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Molecular Advances on Insulin Resistance and Metabolic Dysfunction 2.0
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Molecular Advances on Insulin Resistance and Metabolic Dysfunction 2.0

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 (31 January 2024) | Viewed by 3315

Special Issue Editors

Prof. Dr. Melania Manco

E-Mail Website
Guest Editor
Unit of Endocrinology, Bambino Gesù Children’s Hospital, IRCCS, 00146 Rome, Italy
Interests: obesity; insulin resistance and secretion; type 2 diabetes
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Amalia Gastaldelli

grade E-Mail Website
Guest Editor
Institute of Clinical Physiology, National Research Council, 56124 Pisa, Italy
Interests: insulin resistance; hepatology; diabetes; hypertension; metabolic syndrome; glucose metabolism; fatty liver; metabolism; nutrition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Worldwide, the obesity epidemic has resulted in a surge of metabolic abnormalities and diseases stemming from the condition of insulin resistance that accompanies the obesity status. Insulin resistance represents an impaired biological response to insulin stimulation of target tissues, primarily liver, muscle, and adipose tissue. It is recognized as the root for hypertension, dyslipidemia, non alcholic fatty liver disease, policistic ovary syndome, atherosclerosis, and adverse cardiac remodeling/heart failure. Alterations in glucose and lipid metabolism, insulin secretion and action are among the most important mechanisms that explain the onset of these diseases.

Several modifiable and non-modifiable factors are implicated. Among modifiable risk factors sedentarity and unhealthy diets rich in saturated fat are the most important. However, it is becoming clear that during the last century the production and release of chemicals in the environment has increased and this per se has an effect on health. These chemicals once inhaled or ingested (since they are present in water and in the food chain) may act as endocrine disruptors (EDC) thus increasing the development of metabolic diseases and related comorbidities.

We invite investigators to contribute either original research articles or review articles focusing on the variety of molecular mechanisms that either contribute to the worsening of insulin resistance in obese patients, or that, triggered by insulin resistance, cause the onset and progression of comorbidities associated with obesity.

Prof. Dr. Melania Manco
Prof. Dr. Amalia Gastaldelli
Guest Editors

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

  • dysregulated fatty acid and/or branched chain amino acids metabolism
  • metabolic inflexibility
  • tissue lipid accumulation, lipotoxicity and lipid mediated cell signaling
  • insulin resistance reversal
  • cancer development
  • low-grade inflammation and/or altered expression, synthesis and degradation and bioavailability of IGF binding proteins
  • environmental chemicals
  • mechanisms of T3D
  • microbiota and antimicrobials modulation
  • endocrine disruptors
  • altered immune system homeostasis

Published Papers (3 papers)

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Research

13 pages, 3091 KiB  
Article
Akt Signaling and Nitric Oxide Synthase as Possible Mediators of the Protective Effect of N-acetyl-L-cysteine in Prediabetes Induced by Sucrose
by María Cecilia Castro, Hernán Gonzalo Villagarcía, Luciana Di Sarli Gutiérrez, Luisa González Arbeláez, Guillermo Schinella, María Laura Massa and Flavio Francini
Int. J. Mol. Sci. 2024, 25(2), 1215; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25021215 - 19 Jan 2024
Viewed by 659
Abstract
The aim of this work was to evaluate possible mechanisms involved in the protective effect of N-acetyl-L-cysteine (NAC) on hepatic endocrine-metabolic, oxidative stress, and inflammatory changes in prediabetic rats. For that, normal male Wistar rats (60 days old) were fed for 21 days [...] Read more.
The aim of this work was to evaluate possible mechanisms involved in the protective effect of N-acetyl-L-cysteine (NAC) on hepatic endocrine-metabolic, oxidative stress, and inflammatory changes in prediabetic rats. For that, normal male Wistar rats (60 days old) were fed for 21 days with 10% sucrose in their drinking water and 5 days of NAC administration (50 mg/kg, i.p.) and thereafter, we determined: serum glucose, insulin, transaminases, uric acid, and triglyceride levels; hepatic fructokinase and glucokinase activities, glycogen content, lipogenic gene expression; enzymatic and non-enzymatic oxidative stress, insulin signaling pathway, and inflammatory markers. Results showed that alterations evinced in sucrose-fed rats (hypertriglyceridemia, hyperinsulinemia, and high liver fructokinase activity together with increased liver lipogenic gene expression and oxidative stress and inflammatory markers) were prevented by NAC administration. P-endothelial nitric oxide synthase (P-eNOS)/eNOS and pAKT/AKT ratios, decreased by sucrose ingestion, were restored after NAC treatment. In conclusion, the results suggest that NAC administration improves glucose homeostasis, oxidative stress, and inflammation in prediabetic rats probably mediated by modulation of the AKT/NOS pathway. Administration of NAC may be an effective complementary strategy to alleviate or prevent oxidative stress and inflammatory responses observed in type 2 diabetes at early stages of its development (prediabetes). Full article
(This article belongs to the Special Issue Molecular Advances on Insulin Resistance and Metabolic Dysfunction 2.0)
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13 pages, 1308 KiB  
Communication
Insulin Clearance at the Pubertal Transition in Youth with Obesity and Steatosis Liver Disease
by Roberto Franceschi, Danilo Fintini, Lucilla Ravà, Michela Mariani, Alessia Aureli, Elena Inzaghi, Stefania Pedicelli, Annalisa Deodati, Carla Bizzarri, Marco Cappa, Stefano Cianfarani and Melania Manco
Int. J. Mol. Sci. 2023, 24(19), 14963; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241914963 - 06 Oct 2023
Viewed by 614
Abstract
No data are available on insulin clearance (ClI) trends during the pubertal transition. The aim of this study was to investigate in 973 youths with obesity whether ClI in fasting and post-oral glucose challenge (OGTT) conditions varies at the pubertal [...] Read more.
No data are available on insulin clearance (ClI) trends during the pubertal transition. The aim of this study was to investigate in 973 youths with obesity whether ClI in fasting and post-oral glucose challenge (OGTT) conditions varies at the pubertal transition in relation to the severity of obesity and the presence of steatosis liver disease (SLD). The severity of obesity was graded according to the Centers for Disease Control. SLD was graded as absent, mild and severe based on alanine amino transferase levels. ClI was defined as the molar ratio of fasting C-peptide to insulin and of the areas under the insulin to glucose curves during an OGTT. In total, 35% of participants were prepubertal, 72.6% had obesity class II, and 52.6% had mild SLD. Fasting ClI (nmol/pmol × 10−2) was significantly lower in pubertal [0.11 (0.08–0.14)] than in prepubertal individuals [0.12 (0.09–0.16)] and higher in class III [0.15 (0.11–0.16)] than in class I obesity [0.11 (0.09–0.14)]. OGTT ClI was higher in boys [0.08 (0.06–0.10)] than in girls [0.07 (0.06–0.09)]; in prepubertal [0.08 (0.06–0.11)] than in pubertal individuals [0.07 (0.05–0.09)]; in class III [0.14 (0.08–0.17)] than in class I obesity [0.07 (0.05–0.10)]; and in severe SLD [0.09 (0.04–0.14)] than in no steatosis [0.06 (0.04–0.17)]. It was lower in participants with prediabetes [0.06 (0.04–0.07)]. OGTT ClI was lower in youths with obesity at puberty along with insulin sensitivity and greater secretion. The findings suggest that the initial increase in ClI in youth with severe obesity and SLD is likely to compensate for hyperinsulinemia and its subsequent decrease at the onset of prediabetes and other metabolic abnormalities. Full article
(This article belongs to the Special Issue Molecular Advances on Insulin Resistance and Metabolic Dysfunction 2.0)
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13 pages, 2113 KiB  
Article
Fatty Liver Index (FLI) Identifies Not Only Individuals with Liver Steatosis but Also at High Cardiometabolic Risk
by Fabrizia Carli, Silvia Sabatini, Melania Gaggini, Anna Maria Sironi, Giorgio Bedogni and Amalia Gastaldelli
Int. J. Mol. Sci. 2023, 24(19), 14651; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241914651 - 27 Sep 2023
Cited by 1 | Viewed by 1650
Abstract
A fatty liver index (FLI) greater than sixty (FLI ≥ 60) is an established score for metabolic dysfunction-associated steatotic liver disease (MASLD), which carries a high risk for diabetes and cardiovascular disease, while a FLI ≤ 20 rules out the presence of steatosis. [...] Read more.
A fatty liver index (FLI) greater than sixty (FLI ≥ 60) is an established score for metabolic dysfunction-associated steatotic liver disease (MASLD), which carries a high risk for diabetes and cardiovascular disease, while a FLI ≤ 20 rules out the presence of steatosis. Thus, we investigated whether FLI was associated with cardiometabolic risk factors, i.e., visceral (VAT), subcutaneous (SC), epicardial (EPI), extrapericardial (PERI), and total cardiac (CARD-AT) adipose tissue, hepatic fat ((by magnetic resonance imaging, MRI, and spectroscopy, MRS), and insulin resistance (IR, HOMA-IR and OGIS-index), and components of metabolic syndrome. All individuals with FLI ≥ 60 had MASLD, while none with FLI ≤ 20 had steatosis (by MRS). Subjects with FLI ≥ 60 had a higher BMI and visceral and cardiac fat (VAT > 1.7 kg, CARD-AT > 0.2 kg). FLI was positively associated with increased cardiac and visceral fat and components of metabolic syndrome. FLI, VAT, and CARD-AT were all associated with IR, increased blood pressure, cholesterol, and reduced HDL. For FLI ≥ 60, the cut-off values for fat depots and laboratory measures were estimated. In conclusion, FLI ≥ 60 identified not only subjects with steatosis but also those with IR, abdominal and cardiac fat accumulation, increased blood pressure, and hyperlipidemia, i.e., those at higher risk of cardiometabolic diseases. Targeted reduction of FLI components would help reduce cardiometabolic risk. Full article
(This article belongs to the Special Issue Molecular Advances on Insulin Resistance and Metabolic Dysfunction 2.0)
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