A global perspective on the crosstalk between saturated fatty acids and Toll-like receptor 4 in the etiology of inflammation and insulin resistance |
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| Affiliation: | 1. Department of Psychiatry, University of Vermont, Burlington, VT, USA;2. Department of Medical Biostatistics, University of Vermont, Burlington, VT, USA;3. Department of Radiology, University of Vermont, Burlington, VT, USA;4. Department of Medicine, University of Vermont, Burlington, VT, USA;5. College of Medicine Clinical Research Center, University of Vermont, Burlington, VT, USA;6. Department of Pediatrics, University of Vermont, Burlington, VT, USA;1. School of Public Health and Joint China-US Research Center for Environment and Pulmonary Diseases, Zhejiang Chinese Medical University, Hangzhou, China;2. College of Medicine, Hangzhou Normal University, Hangzhou, China;3. Department of Gynecology, Tongde Hospital of Zhejiang Province, Hangzhou, China;4. College of Life Science, Zhejiang Chinese Medical University, Hangzhou, China;5. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China;6. Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan, USA;7. Department of Physiology & Biophysics, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA;8. College of Public Health, The Ohio State University, Columbus, Ohio, USA |
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| Abstract: | Obesity is featured by chronic systemic low-grade inflammation that eventually contributes to the development of insulin resistance. Toll-like receptor 4 (TLR4) is an important mediator that triggers the innate immune response by activating inflammatory signaling cascades. Human, animal and cell culture studies identified saturated fatty acids (SFAs), the dominant non-esterified fatty acid (NEFA) in the circulation of obese subjects, as non-microbial agonists that trigger the inflammatory response via activating TLR4 signaling, which acts as an important causative link between fatty acid overload, chronic low-grade inflammation and the related metabolic aberrations. The interaction between SFAs and TLR4 may be modulated through the myeloid differentiation primary response gene 88-dependent and independent signaling pathway. Greater understanding of the crosstalk between dietary SFAs and TLR4 signaling in the pathogenesis of metabolic imbalance may facilitate the design of a more efficient pharmacological strategy to alleviate the risk of developing chronic diseases elicited in part by fatty acid overload. The current review discusses recent advances in the impact of crosstalk between SFAs and TLR4 on inflammation and insulin resistance in multiple cell types, tissues and organs in the context of metabolic dysregulation. |
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