It should be noted that citrate does not contain acetyl-CoA, but simply acetyl. So the CoA-group is added to the citrate in the cytosol by the means of ATP-citrate lyase after the citrate is transported into the cytosol.
Like, you're right but it's irrelevant and ruins someone's understanding of the pathway. Acetyl-CoA makes citrate, and that's an important part of understanding where citrate comes from and why it is a good regulatory molecule for FA synthesis.
Requiring a citrate shuttle in order to get the acetyl-coA from mitochondria out into the cytoplasm seemed like a waste until we realized that once it breaks down to OAA and then to pyruvate, we get NADPH, which is essential to FA synthesis. The cell is such a well oiled machine!
This was so helpful, thanks! I agree with the small already made suggestions of clarifying that citrate doesn't actually contain acetyl-CoA but acetyl itself and also that the pdh is a complexe. also i've never heard of the nadph // oxalacetat --> pyruvat conversion. Instead I was taught that there is an exchange between malat and oxalacetat? Anyways, those are just minor things - and your voice is not annoying at all! I personally think it's super important for these rather long videos to not be to monotone. Without proper enunciation, which you clearly delivered, it just get's lenghty. Keep it up!
2:05....post meal.insulin drops and glucagon rises 1-2hours after a meal (thats correct) BUT glucagon's main effect is on liver not on adipose..Epinephrine and cortisol are the ones that mainly stimulate HSL in adipose(lipolysis) :-)
OAA is not converted directly to pyruvate, but first converted to malate which is the converted to pyruvate through malate dehydrogenase, and only in this reaction we earn that nadph you were talking about.
So when you consume fat from your diet, it eventually gets into your blood stream via chylomicrons. Can the triglycerides be then stored directly as fat in your adipose tissue? Or does it have to first go through glycolysis and turn into Acetyl-CoA and then back to Triglycerides via Fatty Acid Synthesis?
Thanks for your excellent videos. Can you very kindly clarify the following. Can dietary fat only be burnt by mitochondria if it has first been ‘processed through’ fat cells and released as FFA? Or can mitochondria also burn dietary fat that hasn’t come from a fat cell? Thanks for any comments.
Hi Kyle, you say: "all Fat will be burned in the mitochondria, however yours is more of a question of Fatty acid transport. Basically your mitochondria will burn fatty acid chains from whatever source they can get them from if the hormone Glucagon is present. whereas if insulin is present it will be stored in adipose. Bear in mind that a small amount of fatty acids will travel around in the blood as part of your VLDL and also attached to Albumin." You seem to be saying that mitochondria can burn fatty acids even if they have not been released by (come from) fat cells as 'free fatty acids'. Please clarify. My question is simple: apart from glucose, can mitochondria only burn FFA's released by fat cells, or can mitochondria also burn fatty acids that have not been processed through fat cells?
Didn't we just lose an OAA from the Kreb Cycle? OAA gets combined with Acetyl-co-A to form Citrate, which is moved out of the mitrochondria. How can it cycle, if it loses one of the key components of the cycle?
+Allan Kirk acetyl CoA carboxylase (ACC) is the enzyme that "activates" mitochondrial acetyl CoA so that the acetyl portion is transported into the cytosol in the shape of citrate. ACC is allosterically activated by citrate, and a high mitochondrial concentration of citrate comes from the inactivation of citrate dehydrogenase (TCA). ... So I think that citrate is in excess in the TCA. The cell puts this to good use by committing to fatty acid synthesis (which requires lots of energy, so it makes sense that citrate dehydrogenase is inactivated by high levels of ATP).
There's a cytosolic isoform of malate dehydrogenase that catalyzes the reduction OAA back to malate (the precursor for OAA in the TCA cycle). This malate is then oxidized to pyruvate via an enzyme called malic enzyme (the NADP+ dependent step), releasing a CO2. (Malic enzyme and the PPP are the two sources of NADPH production in our bodies).
Pyruvate Dehydrogenase complex is to produce AcetylCoA. While Pyruvate Carboxylase is to produce Oxaloacetate. Too much AcetylCoA inhibits Pyruvate Dehydrogenase, so that the continuous production of Oxaloacetate through Pyruvate Carboxylase can produce a lot of Oxaloacetate which will combine with the many AcetylCoA to form Citrates so that they can traverse the mitochondrial membrane and proceed with the Fatty acid synthesis. Pyruvate decarboxylase is something else.
you'd better not keep the pen moving without any indication which could bother us, because we are always concentrating on your voice and the pen all the time. anyway the video is still great! thanks!
This comment section is divided between people who absolutely despise her voice and people who are wayyy too seduced by it.... get it together people lmao
I can't get past the first 30 seconds... so when I find that Khan's not doing these videos, I just go back the way I came in. It would be fine if I wasn't so damn sure she's faking it. Stop slurring and get it together woman!
