By Novartis Foundation
The aptitude lipotoxic impact of accumulation of fatty acids in non-adipose tissues is believed to be an immense part within the improvement of insulin resistance. continual publicity to excessive concentrations of unfastened fatty acids within the blood impacts pancreatic ? mobile functionality, insulin secretion and lipid synthesis within the liver, and garage in adipose tissue. holding the conventional degrees of fatty acids calls for coordinated legislation among the liver, adipose tissue and skeletal muscle.This ebook offers with the molecular features of fatty acid motion in weight problems and insulin resistance. the themes comprise lipid metabolism and adipose tissue biology, and ? cellphone functionality and insulin resistance. Chapters take care of the molecular genetics and molecular body structure of strength homeostasis.
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Extra resources for Fatty Acid and Lipotoxicity in Obesity and Diabetes (Novartis Foundation Symposium 286)
Compared to the control condition, both starvation and high fat feeding increased 14C labelling of the ASM fraction. Thus, mitochondria from rats fed on a high fat compared to a standard chow diet displayed similar rates of [14C]palmitate oxidation to CO2 , but accumulated more radiolabelled intermediates in an acid-soluble pool (Koves et al 2005a). Additionally, pyruvatemediated inhibition of palmitate oxidation, which was robust in normal mitochondria, was severely blunted after high fat feeding.
Trends Cell Biol 12:65–71 Shoelson SE, Lee J, Yuan M 2003 Inflammation and the IKK beta/I kappa B/NF-kappa B axis in obesity- and diet-induced insulin resistance. Int J Obes Relat Metab Disord 27 Suppl 3:S49–52 Shulman GI 2000 Cellular mechanisms of insulin resistance. J Clin Invest 106:171–176 Sparks LM, Xie H, Koza RA et al 2005 A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle. Diabetes 54:1926–1933 Unger RH 2002 Lipotoxic diseases.
This cascade depends on tyrosine (activating) phosphorylation of proximal signalling molecules such as the insulin receptor (IR) and insulin receptor substrate 1 (IRS1) (Saltiel & Pessin 2002). Mounting evidence from both human and animal studies suggests that lipid-induced insulin resistance is mediated in large part by serine phosphorylation of the IR and IRS1 (Hirosumi et al 2002, Perseghin et al 2003, Saltiel & Pessin 2002, Shoelson et al 2003), and that these modifications are executed by stress-activated serine kinases such as protein kinase C (PKC) and cJun terminal kinase (JNK) (Shulman 2000, Yu et al 2002, Griffin et al 1999).