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Special Issue "Insulin Sensitivity/Resistance: From Physiology to Disease"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editors

Dr. Maria Elisabeth Street
E-Mail Website
Guest Editor
AUSL- IRCCS di Reggio Emilia, Reggio Emilia, Italy
Interests: growth; IGF system; insulin sensitivity; inflammation; endocrine disruptors
Special Issues and Collections in MDPI journals
Prof. Paolo Moghetti
E-Mail Website
Guest Editor
Unit of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Verona, Verona, Italy
Interests: Insulin resistance; Polycystic ovary syndrome; Hyperandrogenism; Exercise; Type 2 diabetes
Prof. Dr. Francesco Chiarelli
E-Mail Website
Guest Editor
Department of Paediatrics, University of Chieti, Chieti, Italy
Interests: type 1 diabetes; insulin resistance; metabolic syndrome; growth

Special Issue Information

Dear Colleagues,

Insulin is of upmost importance not only for the regulation of metabolism but is implicated also with growth and senescence and overall has pleiotropic effects. Many factors regulate and/or interfere with insulin sensitivity including genetic and epigenetic factors, hormones, inflammation and dysregulation of autophagy and reticular endothelial stress. More recently environmental factors, and among these endocrine disrupting chemicals, have been shown to have negative effects on insulin sensitivity. Reduced insulin sensitivity can be both cause and consequence of disease, and common conditions such as polycystic ovarian disease can have an underlying condition of impaired insulin sensitivity.  

This issue will focus comprehensively on all aspects of insulin sensitivity. Molecular and cell biology studies are welcome as well as studies both on humans and animals. New scientific data on standard treatments as well as new options will be considered. We encourage original articles, comprehensive reviews and detailed focused reviews, and reports of research protocols. 

Dr. Maria Elisabeth Street
Prof. Paolo Moghetti
Prof. Dr. Francesco Chiarelli
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 papers will be 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
  • insulin sensitivity
  • insulin action
  • treatment of insulin resistance
  • epigenetics
  • endocrine disruptors
  • polycystic ovary syndrome
  • diabetes

Published Papers (2 papers)

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Research

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Article
β Cell GHS-R Regulates Insulin Secretion and Sensitivity
Int. J. Mol. Sci. 2021, 22(8), 3950; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083950 - 11 Apr 2021
Cited by 3 | Viewed by 791
Abstract
Growth hormone secretagogue receptor (GHS-R) is widely known to regulate food intake and adiposity, but its role in glucose homeostasis is unclear. In this study, we investigated the expression of GHS-R in mouse pancreatic islets and its role in glycemic regulation. We used [...] Read more.
Growth hormone secretagogue receptor (GHS-R) is widely known to regulate food intake and adiposity, but its role in glucose homeostasis is unclear. In this study, we investigated the expression of GHS-R in mouse pancreatic islets and its role in glycemic regulation. We used Ghsr-IRES-tauGFP mice, with Green Fluorescent Protein (GFP) as a surrogate for GHS-R, to demonstrate the GFP co-localization with insulin and glucagon expression in pancreatic islets, confirming GHS-R expression in β and α cells. We then generated β-cell-specific GHSR-deleted mice with MIP-Cre/ERT and validated that GHS-R suppression was restricted to the pancreatic islets. MIP-Cre/ERT;Ghsrf/f mice showed normal energy homeostasis with similar body weight, body composition, and indirect calorimetry profile. Interestingly, MIP-Cre/ERT;Ghsrf/f mice exhibited an impressive phenotype in glucose homeostasis. Compared to controls, MIP-Cre/ERT;Ghsrf/f mice showed lower fasting blood glucose and insulin; reduced first-phase insulin secretion during a glucose tolerance test (GTT) and glucose-stimulated insulin secretion (GSIS) test in vivo. The isolated pancreatic islets of MIP-Cre/ERT;Ghsrf/f mice also showed reduced insulin secretion during GSIS ex vivo. Further, MIP-Cre/ERT;Ghsrf/f mice exhibited improved insulin sensitivity during insulin tolerance tests (ITT). Overall, our results confirmed GHS-R expression in pancreatic β and α cells; GHS-R cell-autonomously regulated GSIS and modulated systemic insulin sensitivity. In conclusion, β cell GHS-R was an important regulator of glucose homeostasis, and GHS-R antagonists may have therapeutic potential for Type 2 Diabetes. Full article
(This article belongs to the Special Issue Insulin Sensitivity/Resistance: From Physiology to Disease)
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Review

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Review
Hyperinsulinemia and Its Pivotal Role in Aging, Obesity, Type 2 Diabetes, Cardiovascular Disease and Cancer
Int. J. Mol. Sci. 2021, 22(15), 7797; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22157797 - 21 Jul 2021
Viewed by 1872
Abstract
For many years, the dogma has been that insulin resistance precedes the development of hyperinsulinemia. However, recent data suggest a reverse order and place hyperinsulinemia mechanistically upstream of insulin resistance. Genetic background, consumption of the “modern” Western diet and over-nutrition may increase insulin [...] Read more.
For many years, the dogma has been that insulin resistance precedes the development of hyperinsulinemia. However, recent data suggest a reverse order and place hyperinsulinemia mechanistically upstream of insulin resistance. Genetic background, consumption of the “modern” Western diet and over-nutrition may increase insulin secretion, decrease insulin pulses and/or reduce hepatic insulin clearance, thereby causing hyperinsulinemia. Hyperinsulinemia disturbs the balance of the insulin–GH–IGF axis and shifts the insulin : GH ratio towards insulin and away from GH. This insulin–GH shift promotes energy storage and lipid synthesis and hinders lipid breakdown, resulting in obesity due to higher fat accumulation and lower energy expenditure. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, cancer and premature mortality. It has been further hypothesized that nutritionally driven insulin exposure controls the rate of mammalian aging. Interventions that normalize/reduce plasma insulin concentrations might play a key role in the prevention and treatment of age-related decline, obesity, type 2 diabetes, cardiovascular disease and cancer. Caloric restriction, increasing hepatic insulin clearance and maximizing insulin sensitivity are at present the three main strategies available for managing hyperinsulinemia. This may slow down age-related physiological decline and prevent age-related diseases. Drugs that reduce insulin (hyper) secretion, normalize pulsatile insulin secretion and/or increase hepatic insulin clearance may also have the potential to prevent or delay the progression of hyperinsulinemia-mediated diseases. Future research should focus on new strategies to minimize hyperinsulinemia at an early stage, aiming at successfully preventing and treating hyperinsulinemia-mediated diseases. Full article
(This article belongs to the Special Issue Insulin Sensitivity/Resistance: From Physiology to Disease)
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