tag:blogger.com,1999:blog-36840063.post2620703332305883585..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: Protons (31) insulin induced thermogenesis in the PimaPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger4125tag:blogger.com,1999:blog-36840063.post-33319836295342325232013-12-23T21:55:33.184+00:002013-12-23T21:55:33.184+00:00This comment has been removed by the author.Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-43487445597594380412013-12-23T07:38:14.653+00:002013-12-23T07:38:14.653+00:00...and of course PUFA should allow excess glycolys......and of course PUFA should allow excess glycolysis, which means we need to look at carnitoyl-PUFA/pyruvate/G3P and try to relate these to the cell membrane GLUT4s and CD36 populations! Way to go yet methinks.Peterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-70657667492726849902013-12-23T07:34:34.342+00:002013-12-23T07:34:34.342+00:00Hi raphi,
Yes, basal lipid oxidation appears to g...Hi raphi,<br /><br />Yes, basal lipid oxidation appears to generate marginally less ROS than pyruvate. But we never do basal pyrivate oxidation and we certainly never, ever do solo G3P dehydrogenation. Pyruvate is likely to be running at full chat before mtG3Pdh kicks in. We need this pattern to look at the damage done by hyperglycaemia. Then we need basal pyruvate plus sat fats, monounsats and PUFA...<br /><br />But Brand is walking in the correct direction...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-63710145809813134312013-12-22T16:08:21.328+00:002013-12-22T16:08:21.328+00:00I went through the paper. I understood their first...I went through the paper. I understood their first worked example and how it relates 'electron leakage' with ROS production & with how the electron distribution amongst various complexes affecting upstream and downstream complexes between the different isopotential redox carrier groups.<br /><br />This paper seems to suggest a great method for starting to pin down and characterize substrate behavior in terms of them being more or less able to provoke ROS production (even at "identical total rates of mitochondrial superoxide production")….damn!<br /><br />So - without going too far out on a ledge - doesn't this lend further credibility to someone wanting to use dietary fats as the primary fuel? ::: because most of the energy extraction from downstream fat-products occurs in the mitochondria and inne-rmembrane space where less 'leakage'/uncoupling should occur? Or have I tripped over my own feet?<br /><br />Thanks,<br /><br />Raphi<br /><br />raphihttps://www.blogger.com/profile/08992252569979714724noreply@blogger.com