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Why should I have hypo?

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Doghouse

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Relationship to Diabetes
Type 1
Why should I have hypo? If I exercise some 5 hours or more after a meal, so there is no rapid acting insulin in my system, why should my blood sugar fall? Why is it that my alpha cells don?t sense the falling glucose level, and respond by outputting glucagons, causing my liver and fat cells to start outputting glucose.

Is it that for a T1 diabetic, alpha cells are also destroyed, along with beta cells? Both types are held inside the Islets of Langerhans.

Alternatively is this the route the body follows during a hypo? If so, why is it sluggish for diabetics, and not for non-diabetics?

Is it that the small level of insulin in the form of Lantus, is sufficient to prevent the alpha cells from doing their thing?

Sorry for not posting more often. I have computers at work, and nowadays when I get home, I would rather take the dog out than sit in front of another one.
Mike
 
I don't think there is a simple answer.

Your basal requirements will vary over the day and it could be that at the time you are exercising they are too high for that time of day.

I have read somewhere that some people have failing alpha cells.

If you are taking Metformin as well as your insulin that could be the culprit as it shows the release of glucose from the liver and makes you more sensitive to the insulin you have.

All of the above could be contributing (well the last depends on whether you take the meds but you know what I mean).

Don't worry about not posting much - just post when you can and/or need to.
 
Read various (conflicting) things that I can no longer clearly remember. One that you need active insulin during exercise or BG levels can actually rise (good ole liver again) another that exercise can allow glucose to pass into cells without insulin (increased sensitivity?) so in a sense exercise acts like insulin.

Runsweet.com had some good stuff about the effect of exercise with T1 I think.
 
Why should I have hypo? If I exercise some 5 hours or more after a meal, so there is no rapid acting insulin in my system, why should my blood sugar fall? Why is it that my alpha cells don’t sense the falling glucose level, and respond by outputting glucagons, causing my liver and fat cells to start outputting glucose.

Is it that for a T1 diabetic, alpha cells are also destroyed, along with beta cells? Both types are held inside the Islets of Langerhans.

Alternatively is this the route the body follows during a hypo? If so, why is it sluggish for diabetics, and not for non-diabetics?

Is it that the small level of insulin in the form of Lantus, is sufficient to prevent the alpha cells from doing their thing?

Sorry for not posting more often. I have computers at work, and nowadays when I get home, I would rather take the dog out than sit in front of another one.
Mike

Exercise uses the glycogen stored in muscles initially, then the glycogen stored in the liver. The liver will then try to replenish its stores of glycogen and can result in levels falling. Mike is correct in saying that glucose can be taken up by cells during exercise without the need for insulin, but exercise also increases the number of insulin receptors on cells to improve the efficiency of any circulating insulin. Unfortunately, all this is very personal to the individual and you need to find out from experience what bits apply to you and learn what the appropriate action is. I have discovered that I need to eat a small amount of carbs after exercise in order (paradoxically) to stop my levels rising - others find they need more insulin instead.

Life is never boring with diabetes! 🙄
 
Exercise uses the glycogen stored in muscles initially, then the glycogen stored in the liver. The liver will then try to replenish its stores of glycogen and can result in levels falling. Mike is correct in saying that glucose can be taken up by cells during exercise without the need for insulin, but exercise also increases the number of insulin receptors on cells to improve the efficiency of any circulating insulin. Unfortunately, all this is very personal to the individual and you need to find out from experience what bits apply to you and learn what the appropriate action is. I have discovered that I need to eat a small amount of carbs after exercise in order (paradoxically) to stop my levels rising - others find they need more insulin instead.

Life is never boring with diabetes! 🙄

I'm re-learning my diabetes care at the basics before I even start on exercise....and this is exactly why!!! Think I need to sort one thing out at a time!

Always love your explanations though Northe. If anyone can explain something - you can!
 
When my son had his first night time hypo his consultant put it down to him going on a cycle ride mid evening, saying the effects are normally felt 5-6 hours later, not immediately as we imagined.
 
Are you sure the cells of the body/muscles can take glucose from the blood stream without insulin............?

What are the mechanic of this process.....?
 
It is soooo complicated! I read some papers promoted on this forum which said the following (I'll try to find the source later) -
It seems to be that GLUT 4, glucose transporters, which enable glucose to get into muscle and skeletal cells are capable of being stimulated by both insulin and muscle contraction. It seems that there is a pool of these transporters, some stimulated by insulin and some by muscle contraction and that either can be used to transport sufficient glucose into the cells .( I'd thought that it was only whilst we were 'exercising' that glucose could get into the cells without insulin)
The authors also seem to suggest that insulin acts in the main by inhibiting the uncontrolled release of glucose from the liver.
 
Insulin: understanding its action in health and disease
P. Sonksen1,* and J. Sonksen2

Indeed, rather than stimulating glucose uptake in tissues such as muscle, insulin in fact reduces glucose uptake. This is because the main factor driving glucose uptake is the ‘mass action’ effect of hyperglycaemia and the concentration gradient between the extracellular and intracellular glucose concentrations. Glucose transporters are not rate limiting under these conditions, even in the face of severe insulin deficiency.
 
What amazes me is that we're meant to interpret BG results/patterns and predict the required insulin doses to match food intake and exercise, but the actual metabolic processes governing all of this are still being researched and disputed.😱

Meanwhile, those advising us are often 20-30 years out of date and less aware than we are.

How are we still alive ? :confused:🙄

Rob
 
is there an english translation of all these answers??? or subtitles???!!

or maybe it's just me and I need to be explained to in Layman's terms!?
 
is there an english translation of all these answers??? or subtitles???!!

or maybe it's just me and I need to be explained to in Layman's terms!?

I think it goes something like this.....

It is soooo complicated! I read some papers promoted on this forum which said the following (I'll try to find the source later) -
It seems to be that GLUT 4, glucose transporters, which enable glucose to get into muscle and skeletal cells are capable of being stimulated by both insulin and muscle contraction. It seems that there is a pool of these transporters, some stimulated by insulin and some by muscle contraction and that either can be used to transport sufficient glucose into the cells .( I'd thought that it was only whilst we were 'exercising' that glucose could get into the cells without insulin)
The authors also seem to suggest that insulin acts in the main by inhibiting the uncontrolled release of glucose from the liver.

The parts of the muscle and skeleton cells that enable glucose to pass through the cell wall (referred to as GLUT4) are stimulated (ie. 'wake up') by ithe presence of insulin in the blood, but also when the muscles contract (ie. start to do work). The suggestion is that insulin stops the liver from secreting glucose (which it does 24/7) rather than just helping glucose to pass into cells for fuel.

Insulin: understanding its action in health and disease
P. Sonksen1,* and J. Sonksen2

Indeed, rather than stimulating glucose uptake in tissues such as muscle, insulin in fact reduces glucose uptake. This is because the main factor driving glucose uptake is the ?mass action? effect of hyperglycaemia and the concentration gradient between the extracellular and intracellular glucose concentrations. Glucose transporters are not rate limiting under these conditions, even in the face of severe insulin deficiency.

This one is a bit more complicated. :confused:

It suggests that the thing that makes glucose pass through the cell walls is a build up of glucose in the bloodstream, so that it passes through to the cells in order to equalise the amount of glucose in the cells and the bloodstream. It does this even if there's very little insulin present in the blood, suggesting that the insulin has some other function, ie. stopping the glucose from being secreted by the liver. I think.

If someone could correct any of this, please do. I'm very much guessing at a lot of it and would love to know what it really means ! :D

Rob
 
A consultant recently explained to me about the alpha cells and their action in type 1. In someone without diabetes the alpha and beta cells work together to control the glucose levels. As the glucose level in blood falls beta cells release less insulin and alpha cells start to produce glucagon. When the beta cells are destroyed the alpha cells get a bit lost on their own. They lose the ability to register what the blood glucose is, so they don't know if they should be producing high or low amounts of glucagon. The result is they produce a middle amount all the time, which is most often if you've got diabetes not what you need.

Which explained to me why glucagon doesn't automatically help with hypos.
It's one of the reasons he is using GLP1 (Victoza, Byetta) in those with type 1 diabetes.
 
Sorry.I appreciated the explanation too! - I was just quoting the article I read, with a sort of vague understanding that lack of insulin alone isn't necessarily the only problem (hence how complicated it is!) Thanks, Robster, for helping explain it better
 
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