Biomarkers and Therapeutic Targets in Insulin Resistance

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 548

Special Issue Editor


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Guest Editor
Biomedical Research Center, Qatar University, Doha, Qatar
Interests: insulin resistance; biomarkers; therapeutic targets; type 2 diabetes

Special Issue Information

Dear Colleagues,

Insulin resistance plays a major role in the pathogenesis of metabolic diseases, including type 2 diabetes, obesity, and cardiovascular disease. Understanding the underlying molecular mechanisms and identification of novel biomarkers and therapeutic targets are critical for early diagnosis and treatment. This Special Issue, entitled "Biomarkers and Therapeutic Targets in Insulin Resistance", will offer a platform to discuss the current progress in this area, with an emphasis on molecular, genetic, and biochemical markers for the prediction and monitoring of insulin resistance. Novel therapeutic approaches, including pharmacologic agents, lifestyle changes, and personalized medicine treatment, to manage insulin resistance and its complications will also be featured. This special seeks to provide a comprehensive overview of the state of knowledge and avenues for future research in this rapidly evolving area.

Dr. Mohamed Elrayess
Guest Editor

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Keywords

  • insulin resistance
  • biomarkers
  • therapeutic targets
  • type 2 diabetes
  • metabolic syndrome
  • obesity
  • molecular mechanisms
  • pharmacologic treatments
  • precision medicine
  • cardiovascular diseases

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Published Papers (1 paper)

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Research

15 pages, 1709 KB  
Article
N-Lactoyl Phenylalanine Disrupts Insulin Signaling, Induces Inflammation, and Impairs Mitochondrial Respiration in Cell Models
by Laila Hedaya, Khaled Naja, Shamma Almuraikhy, Najeha Anwardeen, Asma A. Elashi, Maha Al-Asmakh, Susu M. Zughaier, Meritxell Espino-Guarch, Osama Y. Aldirbashi, Gavin P. Davey and Mohamed A. Elrayess
Cells 2025, 14(16), 1296; https://doi.org/10.3390/cells14161296 - 20 Aug 2025
Viewed by 336
Abstract
N-lactoyl amino acids (Lac-AAs) are key players that regulate appetite and body weight. The most prominent and well-studied member is N-lactoyl phenylalanine (Lac-Phe), which can be induced by food intake, exercise and metformin treatment. However, its broader metabolic impact remains insufficiently characterized. This [...] Read more.
N-lactoyl amino acids (Lac-AAs) are key players that regulate appetite and body weight. The most prominent and well-studied member is N-lactoyl phenylalanine (Lac-Phe), which can be induced by food intake, exercise and metformin treatment. However, its broader metabolic impact remains insufficiently characterized. This study investigates the effects of Lac-Phe on insulin signaling, inflammation, and mitochondrial respiration using HepG2 and differentiated C2C12 cell models, as well as isolated rat brain mitochondria and synaptosomes. Our results demonstrate that Lac-Phe significantly impairs insulin-stimulated phosphorylation of key proteins in the insulin signaling pathway, particularly in skeletal muscle cells, indicating disrupted insulin signaling. Additionally, Lac-Phe exposure increases the secretion of pro-inflammatory cytokines in C2C12 skeletal muscle cells and markedly impairs mitochondrial respiration in HepG2 liver cells and rat brain-derived synaptosomes, but not in isolated mitochondria. These findings highlight potential adverse metabolic effects of Lac-Phe, especially when administered at high concentrations, and underscore the necessity of conducting a comprehensive risk assessment and dose optimization before considering Lac-Phe or related Lac-AAs as therapeutic agents. Our work provides important insights into the molecular liabilities associated with Lac-Phe and calls for further studies to balance its therapeutic promise against possible metabolic risks. Full article
(This article belongs to the Special Issue Biomarkers and Therapeutic Targets in Insulin Resistance)
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