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Biomolecules
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Insulin Resistance: Metabolic Mechanisms and Consequences Both In Vivo and...
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Insulin Resistance: Metabolic Mechanisms and Consequences Both In Vivo and Vitro

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: closed (15 January 2023) | Viewed by 11916

Special Issue Editor

Prof. Dr. Juei-Tang Cheng

E-Mail Website
Guest Editor
Institute of Medical Research, Chang Jung Christian University, Tainan City 71101, Taiwan
Interests: metabolic disorders; insulin resistance; hepatokines; natural products; animal models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Insulin resistance (IR) is a critical social problem around the world, and it is usually accompanied by increased plasma insulin levels in humans and/or animals. Because IR is known to be linked with metabolic disorders and the progression of diabetes, many scientists have contributed to the research of IR. The fruitful results have been beneficial to health and basic research. However, numerous points remained unclear, particularly the metabolic mechanisms. Therefore, this Special Issue aims to present a collection of articles focused on metabolic mechanisms and consequences, both in vivo and in vitro of IR. Additionally, details have recently emerged of important molecules and/or signaling events in the related processes.  In recent, hepatokines are a popular topic in publications. It is important to assess the significance of these molecules in the mechanisms of IR. You are most welcome to share the findings relevant to IR that were obtained in your lab using reliable animal models and/or the established cell models. Moreover, considering the health merits of modern therapies, this Special Issue will cover a wide variety of areas including repurposing of old drugs, with the aim of developing useful agents and/or biomolecules for IR therapy from various aspects. Various forms of manuscripts are welcomed for submission to this Special Issue, including reviews, mini-reviews, commentaries, and original research articles, among others, and we look forward to receiving contributions from all over the world.

Prof. Dr. Juei-Tang Cheng
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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
  • metabolic mechanisms
  • hepatokines
  • disease model
  • human health

Published Papers (3 papers)

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Review

14 pages, 1767 KiB  
Review
Molecular Mechanisms of Obesity-Induced Development of Insulin Resistance and Promotion of Amyloid-β Accumulation: Dietary Therapy Using Weak Organic Acids via Improvement of Lowered Interstitial Fluid pH
by Yoshinori Marunaka
Biomolecules 2023, 13(5), 779; https://doi.org/10.3390/biom13050779 - 30 Apr 2023
Cited by 3 | Viewed by 2190
Abstract
Insulin resistance is one of the etiologies of type 2 diabetes mellitus (T2DM) and has been suggested to contribute to the development of Alzheimer’s disease by promoting amyloid-β accumulation. Various causes of insulin resistance have been suggested; however, mechanisms of insulin resistance development [...] Read more.
Insulin resistance is one of the etiologies of type 2 diabetes mellitus (T2DM) and has been suggested to contribute to the development of Alzheimer’s disease by promoting amyloid-β accumulation. Various causes of insulin resistance have been suggested; however, mechanisms of insulin resistance development remain to be elucidated in many respects. Elucidating the mechanisms underlying the development of insulin resistance is one of the key factors in developing methods to prevent the onset of T2DM and Alzheimer’s disease. It has been suggested that the body pH environment plays an important role in the control of cellular functions by regulating the action of hormones including insulin and the activity of enzymes and neurons, thereby maintaining homeostatic conditions of the body. This review introduces: (1) Mitochondrial dysfunction through oxidative stress caused by obesity-induced inflammation. (2) Decreased pH of interstitial fluid due to mitochondrial dysfunction. (3) Development of insulin resistance due to diminution of insulin affinity to its receptor caused by the lowered interstitial fluid pH. (4) Accelerated accumulation of amyloid-β due to elevated activities of β- and γ-secretases caused by the lowered interstitial fluid pH. (5) Diet therapies for improving insulin resistance with weak organic acids that act as bases in the body to raise the pH of lowered interstitial fluid and food factors that promote absorption of weak organic acids in the gut. Full article
(This article belongs to the Special Issue Insulin Resistance: Metabolic Mechanisms and Consequences Both In Vivo and Vitro)
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12 pages, 687 KiB  
Review
Insulin Resistance in Mitochondrial Diabetes
by Chika Takano, Erika Ogawa and Satoshi Hayakawa
Biomolecules 2023, 13(1), 126; https://doi.org/10.3390/biom13010126 - 07 Jan 2023
Cited by 8 | Viewed by 4208
Abstract
Mitochondrial diabetes (MD) is generally classified as a genetic defect of β-cells. The main pathophysiology is insulin secretion failure in pancreatic β-cells due to impaired mitochondrial ATP production. However, several reports have mentioned the presence of insulin resistance (IR) as a clinical feature [...] Read more.
Mitochondrial diabetes (MD) is generally classified as a genetic defect of β-cells. The main pathophysiology is insulin secretion failure in pancreatic β-cells due to impaired mitochondrial ATP production. However, several reports have mentioned the presence of insulin resistance (IR) as a clinical feature of MD. As mitochondrial dysfunction is one of the important factors causing IR, we need to focus on IR as another pathophysiology of MD. In this special issue, we first briefly summarized the insulin signaling and molecular mechanisms of IR. Second, we overviewed currently confirmed pathogenic mitochondrial DNA (mtDNA) mutations from the MITOMAP database. The variants causing diabetes were mostly point mutations in the transfer RNA (tRNA) of the mitochondrial genome. Third, we focused on these variants leading to the recently described “tRNA modopathies” and reviewed the clinical features of patients with diabetes. Finally, we discussed the pathophysiology of MD caused by mtDNA mutations and explored the possible mechanism underlying the development of IR. This review should be beneficial to all clinicians involved in diagnostics and therapeutics related to diabetes and mitochondrial diseases. Full article
(This article belongs to the Special Issue Insulin Resistance: Metabolic Mechanisms and Consequences Both In Vivo and Vitro)
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27 pages, 1657 KiB  
Review
Links between Insulin Resistance and Periodontal Bacteria: Insights on Molecular Players and Therapeutic Potential of Polyphenols
by Katy Thouvenot, Teva Turpin, Janice Taïlé, Karine Clément, Olivier Meilhac and Marie-Paule Gonthier
Biomolecules 2022, 12(3), 378; https://doi.org/10.3390/biom12030378 - 28 Feb 2022
Cited by 9 | Viewed by 4792
Abstract
Type 2 diabetes is a metabolic disease mainly associated with insulin resistance during obesity and constitutes a major public health problem worldwide. A strong link has been established between type 2 diabetes and periodontitis, an infectious dental disease characterized by chronic inflammation and [...] Read more.
Type 2 diabetes is a metabolic disease mainly associated with insulin resistance during obesity and constitutes a major public health problem worldwide. A strong link has been established between type 2 diabetes and periodontitis, an infectious dental disease characterized by chronic inflammation and destruction of the tooth-supporting tissue or periodontium. However, the molecular mechanisms linking periodontal bacteria and insulin resistance remain poorly elucidated. This study aims to summarize the mechanisms possibly involved based on in vivo and in vitro studies and targets them for innovative therapies. Indeed, during periodontitis, inflammatory lesions of the periodontal tissue may allow periodontal bacteria to disseminate into the bloodstream and reach tissues, including adipose tissue and skeletal muscles that store glucose in response to insulin. Locally, periodontal bacteria and their components, such as lipopolysaccharides and gingipains, may deregulate inflammatory pathways, altering the production of pro-inflammatory cytokines/chemokines. Moreover, periodontal bacteria may promote ROS overproduction via downregulation of the enzymatic antioxidant defense system, leading to oxidative stress. Crosstalk between players of inflammation and oxidative stress contributes to disruption of the insulin signaling pathway and promotes insulin resistance. In parallel, periodontal bacteria alter glucose and lipid metabolism in the liver and deregulate insulin production by pancreatic β-cells, contributing to hyperglycemia. Interestingly, therapeutic management of periodontitis reduces systemic inflammation markers and ameliorates insulin sensitivity in type 2 diabetic patients. Of note, plant polyphenols exert anti-inflammatory and antioxidant activities as well as insulin-sensitizing and anti-bacterial actions. Thus, polyphenol-based therapies are of high interest for helping to counteract the deleterious effects of periodontal bacteria and improve insulin resistance. Full article
(This article belongs to the Special Issue Insulin Resistance: Metabolic Mechanisms and Consequences Both In Vivo and Vitro)
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