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Molecular Insights and Therapy in Diabetes

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: 20 March 2025 | Viewed by 5421

Special Issue Editor


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Guest Editor
1. Department of Medicine, University of California, Irvine, CA 92697, USA
2. Department of Biomedical Engineering, University of California, Irvine, CA 92697, USA
Interests: diabetes; molecular science; immunotherapy

Special Issue Information

Dear Colleagues,

In our Special Issue titled “Molecular Insights and Therapy in Diabetes”, we delve into the latest advancements in understanding the molecular underpinnings of diabetes and the development of innovative therapies. This issue aims to showcase research that bridges the gap between detailed molecular mechanisms and therapeutic applications, offering new horizons in diabetes treatment. We invite contributions that explore the genetic, epigenetic, and metabolic pathways involved in diabetes, alongside novel therapeutic strategies that these insights have spurred, including pharmacological, biotechnological, and lifestyle interventions. Our objective is to highlight studies that not only advance our molecular understanding of diabetes but also demonstrate potential therapeutic breakthroughs, paving the way for more effective management and treatment of this complex disease.

Dr. Chenyu Huang
Guest Editor

Manuscript Submission Information

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Keywords

  • diabetes
  • molecular insights
  • therapeutic strategies
  • genetic pathways
  • metabolic pathways
  • pharmacology
  • biotechnology
  • treatment innovations

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Published Papers (2 papers)

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Research

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14 pages, 2452 KiB  
Article
Nicotinamide Mononucleotide (NMN) Ameliorates Free Fatty Acid-Induced Pancreatic β-Cell Dysfunction via the NAD+/AMPK/SIRT1/HIF-1α Pathway
by Yan Wang, Si Liu, Linyao Ying, Keyi Zhang, Hao Li, Na Liang, Lin Xiao and Gang Luo
Int. J. Mol. Sci. 2024, 25(19), 10534; https://doi.org/10.3390/ijms251910534 - 30 Sep 2024
Cited by 2 | Viewed by 2977
Abstract
As the sole producers of insulin under physiological conditions, the normal functioning of pancreatic β cells is crucial for maintaining glucose homeostasis in the body. Due to the high oxygen and energy demands required for insulin secretion, hypoxia has been shown to play [...] Read more.
As the sole producers of insulin under physiological conditions, the normal functioning of pancreatic β cells is crucial for maintaining glucose homeostasis in the body. Due to the high oxygen and energy demands required for insulin secretion, hypoxia has been shown to play a critical role in pancreatic β-cell dysfunction. Lipid metabolism abnormalities, a common metabolic feature in type 2 diabetic patients, are often accompanied by tissue hypoxia caused by metabolic overload and lead to increased free fatty acid (FFA) levels. However, the specific mechanisms underlying FFA-induced β-cell dysfunction remain unclear. Nicotinamide mononucleotide (NMN), a naturally occurring bioactive nucleotide, has garnered significant attention in recent years for its effectiveness in replenishing NAD+ and alleviating various diseases. Nevertheless, studies exploring the mechanisms through which NMN influences β-cell dysfunction remain scarce. In this study, we established an in vitro β-cell dysfunction model by treating INS-1 cells with palmitate (PA), including control, PA-treated, and PA combined with NMN or activator/inhibitor groups. Compared to the control group, cells treated with PA alone showed significantly reduced insulin secretion capacity and decreased expression of proteins related to the NAD+/AMPK/SIRT1/HIF-1α pathway. In contrast, NMN supplementation significantly restored the expression of pathway-related proteins by activating NAD+ and effectively improved insulin secretion. Results obtained using HIF-1α and AMPK inhibitors/activators further supported these findings. In conclusion, our study demonstrates that NMN reversed the PA-induced downregulation of the NAD+/AMPK/SIRT1/HIF-1α pathway, thereby alleviating β-cell dysfunction. Our study investigated the mechanisms underlying PA-induced β-cell dysfunction, examined how NMN mitigates this dysfunction and offered new insights into the therapeutic potential of NMN for treating β-cell dysfunction and T2DM. Full article
(This article belongs to the Special Issue Molecular Insights and Therapy in Diabetes)
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Review

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20 pages, 3225 KiB  
Review
Converging Pathways between Metabolic Dysfunction–Associated Steatotic Liver Disease (MASLD) and Diabetes in Children
by Maria Felicia Faienza, Ilaria Farella, Mohamad Khalil and Piero Portincasa
Int. J. Mol. Sci. 2024, 25(18), 9924; https://doi.org/10.3390/ijms25189924 - 14 Sep 2024
Cited by 2 | Viewed by 2004
Abstract
In the past thirty years, childhood obesity rates have risen significantly worldwide, affecting over 340 million children in affluent nations. This surge is intricately tied to metabolic disorders, notably insulin resistance, type 2 diabetes mellitus (T2DM), and the continually evolving spectrum of metabolic-associated [...] Read more.
In the past thirty years, childhood obesity rates have risen significantly worldwide, affecting over 340 million children in affluent nations. This surge is intricately tied to metabolic disorders, notably insulin resistance, type 2 diabetes mellitus (T2DM), and the continually evolving spectrum of metabolic-associated (dysfunction) steatotic liver disease (MASLD). This review underscores the alarming escalation of childhood obesity and delves comprehensively into the evolving and dynamic changes of nomenclature surrounding diverse conditions of hepatic steatosis, from the initial recognition of non-alcoholic fatty liver disease (NAFLD) to the progressive evolution into MASLD. Moreover, it emphasizes the crucial role of pediatric endocrinologists in thoroughly and accurately investigating MASLD onset in children with T2DM, where each condition influences and exacerbates the progression of the other. This review critically highlights the inadequacies of current screening strategies and diagnosis, stressing the need for a paradigm shift. A proposed solution involves the integration of hepatic magnetic resonance imaging assessment into the diagnostic arsenal for children showing insufficient glycemic control and weight loss post-T2DM diagnosis, thereby complementing conventional liver enzyme testing. This holistic approach aims to significantly enhance diagnostic precision, fostering improved outcomes in this vulnerable high-risk pediatric population. Full article
(This article belongs to the Special Issue Molecular Insights and Therapy in Diabetes)
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