I KNEW I read that somewhere!
And it was in the context of why DKA is such a risk for T1's.
Insulin supresses glyconeogenesis in the liver, which is where ketone bodies come from.
As long as you have a trickle of insulin, as most T2's do, BG can get quite high without ketoacidosis, as the liver isn't fooled into glyconeogenesis by the non-existent insulin.
The metabolic regulation in the liver between insulin and glucagon is a very complex, delicate balance. No insulin signals the liver that there is no sugar in the blood -- the liver is not sensitive to BG -- which fires up gluconeogenesis in addition to the glycogenolysis already being mediated by the glucagon.
:) you were right! I want to find out more about what happens in type 2 dka- it is more about infection and dehydration and other things that cause it but I wonder if their insulin levels are also low when in dka?
the question is why do they choose to respond to insulin levels and not glucose levels in type 1 dka?
Yeah, forgot about yeast. That's the other single-cell organism that is used in rDNA.
But you said "wheat" in your post...
Naughty meee :-) (j/k -- an easy typo to make!)
Boatload of sugar in just one glycogen molecule, eh? WOW!
yes for sure !
Might want to check the glyconeogenesis part. Insulin suppresses gluconeogenesis and the breakdown of glycogen to glucose as part of the group of mechanisms that decrease blood glucose levels.
You're right about ketone bodies being produced for the most part, if not exclusively, in the liver. It cannot be stressed enough that it is this excess ketone production by the liver that leads directly to DKA.
Ketone production in the liver, however, is a consequence of lipolysis (fat breakdown), as well as protein breakdown. Lipolysis is suppressed by insulin, which also has to work to build fat reserves. This is the mechanism by which the presence of insulin in the blood stream prevents DKA.
While insulin directly suppresses any mechanism that increases blood glucose, that suppression requires comparatively more insulin than the amount it takes to suppress lipolysis and prevent DKA. So, even T2s with greatly decreased insulin production can avoid DKA for the most part, as long as they are producing some insulin themselves..
Interestingly, I just read a summary of case studies on T2s that experience DKA and the suggestion is that stressful events like different illnesses causes an increase in glucagon production. Since glucagon does practically the exact opposite of Insulin, it's a greatly increased ketone production from lipolysis that seems to put T2s into DKA.
Meant gluconeogenesis -- there is no process even called glyconeogenesis, AFAIK. :-)
You still produce glucagon (if you left a hypo long enough you would come round most of the time), but the injections are mainly to speed up the action.
I've noticed that as I age, and have jacked up the protein intake for my body, my liver LOVES to convert protein into sugar. I need to cover a high protein meal with square wave bolus using my pump for 1-3 hrs (depending how much protein I eat) after eating in order to counteract the sugar that is produced by my liver. Anywhere from 40-60% of my protein intake gets slowly converted via gluconeogenesis.
I wanted to add that alpa cells respond to the glucagon level AND the insulin level. If the insulin level is high the alpha cells will not release great amounts of glucagon. The insulin level acts as an indicator that insulin has been produced for carbhydrates that are in the process of being digested. This has to do with the micro-dosing of insulin in a healthy body. Here insulin is just produced in small amounts or little bursts - just enough to influence the insulin level for the next few minutes. Insulin depended diabetics have much more insulin on board. Thus the reaction of the alpha cells to lows is ALWAYS modulated down. Just when the insulin level has fallen below the specific threshold the alpha cells will show a more pronounced response to lows. In mice scientists have destroyed the insulin receptor and thus the alpha cells responded with a high release of glucagon. As scientists have learned the blood vessels for the beta cells are the primary target of the autoimmune attack. It is quite likely that the blood vessels for the alpha cells are attacked too. This will also reduce the alpha cell mass over time. This is another explanation why the first years are easier to manage (some beta and alpha cells are left). The bottom line is that the counter-regulation of the alpha cells is broken by design in insulin dependend diabetics. The less insulin you need (or the more of the micro-dosing beta cells are intact) the more of the capability is left.
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what ratio are you using for protein, fat, carb, and correction?
I've been experiencing something similar when I have a low or no carb meal. Wife made me a 1/3lb Salsbury Steak for dinner last night, with some clever no-carb gravy. It was delicious! However, when I eat something like that, I have the same effect -- long, low-level infusion of glucose into the bloodstream from the liver.
So, I'd like to adjust your ratios for protein and fat relative to your carb and correction ratios, relative to mine.
dwallersv, Hi! I've gotten some advice suggesting not to consume more than 4 oz of fish (I love salmon!) or 8 oz of other meat during any given meal. Salmon and red meat tend to also contain some fat (more than turkey, lean ham, etc.), which will contribute to the protein digestion. So, what seems to be working for me (currently) is to take a dual wave bolus. I account for carbs using the normal bolus, and then I add up the total protein/fat that I also consume and give about half the amount as a square wave bolus for usually about 1 or 2 hours. If given over 2 hours, you can stop the square wave at 1-1.5 hours if you see that you've handled it appropriately. Example:
I have some lemon pepper salmon filets in the freezer. I'll eat one with a baked potato. The potato = 25 g of carbs (no sugar), 0 fat, and 2 g of protein. In one 4-oz filet = 0 g carbs, 2 g fat (0.5 g of which is saturated...the rest is good fat), and 23 g of protein. So, via addition, intake = 25 carbs (with no sugar blast), 2 g fat, 25 g protein. I eat this for lunch or dinner (I:C ratio 1:10), so I'll take a normal bolus of 2.5 U followed with a square wave bolus of 1.35 U given over 1 hour. This is 27 g (fat+protein), then use 1:10 I:C ratio (= 2.7 U) divided by 2 = 1.35 U.
For larger quantities of meat (let's say a 12-oz steak from beef), I'll follow a similar approach, but the square bolus will be given a little longer, maybe anywhere from 2-4 hours given total protein+fat. This approach seems to also work for me for pizza consumption. :)
This seems to be true- my brother and I were researching it more and I forgot to post back on this... alpha cells actually listen to insulin more apparently and with lack of insulin as in type 1 or type2 dka(not enough), they get confused and high glucose isn't enough to stop them from producing more glucagon. He found that same study in mice.
I get that same response too, but not with every low. It depends on how low and how much sugar I use to treat it.
I would say it just depends on the insulin on board. The more IOB the less pronounced the glucagon response. With an extreme low it is quite likely that more of the insulin has been degraded. This makes it more likely to see a glucagon response.
I've always thought Klaus Van Bulen murdered his very wealthy wife with insulin. His defense was that while there were syringes around, none they had droplets on them. That only happens if the insulin isn't actually injected. Bull! When I was on MDI, I often had little droplets ont he side of the needle - and I was younger then, with more taut skin.
I'm just clarifying that Symlin is used in the treatment of Type 1 Diabetes as well as Type 2.
"SYMLIN is a synthetic analog of human amylin, a naturally occurring neuroendocrine hormone synthesized by pancreatic beta cells that contributes to glucose control during the postprandial period."
"INDICATIONS SYMLIN® (pramlintide acetate) is indicated as adjunct treatment in adults with type 1 or type 2 diabetes who use mealtime insulin therapy and who have failed to achieve desired glucose control despite optimal insulin therapy (with or without a concurrent sulfonylurea agent and/or metformin in type 2 diabetes)."
"IMPORTANT SAFETY INFORMATION WARNING: SEVERE HYPOGLYCEMIA SYMLIN is used with insulin and has been associated with an increased risk of insulin induced severe hypoglycemia, particularly in patients with type 1 diabetes. When severe hypoglycemia associated with SYMLIN use occurs, it is seen within 3 hours following a SYMLIN injection. If severe hypoglycemia occurs while operating a motor vehicle, heavy machinery, or while engaging in other high-risk activities, serious injuries may occur. Appropriate patient selection, careful patient instruction, and insulin dose adjustments are critical elements for reducing this risk."