You said that procarboxypeptidase and chymotrypsinogen are also activated by enteropeptidase, like trypsinogen. But isn’t it actually trypsin that activates these two? And is this why we only have a trypsin inhibitor in the pancreas-because if trypsinogen isn’t activated, there’s no way for the others to be activated either?
18:00 you said "some of the FFA can become glucose in gluconeogenesis under the supervision of glucagon". I am pretty sure that in mammals we can't convert FFA into glucose, as we can't convert acetyl-CoA into pyruvate. If now, a smart dude will tell me, "listen, but in the Krebs cycle we can eventually convert the acetyl-CoA into oxaloacetate, and then to pyruvate" , I will reply that in order to do so we must use an oxaloacetate, because the acetyl-CoA enters the cycle by combining with an oxaloacetate to form a citrate. Thus, the end result will be no net gain of oxaloacetate, meaning no net gain of pyruvate or glucose.
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Best explanation so far from my understanding 👏👏👏 Thank you so much!
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Please provide antimicrobial nature and functions of each and every organ or its secreted enzymes and it's mechanisms in detail.
If all microorganisms is within us then how diseases occurs to human. I m microbiologist I want this information.
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Hi dear doctor , would you please make a lecture (video) about lung sounds ?
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Great lecture my dear friend :)
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wow wow Iove the way you tech I hope to continue and success
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please ..I hope you continue this series
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You said that procarboxypeptidase and chymotrypsinogen are also activated by enteropeptidase, like trypsinogen. But isn’t it actually trypsin that activates these two? And is this why we only have a trypsin inhibitor in the pancreas-because if trypsinogen isn’t activated, there’s no way for the others to be activated either?
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18:00 you said "some of the FFA can become glucose in gluconeogenesis under the supervision of glucagon".
I am pretty sure that in mammals we can't convert FFA into glucose, as we can't convert acetyl-CoA into pyruvate.
If now, a smart dude will tell me, "listen, but in the Krebs cycle we can eventually convert the acetyl-CoA into oxaloacetate, and then to pyruvate" , I will reply that in order to do so we must use an oxaloacetate, because the acetyl-CoA enters the cycle by combining with an oxaloacetate to form a citrate. Thus, the end result will be no net gain of oxaloacetate, meaning no net gain of pyruvate or glucose.
Thankyou ✨️✨️
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does tumor secreting GIP cause hypoglycemia?
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