If glycogenolysis and glucose release in the liver is inhibited, e.g. no food, plenty of insulin, and alcohol - the cause of the 'so-called cocktail reception hypoglycaemia'.
by Laura Hieronymus, MSEd, APRN, BC-ADM, CDE, and Belinda O’Connell, MS, RD, CDE
When you think about diabetes and blood glucose control, the first thing that comes to mind is probably avoiding high blood glucose levels. After all, the hallmark of diabetes is high blood glucose, or hyperglycemia. But controlling blood glucose is more than just managing the “highs”; it also involves preventing and managing “lows,” or hypoglycemia.
Most people are aware that keeping blood glucose levels as close to normal as possible helps prevent damage to the blood vessels and nerves in the body. But keeping blood glucose levels near normal can carry some risks as well. People who maintain “tight” blood glucose control are more likely to experience episodes of hypoglycemia, and frequent episodes of hypoglycemia — even mild hypoglycemia and even in people who don’t keep blood glucose levels close to normal — deplete the liver of stored glucose (called glycogen), which is what the body normally draws upon to raise blood glucose levels when they are low. Once liver stores of glycogen are low, severe hypoglycemia is more likely to develop, and research shows that severe hypoglycemia can be harmful. In children, frequent severe hypoglycemia can lead to impairment of intellectual function. In children and adults, severe hypoglycemia can lead to accidents. And in adults with cardiovascular disease, it can lead to strokes and heart attacks.
To keep yourself as healthy as possible, you need to learn how to balance food intake, physical activity, and any diabetes medicines or insulin you use to keep your blood glucose as close to normal as is safe for you without going too low. This article explains how hypoglycemia develops and how to treat and prevent it.For more plz read at following link.
I am a type 1 diabetic and am very curious to find an answer for this. With regards to type 1 diabetic liver glycogen, the overall particle size is the same as healthy (see Besford, et al., Glycoconjugate Journal, 2015), implying that glucose release should be the same. However, this is not the case, so perhaps the problem exists in one of the many signalling pathways.
For type 2 diabetics, I have shown that their liver glycogen exists as very large aggregate structures that results in less enzymatically available glucose in times of need (i.e. hypoglyceamia) (also see Besford, et al., Glycoconjugate Journal, 2015). So there are differences in the glycogen stores which have ramifications for glucose release, but for the type 1 diabetic case there seems to be something different happening (assuming type 1 diabetic mouse models are accurate). The answer may involve the synthetic insulins used in the condition (can they perform all the duties as natural insulin?), or perhaps some other phenomenon.
You have to get hold of a decent biochemistry or diabetes text book and read about the neurohumoral control of glucose homeostasis. As a quick primer, try
Muscle glycogen cannot contribute to the blood glucose because muscle does not have the enzyme Glucose 6 phosphatase. Glucose cannot come out of the muscle because insulin recruits the GLUT4 only in hyperglycemia to stimulate the up take by the muscle cells.