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Insulin Resistance and Insulin Production

I think I am some sort of anomaly. When I was diagnosed the only sign of metabolic syndrome I had was being over weight. My blood pressure was normal, my cholesterol and lipids were all normal, my liver and kidney functions were normal, and my fasting BG was reasonable. I had survived a heck of a year prior to diagnosis with a cancer diagnosis, surgery, chemo, hospitalised with neutropenia sepsis requiring injections before each future chemo session to avoid recurrence, radiotherapy, and a biological drug by infusion, not to mention a few steroids during the chemo and all the stress involved. In fact, I still had 4 months to go on the biological drug. Or maybe I am just making excuses. The past is history. Whatever, I was diagnosed with no symptoms.
 
Bluetit1802 said:
My blood pressure was normal, my cholesterol and lipids were all normal, my liver and kidney functions were normal,
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mine too, and still are. It was only my fasting blood sugars which showed up on a routine blood test which told the GP to look further, although I was (and still am) very overweight.
 
Brunneria said:
Suggesting that just losing more weight will solve his insulin resistance is, in my opinion, just making too many unverified assumptions.
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Probably just as well I didn’t mention losing weight then.

FYI I was agreeing with @LittleGreyCat by confirming that from the data provided in the OP, there is evidence of insulin deficiency. No further comments to add.
 
To make more of the results as presented by @LittleGreyCat we probably need to compare the figures and graphing to a non-diabetic as i suspect that the insulin rise is later than would be normal ( normal as in a non-diabetic) and that this mistiming is part of the problem which would likely become more apparent if the glucose/ blood sugar rise amount from the meal was high enough.
Conversely the lower the stimulus from carb intake to better.
 
LittleGreyCat said:
@bulkbiker @Jim Lahey

Insulin Resistance is generally held to be when you are producing insulin but your BG is above normal levels.

One typical example is an overweight/obese T2 with very high insulin levels but also very high BG levels.

However this is not the only scenario. As long as your pancreas isn't producing enough insulin to keep your BG within normal levels you can have a combination of IR and insulin production across a very wide range.

View attachment 33455

As you can see from these results my fasting BG is a bit high but I am still producing (lower) normal amounts of insulin.

The test was in December 2017 almost 10 years after first diagnosis so this is unlikely to be a honeymoon period for a T1.

I'm not sure what is causing the IR apart from a sad tendency to retain fat around my middle.
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As I understand it, the liver is producing too much glucose. The excessive amount released over flows into the blood stream driving up the BG level and this causes the pancreas to respond by releasing more insulin. In T2 it's a viscous cycle that just keeps repeating itself. The liver just ignores the pancreas's response and continues on.

Your levels are fasted, so who knows what the insulin level is post meal when it is doing everything it can to try and return BG levels to normal. You'd see the first and second phase insulin responses, which should stop the liver from releasing glucose and should stop it from producing new fat, but due to IR it doesn't stop and can increase the amount of fat produced. Causing weight gain or stalling weight loss. I would wonder what your levels are like now, it's been 18months since the result you posted?

Perhaps they are different?

There is still a lot of info missing, so I can't say what is causing it. Or should I say guess what is causing the IR....There are other things that can effect the performance of the liver, we know T2 has a big effect and in T2 it seems to me like the liver and pancreas are a married couple with serious communication problems. Neither is listening to other via signalling.

Other missing info includes. Diet, ability to store fat physically and other drugs, steroids for example can dramatically elevate BG levels increasing and the work load on the pancreas and indeed be the straw that breaks the camels back, inducing T2. Other conditions can effect the livers performance. Any impairment, say fatty liver or injury to the liver, physically, toxin wise (Known or unknown) or other reasons can impair it's performance and potentially lesson its ability to deal with all the demands. If it doesn't work so well, then that effects your overall health.

Anyway, I've probably waffled on enough. Maybe updating the results posted with a new set would be a good idea?
 
LittleGreyCat said:
I'm not sure what is causing the IR apart from a sad tendency to retain fat around my middle.
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I've had four IR tests. The aim is to be as close to 1 as possible. I've gone from 1.7 to 2.4, back to 1.7 and then 2.4 again. The higher numbers have occurred when I've been eating more meat and fat but I would have to do more tests to confirm that. It's just an observation.
 
Caeseji said:
What always gets me is how curious a pathology this condition is at the end of the day. It is so multi-faceted and is precluded by so much metabolic derangement that there is a near infinite way to manage or mitigate the disease. There is always going to be oddness with how the body works, sometimes it can be that the pancreas has halted production in some way or that it is just the fact that the body itself has ran out of stores and cannot deal with the production. I doubt that there will ever be a definitive answer to any of this however, there are so many subtypes now that it boggles the mind but I always say it is best to find a way of managing that works for you and keep going with it. IR is always going to be the culprit behind a LOT of this but how we live afterwards is going to have the biggest impact.
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Caeseji - I often refer to T2 diabetes as a portfolio condition, because there are so many aspects of it, and so many factors potentially in play. Sadly, this is compounded by the commonality of a diagnosis by best guess.

My phrase "diagnosis by best guess" isn't meant as an insult to anyone.
 
kitedoc said:
To make more of the results as presented by @LittleGreyCat we probably need to compare the figures and graphing to a non-diabetic as i suspect that the insulin rise is later than would be normal ( normal as in a non-diabetic) and that this mistiming is part of the problem which would likely become more apparent if the glucose/ blood sugar rise amount from the meal was high enough.
Conversely the lower the stimulus from carb intake to better.
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Noting that the test was a fasting one. the results should indicate how the body is coping in the absence of food and without the post meal stimulus for insulin production.

I read it as my body maintaining a higher than optimum BG level in a fasted state.

Possibly due to a miscommunication between the pancreas and the liver.

It could be the pancreas isn't producing enough insulin to match the BG level.

It could be that the liver isn't responding to the insulin and is continuing to release glucose into the bloodstream.

Edit: Aaaargh! Misread what glucagon does. Following bit revised.

It could be that the Alpha cells in the pancreas are releasing too much glucagon to boost the release of glucose by the liver or the liver is not responding to the glucagon correctly.

Hmmmm.....that is an interesting one!

Beta cells release insulin to get glucose out of the blood stream.
Alpha cells release glucagon to stop the BG level falling and get liver releasing glucose into the bloodstream.
I wonder if Alpha cell dysfunction could lead to dawn phenomenon and slow insulin response?

I also wonder if the pancreas switches from insulin to glucagon production in a synchronised manner and "assumes" that the liver will do as it is told? Which could result in lower insulin levels and higher BG levels in a fasting state.

Or that glucagon is released and then the BG overshoots because the liver is not listening to the insulin?

Or.......

Whatever, the main discussions seem to be about Beta cells, which are only one half of the balancing mechanism.
 
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DCUKMod said:
Caeseji - I often refer to T2 diabetes as a portfolio condition, because there are so many aspects of it, and so many factors potentially in play. Sadly, this is compounded by the commonality of a diagnosis by best guess.

My phrase "diagnosis by best guess" isn't meant as an insult to anyone.
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I would not say Best Guess but just 'Diagnosis by Guesswork' as many GPs (like mine did) just assume T2 as an adult without any further thought.
 
Daibell said:
I would not say Best Guess but just 'Diagnosis by Guesswork' as many GPs (like mine did) just assume T2 as an adult without any further thought.
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When I was diagnosed I knew nothing about diabetes. I asked the nurse how she knew I was T2 and not T1. She just replied that had I been T1 I would have been feeling poorly and not feeling as well as I did. That was it. It turned out she was right. Very definitely T2.
 
Scott-C said:
Glucagon does the exact opposite - it causes the liver to release stored glycogen as glucose to raise bg.
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Got in before I posted a correction. :oops:
 
For further reference:
https://www.ncbi.nlm.nih.gov/pubmed/15655708
which seems to say that raised glucagon levels are part and parcel of T2 and can result in raised fasting BG and the liver continuing to release glucose into the blood stream after a meal.

"The disturbance in the endocrine activity of the pancreas is not limited to insulin, since a concomitant increase in fasting plasma glucagon and impaired suppression after the ingestion of an oral glucose load are often observed. This alteration becomes prominent after the ingestion of a mixed meal, when plasma glucagon remains much higher in the diabetic patient as compared to normal individuals. The disproportionate changes in the plasma concentration of the two pancreatic hormones is clearly evident when the insulin:glucagon molar ratio is considered. It is the latter that mainly affects hepatic glucose production. Because of the reduction of the insulin:glucagon molar ratio basal endogenous glucose concentration will be higher causing fasting hyperglycemia, while the hepatic glucose output will not be efficiently suppressed after the ingestion of a meal, contributing to excessive post-prandial glucose rise. "

Which raises the question: "Has anyone had their fasting glucagon levels tested?".
 
As far as I understand it, glucogen is not the only hormone responsible for the rise in glucose from the liver. Growth hormone, cortisol and adrenalin also play a part as they also have a surge in the mornings and the 4 of them work together with the glucogen to trigger the liver to produce its glucose.
 
DCUKMod said:
Caeseji - I often refer to T2 diabetes as a portfolio condition, because there are so many aspects of it, and so many factors potentially in play. Sadly, this is compounded by the commonality of a diagnosis by best guess.

My phrase "diagnosis by best guess" isn't meant as an insult to anyone.
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Unfortunately, several flavours of diabetes are 'diagnosed' on that basis...
 
Daibell said:
Did the endo discuss diet with you as well to check that you were having a low-carb diet to help get any insulin resistance down?
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No he did not ask any of this as reading my notes he knows all this is in place and hba1c has been good for years its only because i wanted to know my type that the overproduction of insulin was discovered now i wish that i hadnt bothered as really worries me to be running high bgs so will put all this to him at the end of this month hoping for explanation as so gobsmaked when he told me about this etc didnt ask questions
 
Just to muddy the waters further, one can become Glucagon Resistant. See videos by Ben Bikman on YouTube.
 
Shiba Park said:
Unfortunately, several flavours of diabetes are 'diagnosed' on that basis...
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Many conditions are diagnosed that way, but this thread is mainly discussing matters relating to the T2 OP.
 
Guzzler said:
Just to muddy the waters further, one can become Glucagon Resistant. See videos by Ben Bikman on YouTube.
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:banghead: (I think).

I am getting a lot of useful (and probably potentially useless) information from this thread.

Glucagon Resistance (GR) would presumably manifest as reverse dawn phenomenon?
That is, BG drops overnight and you don't get a liver dump so wake up hypo?
 
LittleGreyCat said:
:banghead: (I think).

I am getting a lot of useful (and probably potentially useless) information from this thread.

Glucagon Resistance (GR) would presumably manifest as reverse dawn phenomenon?
That is, BG drops overnight and you don't get a liver dump so wake up hypo?
Click to expand...


This is about an hour but it is worth watching.

 
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