This is very confusing. The terms 'bolus' and 'basal' insulin are related to injected insulin, not to endogenous insulin.The question is at what blood glucose level your bolus insulin (first response) releases? I notice in my case that my BG regulation is mainly managed by my basal insulin.
Thank you for posting. There is a typo in ~Table 1This is a great read for anyone who needs to understand their diabetes and hyperglycaemia. It cleared several of my questions that I always wondered based on my experiments.
In particular the affect of GLP and incretins over the stimulation of insulin secretion was an interesting read.
https://www.pancreapedia.org/reviews/secretion-of-insulin-in-response-to-diet-and-hormones
However, I still have one question that i can not find a satisfactory answer so far, so what are your personal experiences or guestimate on it. The question is at what blood glucose level your bolus insulin (first response) releases? I notice in my case that my BG regulation is mainly managed by my basal insulin. Its only when my BG reaches close to 7 mmol that the bolus gets released and i am guess it because that is the point where it goes back very quickly. However, when its in mid 6's, its always slow to go back into 5's.
Happy reading.
I think Bolus is an appropriate term to describe the Phase 1 Insulin ResponseThis is very confusing. The terms 'bolus' and 'basal' insulin are related to injected insulin, not to endogenous insulin.
I suppose you are talking about your own insulin response, not injected insulin, right?
If I were you, I would edit my post to prevent totally confusing answers.
Or just delete it and start a new thread.
While the terms might make sense from a linguistics point of view, it's very confusing on a forum of diabetics on insulin and diabetics not on insulin, because they're not usually used in this sense.I think Bolus is an appropriate term to describe the Phase 1 Insulin Response
The question is at what blood glucose level your bolus insulin (first response) releases?.
I do not recognise the units you quote. (nM) Is this nanomol or nanomol/l? The first is a molecular weight, the latter is a density."Glucose-induced β-cell electrical activity, recorded with glass microelectrodes, is characterized by trains of fast action potentials (“spikes”). The membrane depolarizes before each train of spikes and then depolarizes. This pattern is termed a “burst.” There is a characteristic biphasic response to a square wave of 11.1 mM glucose. Pulses at higher glucose concentrations (22.2 mM or more) evoke transient, constant spike activity."
Possibly this is why some schools say you should stay below 11.1 precisely (I always assumed that number came from 200mg/dl/18).
The theory of beta cell de-differentiation may be mind bending but fact is high glucose changes the alpha to beta cells ratio, which may be why it is so important to give your overworked pancreas some rest.
Thanks updated with first and second phase.This is very confusing. The terms 'bolus' and 'basal' insulin are related to injected insulin, not to endogenous insulin.
I suppose you are talking about your own insulin response, not injected insulin, right?
If I were you, I would edit my post to prevent totally confusing answers.
Or just delete it and start a new thread.
According to the papers i reviewed, the output of insulin is indeed pulsative. but the period of oscillation is around 15 minutes for non diabetics, but diabetics do tend to be faster ( but in the range 5 to 15 minutes per pulse period. So the term 'fast pulse train' is perhaps misleading."Glucose-induced β-cell electrical activity, recorded with glass microelectrodes, is characterized by trains of fast action potentials (“spikes”). The membrane depolarizes before each train of spikes and then depolarizes. This pattern is termed a “burst.” There is a characteristic biphasic response to a square wave of 11.1 mM glucose. Pulses at higher glucose concentrations (22.2 mM or more) evoke transient, constant spike activity."
Possibly this is why some schools say you should stay below 11.1 precisely (I always assumed that number came from 200mg/dl/18).
The theory of beta cell de-differentiation may be mind bending but fact is high glucose changes the alpha to beta cells ratio, which may be why it is so important to give your overworked pancreas some rest.
Thanks for that, lots of interesting information which will take me a long time to study properly. I did note in a quick scan that amino acids and fatty acids also result in an increase in Insulin but I haven't had time to find out why.This is a great read for anyone who needs to understand their diabetes and hyperglycaemia. It cleared several of my questions that I always wondered based on my experiments.
In particular the affect of GLP and incretins over the stimulation of insulin secretion was an interesting read.
https://www.pancreapedia.org/reviews/secretion-of-insulin-in-response-to-diet-and-hormones
However, I still have one question that i can not find a satisfactory answer so far, so what are your personal experiences or guestimate on it. The question is at what blood glucose level your endogenous insulin (first response) releases? I notice in my case that my BG regulation is mainly managed by my endogenous insulin (second phase response). Its only when my BG reaches close to 7 mmol that the first phase insulin gets released and i am guess it because that is the point where it goes back very quickly. However, when its in mid 6's, its always slow to go back into 5's.
Happy reading.
lipid storage requires insulin to open the gates similar to storing glycogen.Thanks for that, lots of interesting information which will take me a long time to study properly. I did note in a quick scan that amino acids and fatty acids also result in an increase in Insulin but I haven't had time to find out why.
Yes, its well known that proteins do spike Insulin that is why in keto diet they don't recommend high proteins as it kicks them out of ketosis. Per Dr. Bernstein, 36% of protein converts to sugar.Thanks for that, lots of interesting information which will take me a long time to study properly. I did note in a quick scan that amino acids and fatty acids also result in an increase in Insulin but I haven't had time to find out why.
The sources are both from biopsy and post mortem and I also have an interesting study that found alpha/beta ratio in type 2 diabetics was exactly twice as high as in those with normal glucose tolerance. And very very important; the alpha/beta ratio correlates with diabetes duration!What is the source of the alpha/beta ratio? Is it post mortem, or biopsy
How about reducing the alpha to beta ratio instead?This would clarify a few more things i believe ...
https://www.frontiersin.org/articles/10.3389/fendo.2020.00378/full#B1
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3110273/The sources are both from biopsy and post mortem and I also have an interesting study that found alpha/beta ratio in type 2 diabetics was exactly twice as high as in those with normal glucose tolerance. And very very important; the alpha/beta ratio correlates with diabetes duration!
But this is all of topic.
How about reducing the alpha to beta ratio instead?
“In conclusion, the pancreatic α/β increased after type 2 diabetes onset and correlated with diabetes duration, while relative alpha-cell area correlated with HbA1c.”
In conclusion, the following report is an analysis of beta cell dysfunction which is relevant to the dedifferentiation discussion, but not the OP
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4010577/
This is a great read for anyone who needs to understand their diabetes and hyperglycaemia. It cleared several of my questions that I always wondered based on my experiments.
In particular the affect of GLP and incretins over the stimulation of insulin secretion was an interesting read.
https://www.pancreapedia.org/reviews/secretion-of-insulin-in-response-to-diet-and-hormones
However, I still have one question that i can not find a satisfactory answer so far, so what are your personal experiences or guestimate on it. The question is at what blood glucose level your endogenous insulin (first response) releases? I notice in my case that my BG regulation is mainly managed by my endogenous insulin (second phase response). Its only when my BG reaches close to 7 mmol that the first phase insulin gets released and i am guess it because that is the point where it goes back very quickly. However, when its in mid 6's, its always slow to go back into 5's.
Happy reading.
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