Download Fatty Acids and Lipotoxicity in Obesity and Diabetes: by Novartis Foundation PDF

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By Novartis Foundation

The capability lipotoxic influence of accumulation of fatty acids in non-adipose tissues is believed to be an important part within the improvement of insulin resistance. persistent 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. retaining the conventional degrees of fatty acids calls for coordinated law among the liver, adipose tissue and skeletal muscle.

This e-book bargains with the molecular features of fatty acid motion in weight problems and insulin resistance. the subjects comprise lipid metabolism and adipose tissue biology, and ? mobile functionality and insulin resistance. Chapters take care of the molecular genetics and molecular body structure of power homeostasis.Content:

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Extra info for Fatty Acids and Lipotoxicity in Obesity and Diabetes: Novartis Foundation Symposium 286

Example text

The exercise-activated transcriptional co-activator, PGC1α , plays a key role in co-ordinating metabolic flux through these two intersecting metabolic pathways, and its suppression by overfeeding may contribute to obesity-associated mitochondrial dysfunction. Our emerging model predicts that muscle insulin resistance arises from mitochondrial lipid stress and a resultant disconnect between β -oxidation and TCA cycle activity. Understanding this ‘disconnect’ and its molecular basis may lead to new therapeutic targets for combating metabolic disease.

2A). This emergent model holds that lipid-induced upregulation of the enzymatic machinery for β -oxidation of fatty acids is not always supported by a co-ordinated increase in downstream metabolic pathways such as the tricarboxylic acid (TCA) cycle and electron transport chain (Koves et al 2005a, Muoio & Newgard 2006). The concept of incomplete fuel oxidation was initially guided by the foregoing microarray studies, and later substantiated in experiments that contrasted the metabolic consequences of enhancing fatty acid supply to muscle via changes in fibre type, exercise, overnight starvation or high fat feeding (Koves et al 2005a, 2005b).

Kadowaki: Why do you think that PPARα agonists have an insulin sensitising effect on the liver, even though it stimulates β oxidation of lipids? Spiegelman: That might be an anti-steatotic effect. If we step away from the energetics, it could be that liver steatosis is a bad thing. We can make a unifying hypothesis: on the one hand, activation of PPARα in the liver has a beneficial effect through anti-steatosis. It also causes cancer in the rats, which could be from ROS production. You are getting β oxidation that exceeds ATP utilization, with an electron leak into the ROS, but you are also getting rid of the steatosis.

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