I used to avoid your videos because they were kinda long. But you really explain things well and I wind up saving time because I don't have to replay the video a million times or hunt down another explanation. For whats it worth, thanks. And keep up the good work!
When in a fasted state what controls glucagon to limit over production of Blood Glucose? Insulin? For instance when I fast my BG levels run steady at 120-130. Is this the simply the result of high glucagon and low insulin ratio? I produce either too much glucagon or too little insulin?
Can u please please please move away from the board at the end of the section so we can screenshot that's my only thing other than that ur perfect thanx a bunch
+Adam Johnston ... Where does he state that PP1 is bound to phosphorylase-a? Are you thinking of the liver? I think the diagram he has drawn is representative of PP1 in the muscle... In which case it is only bound to the regulatory subunit (not phosphorylase-a).
+Adam Johnston Thank you. I appreciate your thoughtful responses. In that lecture "insulin and glucose regulation of glycogenesis" he talks specifically about liver cells. Glycogen degradation is regulated differently in the muscle and liver. I understand the way in which it is regulated in the liver, I'm just a tad unclear on how it is in it's active form in the muscle. But, I'm guessing that if glucose levels are high, glycogen degradation will be inhibited because glucagon and epinephrine signals won't be released. So PKA won't be activated, putting a complete halt on the entire signal cascade... Therefore, PKA won't be able to simultaneously deactivate PP1 either, allowing it to dephosphorylate glycogen synthase b to glycogen synthase a.
+Adam Johnston That's okay :) Thank you! I think was/am also confused about what you meant by PKA and phosphorylase binding directly to the active site of PP1, as to my understanding (and my notes! Haha) PP1 is always bound to a regulatory subunit and is always indirectly inhibited in both the muscle and liver. In the muscle, PP1 inhibited by the activated inhibitory molecule. In the liver, it's a different story, lol. That's when phosphorylase gets involved. Phosphorylase and PP1 are both bound to the regulatory subunit in the liver. If glucose levels are low in the liver, PP1 stays bound to the regulatory subunit and therefore, remains inactive. For PP1 to be active in the liver, glucose levels are high in the cell, triggering the pathway I believe you're thinking about. As far as I know, phosphorylase is not involved in the regulation of PP1 in the muscle. Only PKA (as he has drawn in this video), which indirectly inactivates PP1 by activating an inhibitor to do the dirty work, lol. Biochemistry can throw you for a loop sometimes.
i think it's always activated because we always need to store glycogen But when a special incident occurs like(heavy training or fasting) PP1 is deactivated and we break down glycogen to produce glucose
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I used to avoid your videos because they were kinda long. But you really explain things well and I wind up saving time because I don't have to replay the video a million times or hunt down another explanation. For whats it worth, thanks. And keep up the good work!
Play his videos at 1.25 speed. He talks fast so you can't play them in 1.50 speed or you won't understand what he's saying.
I'm just loving this guy's fluency in this biomedical language. It definitely inspires me to be a better student. Thanks Dr. Kopot!
Perfect Explanation! This guy is single handedly saving my biochem at med school.Thank you so much!
You explained this so much better than my professor! Thank you! I'm much less worried about my biochem final now.
AMAZING! straight to the point, aesthetically pleasing background and very well explained.
These videos were great during undergrad, and are now just as useful during medschool. Thanks!
thanks for all of the help
you are an OG. that was very helpful
This guy is amazing. Thank you
Thank you so much it really helps
You are awesome, i love your videos
When in a fasted state what controls glucagon to limit over production of Blood Glucose? Insulin? For instance when I fast my BG levels run steady at 120-130. Is this the simply the result of high glucagon and low insulin ratio? I produce either too much glucagon or too little insulin?
Wonderful. I love Biochemistry from your teaching.can you appreciate a good reference for biochemistry science?
You are the best ❤️
Great explanation save me a lot of time
Great video! Does this mean that exercise and fasting (inactive pp1) prevent forgetfulness and enhance learning?
Omgg I love you ❤️❤️❤️ You are the God of explanation the most extreme pathways in biochemistry xxxx love itttt thank you so much x
oh Zoeya R I love you too...
Huh ? Lol
Yes Zoeya R 😉
GUAU
excellent video
BIOC 311 squad. Where are you at?
sup
HAHA forced to flipped learning
Fantasia 17 sadly😞
I really don't like this way of learning = =
Fantasia 17 annoying af
For the Protein phosphatase 1 bullet point:
Shouldn't it deactivate Phosphorylase a not b?
Really helpful
Good video!
special Thanks ,
But how's PKA stopped again?
Bad ass dude so simple. thx
you'r a lifesaver welmos7af :'D
Tnx liam paine
VERY USEFULL thanks!!!
Lidia Martinenghi
this wonderful....
Can u please please please move away from the board at the end of the section so we can screenshot that's my only thing other than that ur perfect thanx a bunch
u r aaaamziiiiing
I LOVE YOU.
Thanku sir
good
Is PP1 always "active" unless glycogen degradation is taking place?
If not, what activates it to stimulate glycogen synthesis?
+Adam Johnston ... Where does he state that PP1 is bound to phosphorylase-a? Are you thinking of the liver? I think the diagram he has drawn is representative of PP1 in the muscle... In which case it is only bound to the regulatory subunit (not phosphorylase-a).
+Adam Johnston Thank you. I appreciate your thoughtful responses. In that lecture "insulin and glucose regulation of glycogenesis" he talks specifically about liver cells. Glycogen degradation is regulated differently in the muscle and liver. I understand the way in which it is regulated in the liver, I'm just a tad unclear on how it is in it's active form in the muscle.
But, I'm guessing that if glucose levels are high, glycogen degradation will be inhibited because glucagon and epinephrine signals won't be released. So PKA won't be activated, putting a complete halt on the entire signal cascade... Therefore, PKA won't be able to simultaneously deactivate PP1 either, allowing it to dephosphorylate glycogen synthase b to glycogen synthase a.
+Adam Johnston That's okay :) Thank you! I think was/am also confused about what you meant by PKA and phosphorylase binding directly to the active site of PP1, as to my understanding (and my notes! Haha) PP1 is always bound to a regulatory subunit and is always indirectly inhibited in both the muscle and liver.
In the muscle, PP1 inhibited by the activated inhibitory molecule.
In the liver, it's a different story, lol. That's when phosphorylase gets involved. Phosphorylase and PP1 are both bound to the regulatory subunit in the liver. If glucose levels are low in the liver, PP1 stays bound to the regulatory subunit and therefore, remains inactive.
For PP1 to be active in the liver, glucose levels are high in the cell, triggering the pathway I believe you're thinking about.
As far as I know, phosphorylase is not involved in the regulation of PP1 in the muscle. Only PKA (as he has drawn in this video), which indirectly inactivates PP1 by activating an inhibitor to do the dirty work, lol.
Biochemistry can throw you for a loop sometimes.
i think it's always activated because we always need to store glycogen
But when a special incident occurs like(heavy training or fasting) PP1 is deactivated and we break down glycogen to produce glucose
Thank you!
thanks man
i'm a kid and i understand this i have no clue how i understand it
You can use a pointer
will you marry me