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      Obesity, Insulin Resistance, and Type 2 Diabetes: Associations and Therapeutic Implications

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          Abstract

          Obesity is a triggering factor for diabetes associated with insulin resistance. In individuals who are obese, higher amounts of non-esterified fatty acids, glycerol, hormones, and pro-inflammatory cytokines that could participate in the development of insulin resistance are released by adipose tissue. Besides, endoplasmic reticulum stress, adipose tissue hypoxia, oxidative stress, lipodystrophy, and genetic background have a role in insulin resistance. However, no effective drug therapy was developed for type 2 diabetes mellitus targeting these physiological factors. This is might be due to a lack of agreement on the comprehensive mechanism of insulin resistance. Therefore, this review assesses the cellular components of each physiologic and pathophysiologic factors that are involved in obesity associated insulin resistance, and may encourage further drug development in this field.

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          Pathogen recognition and inflammatory signaling in innate immune defenses.

          Trine Mogensen (2009)
          The innate immune system constitutes the first line of defense against invading microbial pathogens and relies on a large family of pattern recognition receptors (PRRs), which detect distinct evolutionarily conserved structures on pathogens, termed pathogen-associated molecular patterns (PAMPs). Among the PRRs, the Toll-like receptors have been studied most extensively. Upon PAMP engagement, PRRs trigger intracellular signaling cascades ultimately culminating in the expression of a variety of proinflammatory molecules, which together orchestrate the early host response to infection, and also is a prerequisite for the subsequent activation and shaping of adaptive immunity. In order to avoid immunopathology, this system is tightly regulated by a number of endogenous molecules that limit the magnitude and duration of the inflammatory response. Moreover, pathogenic microbes have developed sophisticated molecular strategies to subvert host defenses by interfering with molecules involved in inflammatory signaling. This review presents current knowledge on pathogen recognition through different families of PRRs and the increasingly complex signaling pathways responsible for activation of an inflammatory and antimicrobial response. Moreover, medical implications are discussed, including the role of PRRs in primary immunodeficiencies and in the pathogenesis of infectious and autoimmune diseases, as well as the possibilities for translation into clinical and therapeutic applications.
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            Global Prevalence of Diabetes: Estimates for the year 2000 and projections for 2030

            P S Wild, G Roglic, Carla Green … (2004)
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              Thioredoxin-interacting protein links oxidative stress to inflammasome activation.

              Rongbin Zhou, Aubry Tardivel, Bernard Thorens … (2010)
              The NLRP3 inflammasome has a major role in regulating innate immunity. Deregulated inflammasome activity is associated with several inflammatory diseases, yet little is known about the signaling pathways that lead to its activation. Here we show that NLRP3 interacted with thioredoxin (TRX)-interacting protein (TXNIP), a protein linked to insulin resistance. Inflammasome activators such as uric acid crystals induced the dissociation of TXNIP from thioredoxin in a reactive oxygen species (ROS)-sensitive manner and allowed it to bind NLRP3. TXNIP deficiency impaired activation of the NLRP3 inflammasome and subsequent secretion of interleukin 1beta (IL-1beta). Akin to Txnip(-/-) mice, Nlrp3(-/-) mice showed improved glucose tolerance and insulin sensitivity. The participation of TXNIP in the NLRP3 inflammasome activation may provide a mechanistic link to the observed involvement of IL-1beta in the pathogenesis of type 2 diabetes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Diabetes Metab Syndr Obes
                Journal ID (iso-abbrev): Diabetes Metab Syndr Obes
                Journal ID (publisher-id): dmso
                Journal ID (pmc): dmso
                Title: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
                Publisher: Dove
                ISSN (Electronic): 1178-7007
                Publication date (Electronic): 09 October 2020
                Publication date Collection: 2020
                Volume: 13
                Pages: 3611-3616
                Affiliations
                [1 ]Department of Pharmacology and Clinical Pharmacy, School of Pharmacy, College of Health Sciences, Addis Ababa University , Addis Ababa, Ethiopia
                Author notes
                Correspondence: Yohannes Tsegyie Wondmkun Department of Pharmacology and Clinical Pharmacy, School of Pharmacy, College of Health Sciences, Addis Ababa University , P.O. Box 1176, Addis Ababa, Ethiopia Email yonitse2015@gmail.com
                Article
                Publisher ID: 275898
                DOI: 10.2147/DMSO.S275898
                PMC ID: 7553667
                PubMed ID: 33116712
                SO-VID: 6d47526f-b8ba-4302-a346-103754e7ec65
                Copyright © © 2020 Wondmkun.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 06 August 2020
                Date accepted : 23 September 2020
                Page count
                Figures: 0, References: 43, Pages: 6
                Funding
                Funded by: no funding;
                There is no funding to report.
                Categories
                Subject: Review

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: obesity,insulin,insulin resistance,type 2 diabetes mellitus
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: obesity, insulin, insulin resistance, type 2 diabetes mellitus

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