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Post by pengiep on Aug 31, 2017 8:59:16 GMT -5
Actually, those factors are something to consider in any pharmacological study. Women are known to respond differently from men in a wide range of physiological situations. As are different ethnic backgrounds.
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Post by agedhippie on Aug 31, 2017 9:05:23 GMT -5
When insulin is released you also get amylin and glucagon released, as well as c-peptide formed by the creation of insulin from proinsulin. When you take insulin all those components are missing. When you take insulin, and this applies to all artificial insulin (RHI and analogs), you are missing c-peptides because the the conversion from proinsulin to insulin never happened - this was one of the objections people had in moving to RHI when it first came out. The last I checked the pancreas releases glucagon when the concentration of glucose in the bloodstream falls too low. Maybe my understanding is incorrect as I always thought glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream. Can you point me to some info so I can get a better understanding of what you are trying to say? Having some amylin may be nice but its main role is to inhibit glucagon secretion. Since afrezza works as fast as it does not having it seems minor. Additionally for the T2 they are producing some amylin and c-peptide. As they use afrezza more and more and allow the beta cells to heal they should get back to near normal levels. It might be nice to have a second cartridge for the c-peptide but probably not worth it at this point. Lets get the BG back to near normal levels first. Glucagon is released as a balance to the insulin, it's the reason why when they treat DKA in hospital they give you glucose as well as insulin. The glucagon is released to prevent an overshoot, the classic case is eating something with a very high glycemic index that spikes your levels. The speed of the rise makes the body release more insulin that it should as it attempts to head off the rise. When the rise abruptly stops the insulin has overshot, but the glucagon can partially blunt the overshoot which buys time to recover. Amylin's chief purpose is not to inhibit glucagon secretion, but rather to control gastric emptying. This is important because it interacts with the GLP-1 and GIP incretins which controls the behavior of the insulin. It used to be that you used Symlin (an amylin analog) to replace amylin where necessary but these days they tend to use GLP-1 analogs like Victoza instead and directly replace the broken interaction. Victoza also slows gastric emptying and is used for weight control as well (slowing gastric emptying makes you feel fuller so you don't eat as much). I have no argument with controlling glucose levels, but that is not the only part of the glucose metabolism so you are only fixing part of the problem.
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Post by agedhippie on Aug 31, 2017 9:17:54 GMT -5
It was porcine or bovine. so aged, which is better? The analogs or RHI porcine or bovine?
Quote: When insulin is released you also get amylin and glucagon released, as well as c-peptide formed by the creation of insulin from proinsulin. When you take insulin all those components are missing. When you take insulin, and this applies to all artificial insulin (RHI and analogs), you are missing c-peptides because the the conversion from proinsulin to insulin never happened - this was one of the objections people had in moving to RHI when it first came out.
Oh, RHI was a huge step forwards when it came out, but analogs win by a mile! They are missing all the other components of the animal insulins but I will happily (and possibly misguidedly) trade those for analog's ease of use and predictability. There is some interesting research around the roles of c-peptide which used to be thought of as just a by-product of insulin production. There was a school of thought that said you got better hypo awareness on the animal insulins. Some people swear by it for that reason and still use it although I think the last manufacturer shut down a couple of years ago so I don't know what they will do now. Personally I think it was probably psychological but over the years I have learnt that what works for one person sometimes doesn't work for another (the source of all the YMMV comments in diabetic board posts) so I keep quiet.
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Post by peppy on Aug 31, 2017 9:21:26 GMT -5
I suspect afrezza will be the same. Quote: "Oh, RHI was a huge step forwards when it came out, but analogs win by a mile!"
Thank you Aged, I love you.
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Post by sayhey24 on Aug 31, 2017 9:29:35 GMT -5
The last I checked the pancreas releases glucagon when the concentration of glucose in the bloodstream falls too low. Maybe my understanding is incorrect as I always thought glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream. Can you point me to some info so I can get a better understanding of what you are trying to say? Having some amylin may be nice but its main role is to inhibit glucagon secretion. Since afrezza works as fast as it does not having it seems minor. Additionally for the T2 they are producing some amylin and c-peptide. As they use afrezza more and more and allow the beta cells to heal they should get back to near normal levels. It might be nice to have a second cartridge for the c-peptide but probably not worth it at this point. Lets get the BG back to near normal levels first. Glucagon is released as a balance to the insulin, it's the reason why when they treat DKA in hospital they give you glucose as well as insulin. The glucagon is released to prevent an overshoot, the classic case is eating something with a very high glycemic index that spikes your levels. The speed of the rise makes the body release more insulin that it should as it attempts to head off the rise. When the rise abruptly stops the insulin has overshot, but the glucagon can partially blunt the overshoot which buys time to recover. Amylin's chief purpose is not to inhibit glucagon secretion, but rather to control gastric emptying. This is important because it interacts with the GLP-1 and GIP incretins which controls the behavior of the insulin. It used to be that you used Symlin (an amylin analog) to replace amylin where necessary but these days they tend to use GLP-1 analogs like Victoza instead and directly replace the broken interaction. Victoza also slows gastric emptying and is used for weight control as well (slowing gastric emptying makes you feel fuller so you don't eat as much). I have no argument with controlling glucose levels, but that is not the only part of the glucose metabolism so you are only fixing part of the problem. Please!!! - the glucagon is released to prevent an overshoot, are you kidding me. They may give it to you in the hospital in DKA but the body doesn't work that way. The pancreas and liver are simple machines working in harmony and a flow control model. When the pancreas dumps insulin for first phase it pretty much bases it on what was newly made from the last meal. Then after awhile it may release glucagon but not in the beginning. Since step one is controlling BG levels and for 95 years we have not done a great job at it I vote for doing this in a step program. Lets get the BG under control and in a non-diabetic range and then we can worry about c-peptide and GLP-1 levels. What we are seeing in giving external GLP-1 is causing more harm than good. IMO, one step at a time and afrezza is one huge step for mankind.
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Post by dreamboatcruise on Aug 31, 2017 15:38:26 GMT -5
so aged, which is better? The analogs or RHI porcine or bovine?
Quote: When insulin is released you also get amylin and glucagon released, as well as c-peptide formed by the creation of insulin from proinsulin. When you take insulin all those components are missing. When you take insulin, and this applies to all artificial insulin (RHI and analogs), you are missing c-peptides because the the conversion from proinsulin to insulin never happened - this was one of the objections people had in moving to RHI when it first came out.
Oh, RHI was a huge step forwards when it came out, but analogs win by a mile! They are missing all the other components of the animal insulins but I will happily (and possibly misguidedly) trade those for analog's ease of use and predictability. There is some interesting research around the roles of c-peptide which used to be thought of as just a by-product of insulin production. There was a school of thought that said you got better hypo awareness on the animal insulins. Some people swear by it for that reason and still use it although I think the last manufacturer shut down a couple of years ago so I don't know what they will do now. Personally I think it was probably psychological but over the years I have learnt that what works for one person sometimes doesn't work for another (the source of all the YMMV comments in diabetic board posts) so I keep quiet. I've been doing some reading on c-peptide recently. That is an interesting topic. In addition to free c-peptide released by the pancreas, there is also proinsulin released, which still has the c-peptide linked to the insulin chains. Apparently proinsulin weakly binds to insulin receptors and has a much longer half life than insulin after release. It seems there is still research to be done to fully understand glucose metabolism. I lost my thyroid to autoimmune disorder, so reliant on synthetic thyroxine hormone. When I was diagnosed quite some time ago they still had animal thyroid hormones, and as you say with the insulin, some swore it worked better than the synthetic. I never tried it.
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Post by mnholdem on Aug 31, 2017 17:06:26 GMT -5
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Post by brotherm1 on Sept 1, 2017 0:46:31 GMT -5
That Wikipedia article and it's sub-articles are good. They provide a basic understanding of pancreatic functions but the contents in the above conversations surpass it. Interesting stuff but for now anyone of the above could just be full of amylin and I would not know it as my knowledge to their's is as good as glucagon with the wind. Catch you all langerhan.
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Post by dreamboatcruise on Sept 1, 2017 11:53:50 GMT -5
That Wikipedia article and it's sub-articles are good. They provide a basic understanding of pancreatic functions but the contents in the above conversations surpass it. Interesting stuff but for now anyone of the above could just be full of amylin and I would not know it as my knowledge to their's is as good as glucagon with the wind. Catch you all langerhan. I do try to make distinctions when I present things as to whether it is something that seems universally accepted vs something still being studied... or rarely my own speculation. Since physiology/biology is not my academic field I don't do a lot of the latter. Taking things with a grain of salt never hurts, as well as sometimes verifying. Especially on a discussion forum like this, I think "facts" can morph over time from something that was true into something that perhaps isn't... and often gaining a certain presumption of accuracy as it is repeated. Not helped by some that treat discussions like high school debates where scoring points is more important than accuracy... I was a science/math nerd not a debater in high school.
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Post by stew3409 on Sept 1, 2017 12:15:48 GMT -5
Many resident experts here. I wonder if practitioners know as much and Afrezza scripts would have been in 1000's now.
Obligatory ☺️
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Post by dreamboatcruise on Sept 1, 2017 12:41:51 GMT -5
Many resident experts here. I wonder if practitioners know as much and Afrezza scripts would have been in 1000's now. Obligatory ☺️ Though insurance/PBMs could still be resistant. It will be much easier to get new prescribers on board if insurance coverage improves... and if MNKD can build momentum to the point where there would be no question about the market viability of Afrezza. I suspect there are docs that may realize the fast action benefits of Afrezza and yet still are hesitant to write a lot of prescriptions because of these two issues.
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