Protection Strategies Against Palmitic Acid-Induced Lipotoxicity in Metabolic Syndrome and Related Diseases

Ceja-Galicia, Zeltzin Alejandra; Cespedes-Acuña, Carlos Leonardo Armando; El-Hafidi, Mohammed

doi:10.3390/ijms26020788

Cited by 62Lipid metabolism and biosynthesisDiet, Metabolism, and DiseaseCancer, Lipids, and Metabolism

Protection Strategies Against Palmitic Acid-Induced Lipotoxicity in Metabolic Syndrome and Related Diseases

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Ceja-Galicia, Zeltzin Alejandra, Cespedes-Acuña, Carlos Leonardo Armando, El-Hafidi, Mohammed·2025·International Journal of Molecular Sciences

DOI 10.3390/ijms26020788PMC PMC11765695

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Abstract

Diets rich in carbohydrate and saturated fat contents, when combined with a sedentary lifestyle, contribute to the development of obesity and metabolic syndrome (MetS), which subsequently increase palmitic acid (PA) levels. At high concentrations, PA induces lipotoxicity through several mechanisms involving endoplasmic reticulum (ER) stress, mitochondrial dysfunction, inflammation and cell death. Nevertheless, there are endogenous strategies to mitigate PA-induced lipotoxicity through its unsaturation and elongation and its channeling and storage in lipid droplets (LDs), which plays a crucial role in sequestering oxidized lipids, thereby reducing oxidative damage to lipid membranes. While extended exposure to PA promotes mitochondrial reactive oxygen species (ROS) generation leading to cell damage, acute exposure of ß-cells to PA increases glucose-stimulated insulin secretion (GSIS), through the activation of free fatty acid receptors (FFARs). Subsequently, the activation of FFARs by exogenous agonists has been suggested as a potential therapeutic strategy to prevent PA-induced lipotoxicity in ß cells. Moreover, some saturated fatty acids, including oleic acid, can counteract the negative impact of PA on cellular health, suggesting a complex interaction between different dietary fats and cellular outcomes. Therefore, the challenge is to prevent the lipid peroxidation of dietary unsaturated fatty acids through the utilization of natural antioxidants. This complexity indicates the necessity for further research into the function of palmitic acid in diverse pathological conditions and to find the main therapeutic target against its lipotoxicity. The aim of this review is, therefore, to examine recent data regarding the mechanism underlying PA-induced lipotoxicity in order to identify strategies that can promote protection mechanisms against lipotoxicity, dysfunction and apoptosis in MetS and obesity.

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ROS accumulation triggers damaging cascades: a decrease in mitochondrial membrane potential, activation of caspases 3/7, apoptosis, and ER stress and inflammation via NF-κB.
“ROS accumulation triggers damaging cascades: a decrease in mitochondrial membrane potential, activation of caspases 3/7, apoptosis, and ER stress and inflammation via NF-κB [90,152,153,154,155].”
From The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease (2026) · cites this paper as [155]
Section 3.2 (page unavailable) links palmitic-acid-induced mitochondrial dysfunction with ROS generation, collapse of mitochondrial membrane potential, caspase-3 activation and apoptosis. Section 3.3 describes ROS-associated inflammation through NF-κB. The copy does not establish caspase-7 activation, and section 3.1 describes ER stress as contributing to ROS accumulation rather than ROS triggering ER stress. (LLM, conf=0.86)
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Palmitic acid induces β-cell ferroptosis by activating ceramide signaling pathway
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Increased oxidative stress and mitochondrial impairments associated with increased expression of TNF‐α and caspase‐3 in palmitic acid‐induced lipotoxicity in myoblasts
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Quercetin and Its Derivative Counteract Palmitate-Dependent Lipotoxicity by Inhibiting Oxidative Stress and Inflammation in Cardiomyocytes
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The fate of intracellular S1P regulates lipid droplet turnover and lipotoxicity in pancreatic beta-cells
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Inhibition of Lipid Accumulation and Oxidation in Hepatocytes by Bioactive Bean Extracts
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Progress and potentialities in wood extractives-based materials for active food packaging applications
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EGCG regulation of non-insulin-responsive endosomal compartments in insulin-resistant skeletal muscle
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Baicalein ameliorates lipid accumulation in HepG2 cells via the pregnane X receptor signaling pathway
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Deletion of serine palmitoyl transferase 2 in hepatocytes impairs ceramide/sphingomyelin balance, prevents obesity and leads to liver damage in micePreprint
Lallement, J., Raho, I., Merlen, G., Rainteau, D. P., Croyal, M., Schiffano, M., Kassis, N., Doignon, I., Soty, M., Lachkar, F., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.09.16.460588 · Cited by 1 · see citing works
Subcellular Organelles
Lin, P., & Zhou, D. H. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811297-7.00007-x · Cited by 1 · see citing works

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[65]Zuccaro K.E. Abriata L.A. Meireles F.T.P. Moss F.R. Frost A. Dal Peraro M. Aydin H. Cardiolipin clustering promotes mitochondrial membrane dynamics bioRxiv 2024 10.1101/2024.05.21.595226 · DOI

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Authors: Ceja-Galicia, Z. A., Cespedes-Acuña, C. L. A., & El-Hafidi, M.
Affiliations: Instituto Nacional de Cardiología (MX)
Departamento de Ciencias Básicas, Facultad de Ciencias, Universidad del Bio Bio, Avenida Andres Bello 720, Chillan 3780708, Chile
Departamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico
ORCID: Ceja-Galicia, Zeltzin Alejandra
Cespedes-Acuña, Carlos Leonardo Armando
Venue: International Journal of Molecular Sciences
Publisher: MDPI AG
Published: 2025-01-18
Volume: 26
Issue: 2
Pages: 788
ISSN: 1422-0067 (ISSN-L)
DOI: 10.3390/ijms26020788
PMC: PMC11765695
OpenAlex: W4406676971
Cited by: 61
References: 176
Citations by year: 2026: 39 · 2025: 22
FWCI: 6.06
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
Locations: International Journal of Molecular Sciences (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Keywords: palmitic acid, lipotoxicity, metabolic syndrome, obesity, endoplasmic reticulum stress, mitochondrial dysfunction, inflammation, lipid droplets, free fatty acid receptors, glucose-stimulated insulin secretion, pancreatic beta cells, oleic acid, lipid peroxidation, antioxidants, saturated fatty acids, dietary fat
MeSH terms: Animals, Humans, Mitochondria, Obesity, Reactive Oxygen Species, Oxidative Stress, Palmitic Acid, Metabolic Syndrome, Lipid Metabolism, Endoplasmic Reticulum Stress

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Protection Strategies Against Palmitic Acid-Induced Lipotoxicity in Metabolic Syndrome and Related Diseases

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