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Molecular Insights into Multifactorial Causes of Insulin Resistance in Obesity, 2nd Edition

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 1715

Editor

Dr. Bogdana Virgolici

E-Mail Website
Guest Editor
Department of Biochemistry, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania
Interests: obesity; diabetes mellitus; aging; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

A Western diet, high in unhealthy macronutrients, increases oxidative stress and inflammation by disturbing cellular redox balance and activating inflammatory signaling molecules, while reducing mitochondrial function. Elevated levels of glucose and free fatty acids worsen oxidative stress and inflammation through a series of molecular reactions that disrupt normal cellular metabolism, contributing to complications like atherosclerosis, hypertension, and diabetes mellitus. In contrast, fiber-rich meals help to reduce inflammation, improve insulin sensitivity (possibly by modulating the expression of genes related to insulin signaling), and prevent glycemic spikes. Including fruits, vegetables, and caloric restriction in your diet significantly lowers oxidative and inflammatory stress by influencing the molecular pathways involved in stress responses. Insulin resistance often develops years before type 2 diabetes mellitus and is influenced by genetic factors, physical inactivity, abdominal obesity, and excessive adipokines, which interact with various molecular components in insulin-related signaling cascades. Initially, hyperinsulinemia compensates to maintain normal glucose levels, but prolonged insulin resistance and reduced insulin secretion eventually lead to impaired glucose tolerance. Dietary strategies and bariatric surgery play vital roles in preventing insulin resistance, managing obesity, and maintaining metabolic health by acting on the molecular mechanisms underlying these physiological states.

You can read the publications in first volume here:

https://www.mdpi.com/journal/cimb/special_issues/2PVAA34M09.

Dr. Bogdana Virgolici
Guest Editor

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Keywords

  • obesity
  • inflammation
  • oxidative stress
  • insulin resistance
  • caloric restriction

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Published Papers (4 papers)

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Research

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14 pages, 2675 KB  
Article
Carnosic Acid Attenuates TNF-α-Induced Insulin Resistance by Regulating Mitochondrial Function in 3T3-L1 Adipocytes
by Chia-Yuan Lin, Lok-I Chan, Yu-Hsuan Chang, Meng-Chun Lu and Chia-Wen Tsai
Curr. Issues Mol. Biol. 2026, 48(7), 736; https://doi.org/10.3390/cimb48070736 - 20 Jul 2026
Viewed by 358
Abstract
The disruption of mitochondrial homeostasis is a trigger for insulin resistance. The loss of N-acetyltransferase 1 (Nat1) function, an insulin-sensitivity gene, contributes to mitochondrial dysfunction and insulin resistance. Carnosic acid (CA), a diterpene derived from rosemary, has demonstrated an anti-insulin-resistance effect. This study [...] Read more.
The disruption of mitochondrial homeostasis is a trigger for insulin resistance. The loss of N-acetyltransferase 1 (Nat1) function, an insulin-sensitivity gene, contributes to mitochondrial dysfunction and insulin resistance. Carnosic acid (CA), a diterpene derived from rosemary, has demonstrated an anti-insulin-resistance effect. This study hypothesized that CA protects against TNF-α-induced insulin resistance in 3T3-L1 adipocytes by regulating mitochondrial dynamics, biogenesis, and function via Nat1. 3T3-L1 adipocytes were pretreated with CA for 12 h, followed by co-treatment with TNF-α for an additional indicated duration. Results showed that treatment of 3T3-L1 adipocytes with TNF-α decreases mitochondrial membrane potential (MMP) and PGC-1α protein levels and alters mitochondrial fission/fusion dynamics. Pretreatment with CA improved these effects. In parallel, CA prevented the TNF-α-induced reduction in Nat1 protein and improved insulin signaling by suppressing the phosphorylation of insulin receptor substrate-1 (IRS-1) at serine307, while restoring the phosphorylation of IRS-1 at tyrosine628 and Akt. Moreover, transfection with Nat1 siRNA inhibited the protective effect of CA against TNF-α-induced reductions in MMP, PGC-1α, and insulin signaling. In conclusion, CA ameliorated TNF-α-induced insulin resistance by reducing mitochondrial dysregulation by Nat1. Full article
(This article belongs to the Special Issue Molecular Insights into Multifactorial Causes of Insulin Resistance in Obesity, 2nd Edition)
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20 pages, 4135 KB  
Article
Metabolic and Signaling Dysregulation in a Cellular Model of Hepatic Insulin Resistance
by Hawraa Zbeeb, Chourouk Joumaa, Giulia De Negri Atanasio, Alberto Diaspro and Laura Vergani
Curr. Issues Mol. Biol. 2026, 48(7), 729; https://doi.org/10.3390/cimb48070729 - 17 Jul 2026
Viewed by 366
Abstract
Insulin resistance (IR) is the underlying pathogenic mechanism for Type 2 Diabetes Mellitus, which is interconnected with Fatty Liver Disease. To investigate the molecular mechanisms by which different metabolic triggers contribute to hepatic IR onset, we exposed human HepG2 hepatocytes to varying [...] Read more.
Insulin resistance (IR) is the underlying pathogenic mechanism for Type 2 Diabetes Mellitus, which is interconnected with Fatty Liver Disease. To investigate the molecular mechanisms by which different metabolic triggers contribute to hepatic IR onset, we exposed human HepG2 hepatocytes to varying glucose concentrations (25–50 mM), and/or insulin (1 nM), and a free fatty acid mixture (0.3 mM), mimicking moderate or severe hyperglycemia, hyperinsulinemia, and steatosis. Glucose consumption, glycogen and lipid droplet (LD) accumulation, gene expression, oxidative stress, and insulin signaling were assessed. Under severe hyperglycemia, both insulin and fatty acids decreased glucose consumption, whereas under moderate hyperglycemia, only insulin had this effect. Glycogen accumulation was increased across all treated conditions. Both insulin and fatty acids triggered steatosis and downregulated PPARγ and SIRT1 mRNA, with insulin increasing LD number, while FFAs increased both LD number and size. All conditions enhanced ROS production, resulting in oxidative stress, but with differences in antioxidant enzyme response. Insulin receptor expression was reduced by insulin and FFAs under moderate hyperglycemia but increased by these stimuli under severe hyperglycemia. Both stimuli enhanced AKT phosphorylation under both hyperglycemic conditions. We conclude that different triggers cooperate in promoting hepatic IR through distinct molecular and signaling mechanisms, suggesting that effective treatments may need to target multiple pathways simultaneously. Full article
(This article belongs to the Special Issue Molecular Insights into Multifactorial Causes of Insulin Resistance in Obesity, 2nd Edition)
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23 pages, 3207 KB  
Article
Comparative Serum Proteomic Analysis of Different Habitual Coffee Consumption Among Healthy and Obese with and Without Hypertension Groups
by Jintana Sirivarasai, Sorsia Muttrarak, Prapimporn Chattranukulchai Shantavasinkul, Sittiruk Roytrakul, Waraporn Malilas, Pachara Panpunuan and Piyamitr Sritara
Curr. Issues Mol. Biol. 2026, 48(6), 556; https://doi.org/10.3390/cimb48060556 - 25 May 2026
Viewed by 458
Abstract
Coffee consumption has been associated with metabolic and cardiovascular health, but the molecular mechanisms underlying these associations remain unclear. This study investigated the association between coffee intake and circulating proteomic profiles across metabolic conditions using a pooled-serum, exploratory design. Participants were classified into [...] Read more.
Coffee consumption has been associated with metabolic and cardiovascular health, but the molecular mechanisms underlying these associations remain unclear. This study investigated the association between coffee intake and circulating proteomic profiles across metabolic conditions using a pooled-serum, exploratory design. Participants were classified into four groups: normal weight (NW), normal weight with coffee intake (NWC), obese with hypertension (OBHT), and obese with hypertension with coffee intake (OBHTC). Differentially expressed proteins (DEPs) were identified using volcano plot criteria (|log2FC| ≥ 1, FDR < 0.05), followed by Reactome pathway enrichment, Gene Ontology (GO) molecular function, and Enrichr-derived protein–protein interaction (PPI) analyses. Results: In NW vs. NWC, coffee intake was associated with proteins enriched in receptor-mediated signaling and phosphoinositide pathways. In OBHT vs. OBHTC, DEPs were linked to mitochondrial respiration and oxidoreductase activity. The NW vs. OBHT comparison showed downregulation of metabolic and signaling proteins with enrichment of mitochondrial and stress-response functions. In NWC vs. OBHTC, proteins related to cytokine signaling and vascular function were reduced, while redox-associated regulators were increased. PPI networks highlighted interconnected hubs integrating signaling, metabolism, and immune responses. Conclusion: These findings suggest context-dependent proteomic patterns associated with coffee intake. Given the pooled design and small sample size, results are hypothesis-generating and require validation. Full article
(This article belongs to the Special Issue Molecular Insights into Multifactorial Causes of Insulin Resistance in Obesity, 2nd Edition)
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Review

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29 pages, 1524 KB  
Review
Functional Connections Between Insulin and Neurotrophin-3 in Hemodialysis Patients with Type 2 Diabetes
by Mihaela Gheorghiu and Maria-Florina Trandafir
Curr. Issues Mol. Biol. 2026, 48(9), 884; https://doi.org/10.3390/cimb48090884 - 30 Aug 2026
Viewed by 167
Abstract
The bidirectional transfer of biological information between insulin and neurotrophin-3 (NT-3) in hemodialysis patients (end-stage renal disease—ESRD) with type 2 diabetes mellitus (T2DM) is extremely poorly studied. Why was NT-3 chosen? Because, of all the nerve growth factors, this one also exhibits specific [...] Read more.
The bidirectional transfer of biological information between insulin and neurotrophin-3 (NT-3) in hemodialysis patients (end-stage renal disease—ESRD) with type 2 diabetes mellitus (T2DM) is extremely poorly studied. Why was NT-3 chosen? Because, of all the nerve growth factors, this one also exhibits specific actions at the nephron level. The authors of this manuscript also conducted the first study on the serum behavior of NT-3 in this category of patients. Even though the results have already been published, the way in which an endocrine compound (insulin) interacts at the renal level with a growth factor with predominantly autocrine and paracrine action (NT-3), under both normal and pathological conditions, has not been thoroughly studied. This paper will address the following topics: 1. that insulin synthesis and release involve the same molecules that also exert important actions at the renal level; 2. involvement of insulin deficiency/resistance in the development of diabetic nephropathy and end-stage renal disease vs. kidney influences on serum glucose and insulin levels; 3. actions of NT-3 under normal conditions vs. diabetes mellitus; 4. aspects highlighted by personal studies performed on hemodialysis patients with T2DM. Taking an original approach, the functional link between insulin and NT-3 in hemodialysis patients, especially those with T2DM, will be presented. Finally, new therapeutic possibilities and directions for patient monitoring will be proposed, as well as topics for further research. Full article
(This article belongs to the Special Issue Molecular Insights into Multifactorial Causes of Insulin Resistance in Obesity, 2nd Edition)
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