from what we just learned recently in school: insulin is made in the pancreas to lower blood sugar by carrying the sugar into the cells. other than insulin, there are many hormones who rise bg, which means that they give a signal to the liver that it has to release sugar. that way our cells are provided with sugar 24 hours a day, because they cant store that much sugar and also need sugar (energy) while we dont eat. so because of that glucagon is released consistently to let the liver release sugar, and insulin is needed consistently to put that released sugar into the cells where it is burned.
adrenalin, cortisol and other hormones actually do rise glucagon release, cause if you do sports you need more sugar, but adrenalin and cortisol also have the same impact on the liver, so only by passing by the liver these hormones let the liver release more insulin
adrenalin, cortisol and other hormones actually do rise glucagon release.
true, is is also what's know as Dawn Phenonmenon (sp?) these hormones are released upon wake up, naturally, which also makes our blood sugars rise, we, as type 1's, don't make insulin to counter attack the rise.
here's another good link: http://dtc.ucsf.edu/types-of-diabetes/type1/understanding-type-1-diabetes/how-the-body-processes-sugar/the-liver-blood-sugar/
sarah, glucagon is a hormone that affects the liver. the liver will not release sugar on its own. it needs a signal from the hormone glucagon to release sugar. and it needs a signal from insulin to take up sugar. hormone glands get their signals from the brain. so if a insulin and glucagon producing person is low, the brain registers that and gives a signal to the alpha cell to produce glucagon. the glucagon floats around in the blood and if it comes to the liver the liver will take it up and release glucose. same with high bs but the other way around. as we just had that in school, i am pretty sure thats the way it is. now my question was why a diabetic pancreas, where beta cells are destroyed, cant react "healthy" to a low as the alpha cells which produce glucagon should be fine and give a signal to the liver to release sugar. that way we would not have that many lows.
basal insulin on one hand suppresses the glucagon release, which suppresses the glucose release, but the basal insulin also helps the cells to take in that sugar that is still released by the liver, so our cells can work. and our bg doesn't rise.
yes, i know that glucagon is a hormone, released from the alpha cells. the liver also produces and releases sugar: (see below). I think we're confusing glucagon (from alpha cells) and sugar coverted from what we eat and what is stored and also produced in the liver, no?
The liver both stores and produces sugar…
The liver acts as the body’s glucose (or fuel) reservoir, and helps to keep your circulating blood sugar levels and other body fuels steady and constant. The liver both stores and manufactures glucose depending upon the body’s need. The need to store or release glucose is primarily signaled by the hormones insulin and glucagon.
During a meal, your liver will store sugar, or glucose, as glycogen for a later time when your body needs it. The high levels of insulin and suppressed levels of glucagon during a meal promote the storage of glucose as glycogen.
The liver makes sugar when you need it….
When you’re not eating – especially overnight or between meals, the body has to make its own sugar. The liver supplies sugar or glucose by turning glycogen into glucose in a process called glycogenolysis. The liver also can manufacture necessary sugar or glucose by harvesting amino acids, waste products and fat byproducts. This process is called gluconeogenesis.
this is exactly what metformin does for a type 2, Metformin works by suppressing glucose production by the liver.
It has nothing to do with the glucagon produced in the alpha cells in the pancreas and why metformin alone, for a type 1, won't do crap for us, we...type 1's.
Sounds like you have a very knowledgeable Bio teacher.
Yeah, hormones generally have primary, secondary, tertiary, etc etc, actions and cortisol as well as adrenalin, even Growth Hormone can cause rises in BG, either indirectly or directly.
I'm no endocrinologist so I can never keep the big picture clear in my head.
I think Brian raises a good point about T1 versus T2 as well. I would imagine hormone action and response would be slightly, or not so slightly different depending.
Here is some more info... >
Beta Cells
The beta cells of the islets secrete insulin. Insulin is a small protein consisting of
an alpha chain of 21 amino acids linked by two disulfide (S-S) bridges to a
beta chain of 30 amino acids.
Beta cells have channels in their plasma membrane that serve as glucose detectors. Beta cells secrete insulin in response to a rising level of circulating glucose ("blood sugar"). Insulin affects many organs.
Insulin stimulates liver cells to take up glucose from the blood and convert it into glycogen.
Insulin stimulates skeletal muscle fibers to
take up amino acids from the blood and convert them into protein
take up glucose and convert it into glycogen
Insulin acts on fat (adipose) cells to stimulate the synthesis of fat.
Taken together, all of these actions result in:
the storage of the soluble nutrients absorbed from the intestine into insoluble, energy-rich products (glycogen, protein, fat)
a drop in the level of blood sugar
Amylin
Amylin is a peptide of 37 amino acids, which is also secreted by the beta cells of the pancreas.
Some of its actions:
inhibits the secretion of glucagon;
slows the emptying of the stomach;
sends a satiety signal to the brain.
All of its actions tend to supplement those of insulin, reducing the level of glucose in the blood.
A synthetic, modified, form of amylin (pramlintide or Symlin®) is used in the treatment of type 2 diabetes.
Alpha Cells
The alpha cells of the islets secrete glucagon, a polypeptide of 29 amino acids.
Glucagon acts principally on the liver where it stimulates the conversion of
glycogen into glucose ("glycogenolysis") and
fat and protein into intermediate metabolites that are ultimately converted into glucose ("gluconeogenesis")
In both cases, the glucose is deposited in the blood.
Glucagon secretion is
stimulated by low levels of glucose in the blood;
inhibited by high levels, and
inhibited by amylin.
The physiological significance of this is that glucagon functions to maintain a steady level of blood sugar level between meals.
Injections of glucagon (which is readily available thanks to recombinant DNA technology) are sometimes given to diabetics suffering from an insulin reaction in order to speed the return of normal levels of blood sugar.
Delta Cells
The delta cells secrete somatostatin. This consists of two polypeptides, one of 14 amino acids and one of 28.
Somatostatin has a variety of functions. Taken together, they work to reduce the rate at which food is absorbed from the contents of the intestine.
Somatostatin is also secreted by the hypothalamus and by the intestine. Further information about somatostatin can be found by following the links.
Gamma Cells
The gamma cells of the islets secrete a 36-amino-acid pancreatic polypeptide, which reduces appetite.
No function has yet been found for this peptide of 36 amino acids.
Very interesting discussion, guys. I am not as scholarly minded to read all the studies/tracts on glucagon, and glycogenesis. Not to "Hijack" the thread,but: I am wondering why many type ones from the "way back" like me and some others I know, with 40+ years of this disease; do not have as many sudden severe drop lows as those who were relatively ( less than 25 years) diagnosed?. I do not have a pattern of unaware onset, untreatable-by-myself lows at all. I can actually only remember only 5-6 lows in my lifetime where I needed the squad. Less than 15 when I have needed others to help me,: in a total of 45 years.
All of these lows came when I was using the synthetic insulins. All were due to overdoses of insulin while on MDI, and I was too sick to fix it right, or overdoses when I got too much basal/pre-bolus/too much correction; and a meal was inadverdantly delayed or I had unplanned-for exercise.
No pass outs at all when I used the mammalian insulins and one shot a day; even as a very active teenager and young adult, well into my 30's. The causation activities and episodes above occurred but I just popped a peppermint, or OJ, or half of a can of regular coke and took it in stride. No glucometers then, and I never really felt bad enough to pass out.
Does this meant that some of the counter-regulatory functions of glucagon are still in place for me? Could it have been because I took the beef and pork insulins for 25 years, at least? Preservations of alpha and beta cell functions as well as remnants of c-peptides? I have never had mine checked.
There is a study going on at Joslin to find out why certain type 1's do not have significant complications after over 50 years; some even not in the best of best control? Richard157(sp?) is in it.. I think that he does not have hypo unawareness either, after 60 years with type one. Do you think the animal insulins had a protective effect against alpha cell, beta cell reduction and thus renders less complications in some long-term diabetics? I will let you researchers ponder that, if you will. I am motivated to read a bit, but not today since my refrigerator died, and that is quite the priority LOL Thanks.
God bless,
Brunetta
I don't know about animal insulin versus rDNA insulins. I started on animal insulins as well and I think I do experience some symptons of depressed glucagon effectiveness as well. I certainly don't get the same kind of BG bounces after a hypo that I used to get when I first went on insulin. I think the link by meee is a good explanation for why we seem to lose the acuteness of our response to hypos after years of being diabetic.
I don't imagine that we lose glucagon production altogether like we do with insulin production though. We still experience increasing BG without a constant dose of basal insulin and the suggests that glucagon is still working even decades later.
it really is a fascinating yet complicated disease, huh. So much working and not working together. And, we wonder why this is so hard to manage sometimes, so much a play that we can't even see.
We need a white board, ha! my endo always starts making diagrams, pictures, etc..on his white board about the body and type 1 diabetes.
It is... I think it is amazing we can manage this at all really when you think about how complicated it is and how much we don't know... a white board... I wish my endo did that or at least paid attention to my bg records! Someone on my instagram has a white board to manage her diet etc.
That's interesting Brunetta, didn't they test your c peptide at the Faustman lab? They tested mine last August, I haven't gone again yet this year but they said it was higher than when I was first diagnosed. It's still low though. I thought people had worse hypos on regular and the other insulin available at walmart than the non generic newer ones.. I would love to get on an insulin where I had less lows. Mine aren't that severe I don't think although they feel awful, some of them, I have been able to treat them all on my own even when I was really low according to my meter, some I don't test for. Maybe you do have a better glucagon reaction- I was having hypoglycemia ten years or so ago and this suggests I was having trouble with that maybe.
The last time I went to the Faustman lab was in August 2011. If they tested my c-peptide, they told me nothing about it, LOL. I guess I could have asked, but I did not think about it. Mee, my situation with lows has been exactly the opposite with me. I have had worse, more interfering with functional life lows on the synthetic insulins than on the animal based ones.
God Bless,
Brunetta
One thing to clarify is synthetic versus analogues. Almost all insulin made today (unless specifically ordered) is synthetic (made artificially) instead of being obtained from animal organs as happened prior to the 1980s. Insulin analogues were not developed until the late 1990s with Humalog being the first in 1997 or 1998, followed by Lantus in 2000 and then Novolog/NovoRapid, Levemir, Apidra, etc. What makes an insulin an analogue is that it has been modified to have a faster/slower action than usual. Insulin such as NPH isn't an analogue because it's slowed down by adding a substance to it, not modifying the insulin molecule itself. (That is my very non-scientific understanding, anyway!)
So there is Regular insulin made from animals, but there is also Regular insulin made synthetically. Ditto for NPH and some of the other insulin types that don't exist anymore (Lente, etc.). People diagnosed more than about 30 years ago would have used animal insulin. Those of us diagnosed 15-30 years ago may have only used synthetic insulin though insulin analogues hadn't been developed yet. Anyone diagnosed more recently such as in the past 10-15 years may have only used analogues.
For myself, I was diagnosed in 1991 and to my knowledge I have only used synthetic insulin. I have hypo unawareness as a kid and had some severe lows because of it. I feel lows better now as an adult, although that may be partially because I pay more attention to my body and how I'm feeling. My low symptoms are pretty subtle and I have to either be low for a long time or be very low before I feel really shaky or sweaty or otherwise awful. Sometimes symptoms kick in once my blood sugar is coming up, for some reason. I have not had any truly severe lows (being completely unable to help myself, unable to communicate that something was wrong, or being unconscious) since getting onto MDI and then the pump.
oh, I see, I thought you didn't have the worse ones at all... yeah.. maybe it is the new insulins... I'm so afraid of lows lately, they're just coming on when I don't expect it but I still feel it.. you should call and ask them if they tested yours or not.. they told me to email in october last year and then they emailed me back to tell me what it was. That is one of the things they test as well as to see if you have the right type and amount of attacking T cells. They told me if you don't you would not be considered for phase two. I didn't go this year because I was too tired and my control moved to CA and couldn't come back. But they said I can still go without a control and they will provide one. She also asked if I had mono when I said I didn't feel well enough to go because they want to study people with mono too. One of the phase 1 participants came down with mono. good luck with your fridge!
thanks for that explanation Jen, my lows are all so different, sometimes I feel it, sometimes I don't, never know which one it will be, some are mild,some are dropping fast, like going down on a sinking elevator and then when I drink juice I feel myself come back up- a wonderful feeling!
I just read that novolin is made with wheat and humalin is made with ecoli.. I wonder if novolin can cause gluten sensitivity problems?
Hmm. I don't know much about how it's made in terms of the science, but I don't think the substance it's made from has any effect on the medication itself. Penicillin is apparently made from mold, but people with mold allergies aren't allergic to penicillin (I don't know if it makes them have a higher risk).
yeah, that's true... I'm allergic to sulfa antibiotics and I can use some sulfa products.. not sure if it's the same sulfa, I've forgotten now.
I have lots of allergies but *knocks wood* no medication allergies.
Also: Alpha cells respond to insulin, not glucose levels, unlike beta cells. This is why T1's risk DKA, while T2's are safe from that monster.
the information I found said they respond to low glucose levels but that would also mean high insulin most of the time I assume... type 2 can go into dka, I'm not sure what percentage do but it is less common I think and it's usually when they have an infection- the only person sicker than me in the er was someone who had type 2 who was also in kidney failure according to one of my nurses.