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Catalog
Lipid-induced Insulin Resistance: Molecular Mechan ...
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Video Transcription
Video Summary
Dr. Swatinath Mukhopadhyay, professor and head at the Department of Endocrinology and Metabolism, discussed the topic of lipid-induced insulin resistance, its molecular mechanisms, and clinical implications. He explained that an excess of dietary lipids stimulates the production of fetuin A, a pro-inflammatory hepatokine that triggers a pro-inflammatory state and insulin resistance. Lipid loading in metabolically unhealthy adipose tissue produces kamerin, an adipokine that drives inflammation and macrophage polarization. Dr. Mukhopadhyay emphasized the role of organokines, including hepatokines, adipokines, and myokines, as potential targets to mitigate insulin resistance and prevent and treat type 2 diabetes. He discussed the impact of adipose tissue expansion, both through hyperplasia and hypertrophy, on insulin sensitivity. Dr. Mukhopadhyay highlighted the role of toll-like receptor 4 in immune function and inflammation and its relationship with fetuin A. He also discussed the role of pro-inflammatory cytokines, such as TNF alpha and interleukin-6, in causing insulin resistance. Dr. Mukhopadhyay mentioned various therapeutic approaches targeting inflammation for diabetes, including salicylates, low-dose methotrexate, interleukin-1 receptor antagonists, and SGLT2 inhibitors. He also touched on the potential benefits of GLP-1 receptor agonists, thiazolidinediones, and metformin in reducing inflammation and improving insulin sensitivity. Finally, Dr. Mukhopadhyay highlighted the potential of vanadium compounds as insulin mimetics and their ability to rescue phosphotyrosine levels and improve metabolic function.
Keywords
lipid-induced insulin resistance
fetuin A
inflammation
insulin sensitivity
pro-inflammatory cytokines
therapeutic approaches
GLP-1 receptor agonists
vanadium compounds
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