tag:blogger.com,1999:blog-36840063.post788270444687808959..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: Skulachev in 1978Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger8125tag:blogger.com,1999:blog-36840063.post-26799431501068680992017-04-20T05:09:29.688+00:002017-04-20T05:09:29.688+00:00Tucker, oh yes!
PeterTucker, oh yes!<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-55680395261473736092017-04-19T21:40:36.680+00:002017-04-19T21:40:36.680+00:00"Skulachev is still publishing important stuf..."Skulachev is still publishing important stuff today..."<br /><br />I'll say. I was quite annoyed to come to my great (I thought) insight about cardiolipin and metabolic syndrome only to discover Mr. Skulachev was not only aleady there, but had already developed a drug to treat it, and it was in human trials.<br /><br />The guy's a genius, for sure.Tucker Goodrichhttps://www.blogger.com/profile/09455436946187786398noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-37318836057215838832017-04-18T17:56:32.113+00:002017-04-18T17:56:32.113+00:00From your link
"Results show the specific act...From your link<br /><i>"Results show the specific action of insulin on E. coli, inhibiting tryptophanase induction and adenylate cyclase activity, while stimulating growth on glucose and uptake and phosphorylation of alpha-methylglucoside."</i><br /><br />So early insulin dates back to prokaryotes... wow. So what would drive the production and export of insulin in an E. coli? I suppose if sugar gets too high it becomes a 'bad thing' - tell your neighbors to consume it? <br /><br />Looks like a growth factor -- If I imagine a group of E.coli - having some external signal must benefit the group - in some way to preserve the gene. Sort of a first step in subverting the good of the cell to the good of the colony. It would not be good to out grow foodsupply/oxygen <br />,.,<br /><br />In our cells - if insulin is the system-wide feedback - and more available where circulation is good - it could limit overgrowth in areas that where cells would overgrow their oxygen supply. Insulin sensitivity would be the local feedback - more important and dominant in effect.<br /><br />A diet of artificial food that breaks insulin sensitivity regulation seems like a really bad thing.karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-17776673444098615772017-04-18T09:14:11.003+00:002017-04-18T09:14:11.003+00:00karl,
https://www.ncbi.nlm.nih.gov/pubmed/7016870...karl,<br /><br />https://www.ncbi.nlm.nih.gov/pubmed/7016870<br />https://www.ncbi.nlm.nih.gov/pubmed/356893<br /><br />Insulin is so oooooooold!<br /><br />The Na+/K+ buffer for protons has to be post-LUCA because it needs proton tight membranes. The Na+/K+ system probably predates the proton tight membranes so is probably the system LUCA used and proton gradients were added on to this...... But the paper gives insight in to how the system works today. Now we need to know where insulin and it's receptor are derived from. I'm wondering (guessing blindly!) if it might be from a K+ channel pore...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-78740799492683771612017-04-17T21:15:43.486+00:002017-04-17T21:15:43.486+00:00Hmm very complicated paper. I'm wondering if ...Hmm very complicated paper. I'm wondering if the stages of effect might help make sense of it all.<br /><br />If first Insulin shuts down burning fat - then moves potassium - is it part of an energy backup system?<br /><br />This is the middle point of shifting from fat to sugar - is there a need to have one off before the other starts? And thus something needs to power the cell while shifting?<br /><br />I put together some insulin notes <a href="https://xtronics.com/wiki/insulin.html" rel="nofollow"> here </a> as it was bothering me that the "insulin controls blood sugar" narrative is so incomplete that it misleads. If you think of a system with constant insulin - and then think of insulin sensitivity being what controls things - things get closer to the truth.<br /><br />As most evolved proteins, insulin does not have a single function - To say that insulin has one job - to regulate BG levels points people in the wrong direction.<br /><br />If I think of constant insulin - and shifting sensitivity - and the shift is due to <a href="http://high-fat-nutrition.blogspot.com/2012/08/protons-fadh2nadh-ratios-and-mufa.html" rel="nofollow"> FADH2:NADH ratios </a> - we are back to ions.<br /><br /><br />I started thinking of the evolution of insulin and found this:<br /><br /><a href="https://academic.oup.com/endo/article-abstract/104/5/1393/2592325/The-Insulin-Receptor-in-Vertebrates-Is?redirectedFrom=fulltext" rel="nofollow">The Insulin Receptor in Vertebrates Is Functionally More Conserved during Evolution than Insulin Itself </a><br /><br /><br /><br />There are other papers about the evolution with the related IGF - I'm now wondering did insulin start off as a growth factor (IGF or something similar ) or the other way round?karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-909802678576060912017-04-17T16:16:14.426+00:002017-04-17T16:16:14.426+00:00That will be sarcolemma...That will be sarcolemma...Peterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-8708157760418357022017-04-17T16:15:42.668+00:002017-04-17T16:15:42.668+00:00Completely related. He goes from bacteria (simples...Completely related. He goes from bacteria (simplest situation) through mitochondria to sarcolema to axon depolarisation. There are a lot of answers to why cytoplasmic membranes are Na+/K+ based and mitochondria are H+ based. Na+/K+ can be viewed as the default, mitochondria are special. Potassium movement signals/prepares for proton gradient management. The paper is worth the effort! Nicely speculative with some hard supportive facts.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-89416487397311454692017-04-17T15:43:03.063+00:002017-04-17T15:43:03.063+00:00Could this have anything to do with the sodium and...Could this have anything to do with the sodium and potassium ion channels in axons, or is it completely unrelated?cavenewthttps://www.blogger.com/profile/08461541719892430585noreply@blogger.com