tag:blogger.com,1999:blog-36840063.post5902860064678606614..comments2024-03-27T22:57:00.742+00:00Comments on Hyperlipid: Protons (35) TFAM-KO revisitedPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger11125tag:blogger.com,1999:blog-36840063.post-62674997350926618062014-03-09T06:40:18.092+00:002014-03-09T06:40:18.092+00:00The age-split result was the third attempt at frac...The age-split result was the third attempt at fracking the data, the first two attempts gave null effect for the "protein=death" hypothesis.<br />Third time lucky, unless there were other failed attempts they didn't write up.<br />It's not like the correlation was obvious from the raw data. That's always going to look suspicious.<br />Thanks for the info they're longevity wonks rather than vegans. I thought it was one or the other (there are so many authors it's a manifesto).<br />Writing about the null effects they found might have had a detrimental effect on the funding of research into a subject they obviously all feel passionate about.<br /><br />Any way I thought this was interesting:<br />A switch in the source of ATP production and a loss in capacity to perform glycolysis are hallmarks of hepatocyte failure in advance liver disease.<br />http://www.ncbi.nlm.nih.gov/pubmed/24583248<br /><br />In the early phase of cirrhosis, mitochondrial function and ATP generation are maintained by increasing energy production from glycolytic flux as production from oxidative phosphorylation falls. At the terminal stage of hepatic injury, mitochondria respiration and ATP production are significantly compromised, as the hepatocytes are unable to sustain the increased demand for high levels of ATP generation from glycolysis. This impairment corresponds to a decrease in glucose-6-phosphatase catalytic subunit and phosphoglucomutase 1. Similar decreased gene expression was observed in liver tissue from patients at different stages of chronic liver injury. Further, unbiased network analysis of microarray data revealed that these genes' expression was down regulated in the group of patients with poor outcome.<br />CONCLUSIONS:<br />An adaptive metabolic shift, from generating energy predominantly from oxidative phosphorylation to glycolysis, allows maintenance of energy homeostasis during early stages of liver injury, but **leads to hepatocyte dysfunction** during terminal stages of chronic liver disease because hepatocytes are unable to sustain high levels of energy production from glycolysis.<br />Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-66906273378046145082014-03-06T14:14:56.950+00:002014-03-06T14:14:56.950+00:00Hey guys, anyone read or have comments on this man...Hey guys, anyone read or have comments on this manuscript?<br /><br />http://www.cell.com/cell-metabolism/abstract/S1550-4131(14)00062-X<br /><br />Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population<br /><br /><br />These guys appear to be longevity wonks, not vegan activists. I don't know that they locked into the right cause for the association they mined from NHANES III, but seems pretty convincing that something is going on. <br /><br />Might be worth a look?<br /><br />-- <br />PhillipNKSL55https://www.blogger.com/profile/17740938677114441960noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-2185974872011016072014-03-05T19:53:45.611+00:002014-03-05T19:53:45.611+00:00I wonder if DNP does the same thing to mitochondri...I wonder if DNP does the same thing to mitochondria in adipocytes?<br /><br />Sorry to bring this up again, but I noticed while running DNP that weight gain seems impossible. Although I wont lose weight on DNP while still eating alot of carbs, I can absolutely pig out on junk food and not gain anything, except some water weight.Kindkehttps://www.blogger.com/profile/15841418412425329998noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-35518732201828131762014-03-01T20:18:55.946+00:002014-03-01T20:18:55.946+00:00I believe Marion Nestle honestly believes Lustig s...I believe Marion Nestle honestly believes Lustig said fructose wasn't a poison.<br /><br />I doubt that he actually said this--or at least that what he meant was what she understood.<br /><br />He said, she said.donnyhttps://www.blogger.com/profile/02107555662488785352noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-125169353241768462014-02-26T21:21:26.525+00:002014-02-26T21:21:26.525+00:00This comment has been removed by the author.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-14506336472407705582014-02-26T17:50:15.648+00:002014-02-26T17:50:15.648+00:00Dr. Feinman raked him over the coals on this at AH...Dr. Feinman raked him over the coals on this at AHS 2011.Anonymoushttps://www.blogger.com/profile/06619419812590914435noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-59477632221870908212014-02-25T18:50:54.765+00:002014-02-25T18:50:54.765+00:00Remember Robert Lustig, of the youtube video "...Remember Robert Lustig, of the youtube video "Sugar the bitter truth"? <br /><br />http://www.youtube.com/watch?v=dBnniua6-oM<br /><br />I've often felt that he twisted the truth at times, maybe feeling justified because he's fighting for public health and children's in particular. But at least he's fighting the good fight and the hardcore part, where he explains very scientifically how fructose and ethanol are metabolized by the liver in the same way, that part had to be the one unquestionable fact, right?<br /><br />I just watched this interesting lecture by scientist Marion Nestle.<br /><br />http://www.youtube.com/watch?v=IEwRO2nyFKE<br /><br />On minute 053:21 she claims she cornered Lustig and forced him to confirm if he really believes that sugar is literally a poison, as he says on his video (minute 020:25). She claims that he denied ever having said any such thing.<br /><br />If you watch the 020:25 minute mark of Lustig's video you see him say that sugar is indeed a poison -which he then proceeds to repeat quite often throughout his lecture and goes at great lengths to explain the hows and the whys. That's the whole point of his now famous lecture. He didn't even say to Nestle that he's since changed his mind, he denied ever having said it in the first place.<br /><br />Is there any reason why he's turning into a pathological liar? Why would he deny it when the video is evidence? Isn't the whole point of his career that sugar is poison? I just don't understand this.Mhttps://www.blogger.com/profile/14679839426291667211noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-11089470348882711692014-02-24T00:29:00.909+00:002014-02-24T00:29:00.909+00:00Peter you might like to look back at this old pape...Peter you might like to look back at this old paper.http://cancerres.aacrjournals.org/content/30/8/2223.full.pdf Hepatoma in sucrose causes swollen mitochondria. This means Ca efflux and Phosphate concentrated. Water excluded and the EZ decreases........Same thing happens in metsyn. Here is the funny thing......mitochondria also concentrate some transition metals when this happens. This means their mass rises when the swell too. When masses rises things burn fuel at a faster rate. This happens in a star that is dying and a mitochondria that is under assault. Physics 101. Burning fuels at a faster rate means more ROS and RNS. This means that the voltage on the inner mitochondrial membrane is higher when this happens. Now think about your proton series and delta psi and what the mitochondria are doing. And then remember that ketones lower the voltage when they are the primary fuel source. I think you'll get this chain of events. It begins to show you why ketosis cancer and metsyn all walk together. Anonymoushttps://www.blogger.com/profile/06619419812590914435noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-67958691833714865102014-02-23T21:44:48.920+00:002014-02-23T21:44:48.920+00:00Hi Peter
I'm very uneducated when it comes to...Hi Peter<br /><br />I'm very uneducated when it comes to this area. So could you possibly dumb it down a little for me...ok ok a lot :) (I did say I was uneducated in this field) <br /><br />I've been eating lchf for a solid 5 months now, but as far as my understanding goes, if I have high insulin won't that make my body store fat and prevent me from burning it? Even though I'm eating <10 carbs and moderate protein and very high fat? <br /><br />I appreciate any response.....hopefully dumbed down to my level ;) as I know this is a old thread.<br /><br />Jen xAnonymoushttps://www.blogger.com/profile/09812954598682457030noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-78971397473761251002014-02-19T10:17:33.568+00:002014-02-19T10:17:33.568+00:00Sorry, I wrote that in a hurry and got it the wron...Sorry, I wrote that in a hurry and got it the wrong way round. Nox4 knockouts are fat, not thin. Nox4 makes them thin, which means it might be doing that in TFAM knockouts.Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-6222950094415269662014-02-18T16:45:24.304+00:002014-02-18T16:45:24.304+00:00Peter, it looks like the superoxide in adipocytes ...Peter, it looks like the superoxide in adipocytes doesn't come from mitochondria but from NADPH oxidase. Insulin activates Nox4. You'd have thought Nox4 knockouts would be fat, but they're thin, like TFAM knockouts.<br /><br />http://www.jbc.org/content/287/13/10379.full<br />http://www.ncbi.nlm.nih.gov/pubmed/22430302<br />Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.com