine that plays a critical role in the regulation of metabolism. In this study, we demonstrate that chemerin as a circulating adipokine promotes β cell proliferation in vivo and in vitro. Chemerin serum levels and the expression of the main receptors within islets are highly regulated under a variety of challenging conditions, including obesity and type 2 diabetes. As compared to their littermates, mice overexpressing chemerin had a larger islet area and increased β cell mass with both a normal and high-fat diet. Moreover, in chemerin-overexpressed mice, we observed improved mitochondrial homeostasis and increased insulin synthesis. In summary, our findings confirm the potential role of chemerin as an inducer of β cell proliferation, and they provide novel insights into the helpful strategy to expand β cell population. Full article

(This article belongs to the Special Issue Mechanisms of Insulin Resistance and Adipose Tissue Dysfunction 2.0)

► Show Figures

Figure 1

20 pages, 4672 KiB

Open AccessArticle

COBL, MKX and MYOC Are Potential Regulators of Brown Adipose Tissue Development Associated with Obesity-Related Metabolic Dysfunction in Children

by Sarah Abdul Majeed, Helene Dunzendorfer, Juliane Weiner, John T. Heiker, Wieland Kiess, Antje Körner and Kathrin Landgraf

Int. J. Mol. Sci. 2023, 24(4), 3085; https://doi.org/10.3390/ijms24043085 - 4 Feb 2023

Cited by 1 | Viewed by 1730

Abstract

Obesity is already accompanied by adipose tissue (AT) dysfunction and metabolic disease in children and increases the risk of premature death. Due to its energy-dissipating function, brown AT (BAT) has been discussed as being protective against obesity and related metabolic dysfunction. To analyze the molecular processes associated with BAT development, we investigated genome-wide expression profiles in brown and white subcutaneous and perirenal AT samples of children. We identified 39 upregulated and 26 downregulated genes in uncoupling protein 1 (UCP1)-positive compared to UCP1-negative AT samples. We prioritized for genes that had not been characterized regarding a role in BAT biology before and selected cordon-bleu WH2 repeat protein (COBL), mohawk homeobox (MKX) and myocilin (MYOC) for further functional characterization. The siRNA-mediated knockdown of Cobl and Mkx during brown adipocyte differentiation in vitro resulted in decreased Ucp1 expression, while the inhibition of Myoc led to increased Ucp1 expression. Furthermore, COBL, MKX and MYOC expression in the subcutaneous AT of children is related to obesity and parameters of AT dysfunction and metabolic disease, such as adipocyte size, leptin levels and HOMA-IR. In conclusion, we identify COBL, MKX and MYOC as potential regulators of BAT development and show an association of these genes with early metabolic dysfunction in children. Full article

(This article belongs to the Special Issue Mechanisms of Insulin Resistance and Adipose Tissue Dysfunction 2.0)

► Show Figures