Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.7
3.4
Journals
Metabolites
Sections
Insulin Resistance in the 2020's
share announcement

Insulin Resistance in the 2020's

A topical collection in Metabolites (ISSN 2218-1989). This collection belongs to the section "Endocrinology and Clinical Metabolic Research".

Viewed by 27421

Editor

Dr. Amedeo Lonardo

grade E-Mail Website
Guest Editor
1. Formerly Director of the Simple Operating Unit "Metabolic Syndrome", Azienda Ospedaliero-Universitaria, 41126 Modena, Italy
2. Formerly Professor of Internal Medicine, School of Specialization of Allergology and Clinical Immunology, University of Modena and Reggio Emilia, 41121 Modena, Italy
Interests: NAFLD-MAFLD; cirrhosis; hepatocellular carcinoma; metabolic syndrome; insulin resistance; sex differences
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues,

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 physiological states (e.g., puberty and pregnancy) and pathological conditions (e.g., diabesity and metabolic syndrome). In particular, IR is a key determinant of a wide-ranging spectrum of diseases spanning cardio-nephro-metabolic disorders to the end-stage failure of such vital organs as the heart, the kidney and the liver, and also certain types of cancer such as, for example, gastrointestinal and breast cancers.

The obesogenic world in which a large part of the human population resides is a recognized facilitator of IR development and progression. However, genetic traits may predispose to the specific array of complications and manifestations that typically characterize patients. Therefore, owing to its epidemiological and clinical burden, IR is an attractive topic both in basic and clinical research. Interest in molecular mechanisms, translational approaches and strong interdisciplinarity characterize IR research, which brings together investigator-driven studies as well as industry-sponsored investigations.

The aim of this Topic Collection is to publish high-quality review and research papers in IR. We make a call for well-written review articles and original papers spanning the areas of glucose metabolism, lipid metabolism, obesity, cardiovascular and fatty liver disease. The scope of this Topic Collection includes, but is not limited to: homeostatic model assessment, insulin sensitivity, Type 2 diabetes, polycystic ovary syndrome, nonalcoholic fatty liver disease, oxidative stress, inflammation, beta cell function and hepatic steatosis.

Dr. Amedeo Lonardo
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 collection 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. Metabolites 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

  • abdominal obesity
  • adipokines
  • adipose tissue
  • adiposopathy
  • aldosteronism
  • Alzheimer’s disease
  • android obesity
  • apolipoprotein
  • androgens
  • arterial hypertension
  • atherogenic dyslipidemia
  • atherosclerosis
  • beta cell function
  • beta cell secretion
  • bile acids
  • biomarkers
  • body mass index
  • cancer
  • cardiovascular disease
  • cell biology
  • childhood obesity
  • chronic kidney disease
  • cardiovascular risk
  • coronary artery disease
  • COVID-19
  • diabetes
  • diabetic foot
  • diagnosis
  • dyslipidemia
  • drug management
  • endoplasmic reticulum stress
  • estrogens
  • extracellular vesicles
  • fertility
  • genetics
  • geriatric medicine
  • gestational diabetes
  • glp-1 receptor agonists
  • glucose (in)tolerance
  • glucose homeostasis
  • glucose metabolism
  • glucose transport
  • gut microbiota
  • growth hormone
  • hepatic steatosis
  • hepatokines
  • high-fat diet
  • histology
  • HIV
  • homeostatic model assessment (HOMA)
  • hyperadrenalism
  • hypercortisolism
  • hyperinsulinemia
  • imaging techniques
  • insulin-like growth factor
  • insulin resistance
  • insulin receptor
  • insulin sensitivity
  • insulin signaling
  • insulin secretion
  • insulin sensitizers
  • lifestyle
  • lipid metabolism
  • lipotoxicity
  • metabolic syndrome
  • metformin
  • molecular biology
  • natural history
  • nonalcoholic fatty liver disease
  • nonalcoholic steatohepatitis
  • oxidative stress
  • pediatric medicine
  • peripheral artery disease
  • personalized medicine
  • polycystic ovary syndrome
  • prediabetes
  • randomized clinical trial
  • SARS-CoV-2
  • type 2 diabetes
  • peroxisome proliferator
  • protein kinase
  • sex differences
  • skeletal muscle
  • thiazolidinediones
  • thyroid
  • viral hepatitis

Published Papers (6 papers)

Download All Papers

2021

Jump to: 2020

8 pages, 658 KiB  
Article
Safety and Effectiveness of Sodium–Glucose Cotransporter 2 Inhibitor Combined with Medical Nutrition Therapy for Hyperglycemia in Acute Stroke: A Retrospective Study
by Takahisa Mori, Kazuhiro Yoshioka, Yuhei Tanno and Shigen Kasakura
Metabolites 2022, 12(1), 25; https://doi.org/10.3390/metabo12010025 - 28 Dec 2021
Cited by 1 | Viewed by 1904
Abstract
Hyperglycemia, a predictor of poor clinical outcomes in acute stroke, must be lowered safely and promptly. We investigated the safety and effectiveness of sodium-glucose cotransporter 2 inhibitors (SGLT2is) combined with medical nutrition therapy in lowering blood glucose levels. This retrospective study included stroke [...] Read more.
Hyperglycemia, a predictor of poor clinical outcomes in acute stroke, must be lowered safely and promptly. We investigated the safety and effectiveness of sodium-glucose cotransporter 2 inhibitors (SGLT2is) combined with medical nutrition therapy in lowering blood glucose levels. This retrospective study included stroke patients admitted between 2014 and 2019, who (1) had glycated hemoglobin ≥6.5%, blood glucose level ≥ 11.1 mmol/L at admission, (2) took their diet and drugs orally during hospitalization, (3) underwent SGLT2is pharmacotherapy after admission, and (4) underwent a fasting blood glucose (FBG) test on day 7. Patients were provided with a moderate-carbohydrate diet combined with total energy restriction. We assessed the achievement of FBG < 7 mmol/L on day 7 and the need for sulfonylurea or a long-acting insulin analog (LIA) treatment during hospitalization, which carries a risk of hypoglycemia. Fifty-one patients met our inclusion criteria. Of them, 33 (64.7%) achieved the target FBG on day 7. Only eight patients were treated with a small dose of LIA; however, no patients required sulfonylurea. No dehydration occurred. SGLT2is combined with a moderate carbohydrate- and energy-restricted diet achieved the target FBG level safely, effectively, and promptly in mild stroke patients with oral ingestion. Full article
►▼ Show Figures

Figure 1

3 pages, 181 KiB  
Editorial
That’s the Sex, Baby, and There’s Nothing You Can Do about It!
by Nicola De Maria and Erica Villa
Metabolites 2021, 11(5), 291; https://doi.org/10.3390/metabo11050291 - 1 May 2021
Viewed by 1968
Abstract
Dr [...] Full article
15 pages, 1017 KiB  
Review
Insulin Resistance across the Spectrum of Nonalcoholic Fatty Liver Disease
by Angelo Armandi, Chiara Rosso, Gian Paolo Caviglia and Elisabetta Bugianesi
Metabolites 2021, 11(3), 155; https://doi.org/10.3390/metabo11030155 - 8 Mar 2021
Cited by 55 | Viewed by 5603
Abstract
Insulin resistance (IR) is defined as a lower-than-expected response to insulin action from target tissues, leading to the development of type 2 diabetes through the impairment of both glucose and lipid metabolism. IR is a common condition in subjects with nonalcoholic fatty liver [...] Read more.
Insulin resistance (IR) is defined as a lower-than-expected response to insulin action from target tissues, leading to the development of type 2 diabetes through the impairment of both glucose and lipid metabolism. IR is a common condition in subjects with nonalcoholic fatty liver disease (NAFLD) and is considered one of the main factors involved in the pathogenesis of nonalcoholic steatohepatitis (NASH) and in the progression of liver disease. The liver, the adipose tissue and the skeletal muscle are major contributors for the development and worsening of IR. In this review, we discuss the sites and mechanisms of insulin action and the IR-related impairment along the spectrum of NAFLD, from simple steatosis to progressive NASH and cirrhosis. Full article
►▼ Show Figures

Figure 1

12 pages, 1595 KiB  
Article
The Increased Expression of Regulator of G-Protein Signaling 2 (RGS2) Inhibits Insulin-Induced Akt Phosphorylation and Is Associated with Uncontrolled Glycemia in Patients with Type 2 Diabetes
by J. Gustavo Vazquez-Jimenez, M. Stephanie Corpus-Navarro, J. Miguel Rodriguez-Chavez, Hiram J. Jaramillo-Ramirez, Judith Hernandez-Aranda, Octavio Galindo-Hernandez, J. Rene Machado-Contreras, Marina Trejo-Trejo, Agustin Guerrero-Hernandez and J. Alberto Olivares-Reyes
Metabolites 2021, 11(2), 91; https://doi.org/10.3390/metabo11020091 - 5 Feb 2021
Cited by 5 | Viewed by 3113
Abstract
Experimental evidence in mice models has demonstrated that a high regulator of G-protein signaling 2 (RSG2) protein levels precede an insulin resistance state. In the same context, a diet rich in saturated fatty acids induces an increase in RGS2 protein expression, which has [...] Read more.
Experimental evidence in mice models has demonstrated that a high regulator of G-protein signaling 2 (RSG2) protein levels precede an insulin resistance state. In the same context, a diet rich in saturated fatty acids induces an increase in RGS2 protein expression, which has been associated with decreased basal metabolism in mice; however, the above has not yet been analyzed in humans. For this reason, in the present study, we examined the association between RGS2 expression and insulin resistance state. The incubation with palmitic acid (PA), which inhibits insulin-mediated Akt Ser473 phosphorylation, resulted in the increased RGS2 expression in human umbilical vein endothelial-CS (HUVEC-CS) cells. The RGS2 overexpression without PA was enough to inhibit insulin-mediated Akt Ser473 phosphorylation in HUVEC-CS cells. Remarkably, the platelet RGS2 expression levels were higher in type 2 diabetes mellitus (T2DM) patients than in healthy donors. Moreover, an unbiased principal component analysis (PCA) revealed that RGS2 expression level positively correlated with glycated hemoglobin (HbA1c) and negatively with age and high-density lipoprotein cholesterol (HDL) in T2DM patients. Furthermore, PCA showed that healthy subjects segregated from T2DM patients by having lower levels of HbA1c and RGS2. These results demonstrate that RGS2 overexpression leads to decreased insulin signaling in a human endothelial cell line and is associated with poorly controlled diabetes. Full article
►▼ Show Figures

Graphical abstract

13 pages, 1026 KiB  
Article
Glucagon-Like Peptide-1 Receptor Agonists for Treatment of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis: An Updated Meta-Analysis of Randomized Controlled Trials
by Alessandro Mantovani, Graziana Petracca, Giorgia Beatrice, Alessandro Csermely, Amedeo Lonardo and Giovanni Targher
Metabolites 2021, 11(2), 73; https://doi.org/10.3390/metabo11020073 - 27 Jan 2021
Cited by 175 | Viewed by 10435
Abstract
To assess the efficacy of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) for treatment of nonalcoholic fatty liver disease (NAFLD) or steatohepatitis (NASH), we performed a systematic review and meta-analysis of randomized controlled trials (RCTs). Three large electronic databases were systematically searched (up to [...] Read more.
To assess the efficacy of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) for treatment of nonalcoholic fatty liver disease (NAFLD) or steatohepatitis (NASH), we performed a systematic review and meta-analysis of randomized controlled trials (RCTs). Three large electronic databases were systematically searched (up to 15 December 2020) to identify placebo-controlled or active-controlled RCTs using different GLP-1 RAs. We included eleven placebo-controlled or active-controlled phase-2 RCTs (involving a total of 936 middle-aged individuals) that used liraglutide (n = 6 RCTs), exenatide (n = 3 RCTs), dulaglutide (n = 1 RCT) or semaglutide (n = 1 RCT) to specifically treat NAFLD or NASH, detected by liver biopsy (n = 2 RCTs) or imaging techniques (n = 9 RCTs). Compared to placebo or reference therapy, treatment with GLP-1 RAs for a median of 26 weeks was associated with significant reductions in the absolute percentage of liver fat content on magnetic resonance-based techniques (pooled weighted mean difference: −3.92%, 95% confidence intervals (CI) −6.27% to −1.56%) and serum liver enzyme levels, as well as with greater histological resolution of NASH without worsening of liver fibrosis (pooled random-effects odds ratio 4.06, 95% CI 2.52–6.55; for liraglutide and semaglutide only). In conclusion, treatment with GLP-1 RAs (mostly liraglutide and semaglutide) is a promising treatment option for NAFLD or NASH that warrants further investigation. Full article
►▼ Show Figures

Graphical abstract

2020

Jump to: 2021

5 pages, 364 KiB  
Commentary
What’s Past Is Prologue: History of Nonalcoholic Fatty Liver Disease
by Giovanni Targher
Metabolites 2020, 10(10), 397; https://doi.org/10.3390/metabo10100397 - 8 Oct 2020
Cited by 8 | Viewed by 2977
Abstract
Since the initial descriptions in the early 1980s by Dr. Ludwig et al. and Drs. Schaffner and Thaler, who firstly coined the terms nonalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease (NAFLD), this liver disease has become a global health problem worldwide, causing [...] Read more.
Since the initial descriptions in the early 1980s by Dr. Ludwig et al. and Drs. Schaffner and Thaler, who firstly coined the terms nonalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease (NAFLD), this liver disease has become a global health problem worldwide, causing considerable liver-related and extra-hepatic morbidity and mortality. Based on pathophysiological insights gained from the past decades, it has been clearly established that NAFLD is a metabolic liver disease whose etiology and pathogenesis extends beyond the liver and that NAFLD has important clinical implications, especially in terms of an increased risk of developing both cardiovascular disease (which represents the leading cause of death in this patient population) and other extra-hepatic manifestations, such as type 2 diabetes mellitus, chronic kidney disease, and some extra-hepatic cancers. The aim of this brief commentary is to discuss a recent review article written by Dr. Lonardo and colleagues, who raised awareness of the history of NAFLD. Since “What’s past is prologue”, I believe that this review article focusing on the history of NAFLD may contribute to better understanding the disease itself, as well as to anticipating the lines of the future clinical and pharmacological research of this common and burdensome liver disease. Full article
►▼ Show Figures

Figure 1

Back to TopTop