tag:blogger.com,1999:blog-36840063.post60173409758790128..comments2024-03-27T22:57:00.742+00:00Comments on Hyperlipid: Cell surface oxygen consumption (3) Alternative optionsPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger1125tag:blogger.com,1999:blog-36840063.post-66564604411390488382019-02-12T12:29:18.132+00:002019-02-12T12:29:18.132+00:00Nice paper. I will print myself a copy for slow co...Nice paper. I will print myself a copy for slow contemplation in the hope that I'll understand some of it!<br /><br />'Note that the glutamate is not being oxidised, it is running a small section of the TCA backwards to generate citrate for lipid synthesis, ie anabolism. '<br /><br />This is strongly reminiscent of the truncated TCA in hepatocytes due to physiological Salicylate shown in the paper I mentioned recently ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2651525/ ). See in their first diagram that salicylate inhibits the TCA before the KGDH step likewise decreasing production of NADH.<br /><br />They refer to an older paper dealing with truncated TCA under high energy demand Kondrashova, M.N. 1989, abstract at https://europepmc.org/abstract/med/2669978<br /><br />The claim is that the slower part of the TCA is being side-stepped. Makes sense. <br /><br /> Wikip. informs me that deamination of glutamate by GDH is a method of dealing with excess nitrogen, converting it to ammonia which is further processed to Urea in the liver. Reminds me of the aspirin/gout connection.<br /><br /> High salicylate fruit, anyone?Passthecreamhttps://www.blogger.com/profile/01214860448492630477noreply@blogger.com