PeteN11
Well-Known Member
I use the letter "e" in Liver to remember Glycogen and the letter "o" in Hormone to remember Glucagon.
I use the letter "e" in Liver to remember Glycogen and the letter "o" in Hormone to remember Glucagon.(Going off topic, anyone got a good way to remember which is which of glycogen and glucagon, I always have to check I haven't got the names the wrong way round?)
The liver does not hold Glucose it stores Glygogen. The liver needs to be told to break this down and release it as Glucose by the hormone Glucagon. Glucagon is produced by the Pancreas which in most T1's is fairly messed up so there is no guarantee it will do so when needed or in time. And it almost certainly wont if there is already insulin in the body.The liver holds enough glucose to deal with most hypos, so you would probably have been ok even if you had slept through it.
Glad all was OK. I too use Lantus and Novarapid.i’m not sure if i could have accidentely switched the lantus insulin for novorapid.
Hi @Antje77 You are so correct to point out everyone's insulin journey is a very personal one to figure out how to calibrate and administer.No, it isn't. It's only the insulin glargine (Lantus, (a)basaglar, and Toujeo) holding a risk of bizarre hypo's, not any of the other long acting insulins.
I take 84 units of Tresiba at the moment. You say that to your thinking 25 units should be split into 2 for safety. Should I conclude you think I should split my basal insulin over 6 injections? What about people using 200 units of basal? Should they inject 16 times for basal only because you, and not their endocrinologist, think 25 units at once is too much?
Please consider the differences between different people and remember what works for you may not be the best solution for everyone else.
The only time I have ever had a serious hypo was that one time on Lantus. For the last 3 years my bg's have been managed very well without splitting my dose of long acting, and while I'm very much afraid of Lantus, I found my current long acting insulin to be very stable and predictable, I don't feel it as a risk at all to inject it only once a day.
No, it isn't. It's only the insulin glargine (Lantus, (a)basaglar, and Toujeo) holding a risk of bizarre hypo's, not any of the other long acting insulins.
I take 84 units of Tresiba at the moment. You say that to your thinking 25 units should be split into 2 for safety. Should I conclude you think I should split my basal insulin over 6 injections? What about people using 200 units of basal? Should they inject 16 times for basal only because you, and not their endocrinologist, think 25 units at once is too much?
Please consider the differences between different people and remember what works for you may not be the best solution for everyone else.
The only time I have ever had a serious hypo was that one time on Lantus. For the last 3 years my bg's have been managed very well without splitting my dose of long acting, and while I'm very much afraid of Lantus, I found my current long acting insulin to be very stable and predictable, I don't feel it as a risk at all to inject it only once a day.
Isn't it odd that we are encouraged to use a practice that increases the risk?
Thanks for all of your replies
Looks like it could have been a ‘lantus low’ as well, but will probably never know.
I tried Levemir before Antje, but it gave me blue spots. Maybe tresiba which you mention is different, i will check it out. Also the timer that can be added to the pen!
Btw I can def confirm that the liver can not always get you out of a hypo.
Because insulin is injected subcutaneously and insulin switches Glucagon secretion off, T1s usually have too much of it. Not too little. Glucagon is made in the alpha cells, not the beta cells. There is no reason why a hypo induced stress response wouldn't result in the required glucagon being secreted. That T1s can't produce the glucagon required to deal with hypos is a popular myth.The liver does not hold Glucose it stores Glygogen. The liver needs to be told to break this down and release it as Glucose by the hormone Glucagon. Glucagon is produced by the Pancreas which in most T1's is fairly messed up so there is no guarantee it will do so when needed or in time. And it almost certainly wont if there is already insulin in the body.
In the OP's case he was dangerously low and nothing seems to happening on the Glucagon front. Surely it would already have started to kick in?
Glad all was OK. I too use Lantus and Novarapid.
If I had woken up to that reading of 12 I would have used my Novarapid first rather than the Lantus which I would have waited to take at my normal morning time. The dosage would have depended on what I had eaten and especially drank the night before but could have been 25 units.
Was it time for your Lantus injection and is 25 your normal dose?
What have you been advised to do for correction doses as I have been never been told to use Lantus?
As others have said get all your back up glucose ready in different parts of the house, car and work. Going out to get some whilst that low would have slowed down your recovery rate even more due to the exercise involved.
Because insulin is injected subcutaneously and insulin switches Glucagon secretion off, T1s usually have too much of it. Not too little. Glucagon is made in the alpha cells, not the beta cells. There is no reason why a hypo induced stress response wouldn't result in the required glucagon being secreted. That T1s can't produce the glucagon required to deal with hypos is a popular myth.
By 'this' are you referring to the idea that the glucagon driven element of the counterregulatory system works for people with T1 diabetes the same as it does for non-diabetics? This is not an outlandish idea. It simply suggests that this element of the metabolism works the way it should.Hi,
Do you have a reliable link to a sourse/sources to back this up?
Thanx.
This does not mean that the system is broken, though.
I surprised you say it is a popular myth when you have already stated......There is no reason why a hypo induced stress response wouldn't result in the required glucagon being secreted. That T1s can't produce the glucagon required to deal with hypos is a popular myth.
Because insulin is injected subcutaneously and insulin switches Glucagon secretion off,
GIven Lantus is a slow acting insulin, I do not believe it can impact DP.hi, yes it was time for my lantus/abasaglar injection. I always took it around 5/6 am to avoid high bg in the morning (dawn effect) when i get up around 7/8 am.
So on Monday my bg was 12,2 around 6am and i thought the lantus might fix this as well.
On a normal day, if there ever is one, does your Lantus normally have the same effect of lowering your bg to those low levels? I am just surprised that the Lantus had such an affect so rapidly as it is supposed to be slow acting.hi, yes it was time for my lantus/abasaglar injection. I always took it around 5/6 am to avoid high bg in the morning (dawn effect) when i get up around 7/8 am.
So on Monday my bg was 12,2 around 6am and i thought the lantus might fix this as well.
By 'this' are you referring to the idea that the glucagon driven element of the counterregulatory system works for people with T1 diabetes the same as it does for non-diabetics? This is not an outlandish idea. It simply suggests that this element of the metabolism works the way it should.
More to the point, I have not been able to find a compelling argument that this process does not work for T1s. There is lots of speculation, but no suggested underlying mechanism for this supposed dysfunction. Nor is there compelling evidence of it. Only anecdotal reports. On the other hand, if T1s were not able to make glucagon when necessary, we wouldn't make it through the night. Glucagon stimulates both glycolysis and gluconeogenesis, providing much needed glucose during that extended period between meals.
After 43 ears of T1, I have no doubt that my glucagon production is as robust as it ever was. The Somogyi Effect, with blood glucose shooting up after a hypo, is further evidence of it. Yes, the stress response can be down-regulated by repeated hypos, and for me hypo unawareness is an issue. It just means that glycogen gets mobilised at lower blood glucose levels than it used to. This does not mean that the system is broken, though.
The only useful suggestion in this regard is to limit insulin injection amounts to a level that doesn't overwhelm liver glycogen stores. In the average person, the liver holds about 130 grams of glycogen. The similar amount of glycogen in muscles has to be used there and is no use during hypos. So if the carb:insulin ratio is say 1:10, glycogen stores will cover an extra 13 units of insulin. Many people inject way more than this, hence the additional risk. Risk that can be avoided by splitting basal and reducing boluses. Because of their effects on this system, more vigilance is required after exercise and/or alcohol too.... It not advisable to suggest the liver will back you up in a "bar fight" with hypoglycemia....
The only useful suggestion in this regard is to limit insulin injection amounts to a level that doesn't overwhelm liver glycogen stores. In the average person, the liver holds about 130 grams of glycogen. The similar amount of glycogen in muscles has to be used there and is no use during hypos. So if the carb:insulin ratio is say 1:10, glycogen stores will cover an extra 13 units of insulin. Many people inject way more than this, hence the additional risk. Risk that can be avoided by splitting basal and reducing boluses. Because of their effects on this system, more vigilance is required after exercise and/or alcohol too.
Read the second paragraph. The numbers differ somewhat to what at I have seen elsewhere, but in the same ballpark. Note that glucose from muscle glycogen can not get back into the bloodstream, so is no help during a hypo..... I'd love a link to the source regarding your stament on how much the average liver "puts out" in glycogen..?
The only useful suggestion in this regard is to limit insulin injection amounts to a level that doesn't overwhelm liver glycogen stores. In the average person, the liver holds about 130 grams of glycogen.
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