ReviewAntioxidants (Basel, Switzerland)2021
Lipotoxic Impairment of Mitochondrial Function in β-Cells: A Review.
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Mitophagy and Noncoding RNA Regulation in Type 2 Diabetes Mellitus: Molecular Mechanisms, Tissue-Specific Evidence and Translational Perspective.Biomedicines · 2026Review
- Compositional recalibrations of cardiolipin integrate loss of stearoyl-CoA desaturase 1 activity with mitochondrial decay in lipid-laden pancreatic β-cells.Cell communication and signaling : CCS · 2026Article
- Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation.Biogerontology · 2026Review
- Intersecting Molecular Pathways in Cardiovascular Disease and Diabetes Mellitus: Emerging Roles of Inflammation and Therapeutics.Diabetes/metabolism research and reviews · 2026Review
- Toll of Chronic Metabolic Acidosis at Molecular, Cellular, and Systemic Levels: A Conceptual Framework to Revisit Type 2 Diabetes (T2D) Pathophysiology.Biomedicines · 2026Review
- Review
- Characterization and Schematic Modeling of Oxidized Fat Use in Swine Feeding: Metabolic and Productive Consequences-A Review.Animals : an open access journal from MDPI · 2026Review
- Article
- Palmitic but Not Oleic Acid Induces Pro-Inflammatory Dysfunction of Human Endothelial Cells from Different Vascular Beds In Vitro.International journal of molecular sciences · 2025Article
- Optimizing Exercise for Type 2 Diabetes Management: Comparative Insights from Aerobic, Resistance, Interval and Combined Training Protocols.Metabolites · 2025Review
- Metabolic Reprogramming Through Polyphenol Networks: A Systems Approach to Metabolic Inflammation and Insulin Resistance.Medical sciences (Basel, Switzerland) · 2025Review
- TLR4 mediates lipotoxic β-cell dysfunction by inhibiting the TMEM24/PI3K/AKT pathway.Acta biochimica et biophysica Sinica · 2025Article
- The hidden pathway: biological aging as a mediator between diabetes and breast cancer risk: a Mendelian randomized study.Discover oncology · 2025Article
- Early-Life Exposure to Bisphenol A Damaged Pancreas That May Increase Offspring Sensitivity to High-Fat Diets.Journal of toxicology · 2025Article
- Remodeling of the Intracardiac Ganglia During the Development of Cardiovascular Autonomic Dysfunction in Type 2 Diabetes: Molecular Mechanisms and Therapeutics.International journal of molecular sciences · 2024Review
- Article
- Review
- Investigating the Role of Non-Coding RNA in Non-Alcoholic Fatty Liver Disease.Non-coding RNA · 2024Review
- The Influences of Perinatal Androgenic Exposure on Cardiovascular and Metabolic Disease of Offspring of PCOS.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Molecular Processes Involved in the Shared Pathways between Cardiovascular Diseases and Diabetes.Biomedicines · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipotoxicity is a major contributor to type 2 diabetes mainly promoting mitochondrial dysfunction. Lipotoxic stress is mediated by elevated levels of free fatty acids through various mechanisms and pathways. Impaired peroxisome proliferator-activated receptor (PPAR) signaling, enhanced oxidative stress levels, and uncoupling of the respiratory chain result in ATP deficiency, while β-cell viability can be severely impaired by lipotoxic modulation of PI3K/Akt and mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated kinase (ERK) pathways. However, fatty acids are physiologically required for an unimpaired β-cell function. Thus, preparation, concentration, and treatment duration determine whether the outcome is beneficial or detrimental when fatty acids are employed in experimental setups. Further, ageing is a crucial contributor to β-cell decay. Cellular senescence is connected to loss of function in β-cells and can further be promoted by lipotoxicity. The potential benefit of nutrients has been broadly investigated, and particularly polyphenols were shown to be protective against both lipotoxicity and cellular senescence, maintaining the physiology of β-cells. Positive effects on blood glucose regulation, mitigation of oxidative stress by radical scavenging properties or regulation of antioxidative enzymes, and modulation of apoptotic factors were reported. This review summarizes the significance of lipotoxicity and cellular senescence for mitochondrial dysfunction in the pancreatic β-cell and outlines potential beneficial effects of plant-based nutrients by the example of polyphenols.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.