By Novartis Foundation
The capability lipotoxic influence of accumulation of fatty acids in non-adipose tissues is assumed to be a big part within the improvement of insulin resistance. persistent publicity to excessive concentrations of loose fatty acids within the blood impacts pancreatic ? mobile functionality, insulin secretion and lipid synthesis within the liver, and garage in adipose tissue. protecting the traditional degrees of fatty acids calls for coordinated legislation among the liver, adipose tissue and skeletal muscle.This ebook bargains with the molecular elements of fatty acid motion in weight problems and insulin resistance. the themes comprise lipid metabolism and adipose tissue biology, and ? phone functionality and insulin resistance. Chapters take care of the molecular genetics and molecular body structure of strength homeostasis.
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Additional info for Fatty Acid and Lipotoxicity in Obesity and Diabetes (Novartis Foundation Symposium 286)
Hotamisligil: Mitochondrial dysfunction will produce ROS, ROS will activate JNK, JNK will activate cytokines and cytokines will activate ROS. It’s a cycle. Muoio: The stress kinases are most certainly considered in our model. We propose that mitochondrial events feed into those pathways. Hotamisligil: If you could find a way to dissociate these events, this would be very important and a significant advance. Spiegelman: That’s tough. I’m not sure how they could be dissociated. Glass: It may be different in different tissues.
PGC1α enhances complete oxidation of fatty acids. Fatty acid oxidation was evaluated in rat L6 myocytes treated with recombinant adenoviruses encoding β -galactosidase ( β -gal) or PGC1α , compared against a no virus control (NVC) group. 48 h after addition of virus, cells were incubated for 3 h with 100–500 µ M [14C]oleate. Complete (A) and incomplete (B) fatty acid oxidation was determined by measuring 14C label incorporation into CO2 and acid soluble metabolites (ASM), respectively. (C) The relationship between incomplete and complete fatty acid oxidation was expressed as a ratio of label incorporated into ASM divided by labelling of CO2 .
On the other hand, fatty acids and their lipid by-products are thought to play a major role in the pathogenesis of metabolic disease. Research from our laboratory and many others indicates that both adaptive and maladaptive responses to fatty acids are driven in large part by the peroxisome proliferatoractivated receptor (PPAR) family of nuclear hormone receptors. These receptors function as molecular sensors of the cellular lipid milieu (Gilde & Van Bilsen 2003). They are bound and activated by fatty acids and other lipid metabolites, and in turn initiate transcriptional programmes that regulate fatty acid metabolism.
Fatty Acid and Lipotoxicity in Obesity and Diabetes (Novartis Foundation Symposium 286) by Novartis Foundation