What’s Insulin ?
Insulin is a peptide, consisting of 51 amino acids in two peptide chains.
Preproinsulin is the primary translational product of the insulin gene, a biologically inactive precursor of insulin.
This 110 amino acid peptide is converted into proinsulin by signal peptidases, which remove its signal peptide from its N-terminus.
Proinsulin is then converted into the bioactive hormone insulin by removal of the C-peptide.
In addition, amylin, a 37 residue peptide hormone, is co-secreted with insulin (1:100 ratio) from the pancreatic beta cells, which are also deficient in diabetic people.
Structure and function of amylin
Amylin inhibits glucagon secretion, delays gastric emptying and acts as a satiety agent.
It acts as a short-term regulator of blood glucose level by diminishing the rate of glucose entering the bloodstream.
The C-peptide helps to prevent neuropathy and other vascular complications by assisting in the repair of the arterial muscular layers.
The role of insulin and glucagon :
Insulin stimulates glycogen synthesis and inhibits glycogen breakdown.In contrast, glucagon, a peptide hormone produced by alpha cells of the pancreas, raises the concentration of glucose in the blood-stream. Its effect is opposite to that of insulin, which lowers the glucose.
The pancreas A cells release glucagon when the concentration of glucose in the bloodstream falls too low. Glucagon binds to the glucagon receptors of the liver and causes it to convert stored glycogen, which is released into the bloodstream.
Thus, glucagon and insulin are part of a feedback system that keeps blood glucose levels at a stable level (Fig. 1.1).
Antibodies against insulin in type 1 diabetes
About 5% of people, particularly children and young adults, have type 1 diabetes as their bodies cannot produce insulin because their body’s immune system (i.e. white blood cells called T cells) attacks and destroys the beta cells.
Unfortunately, type 1 diabetes is not diagnosed until all beta cells have already been destroyed. Consequently, a person with type 1 depends on insulin to survive.
Insulin itself may be a key trigger of the immune attack on beta cells because antibodies to insulin and other proteins produced by beta cells are found in people with type 1 diabetes.
Researchers test for these antibodies to help identify people at increased risk of developing the disease.
Testing the types and levels of antibodies in the blood can help determine whether a person has type 1 diabetes or latent autoimmune diabetes of adults (LADA), a slow onset type 1 diabetes, or another type of diabetes.
Insulin resistance in Type 2 diabetes
In type 2 diabetes, the body does not use insulin properly; that is, there is insulin resistance. For a short term, the insulin resistance can be overcome as the pancreas will make extra insulin for glucose regulation.
However, in the long term, the pancreas cannot make enough insulin, and elevated glucose level begins its detrimental effects on the body if not regulated by drug intervention or insulin injection.
Both type 1 and type 2 diabetes result from a complete or partial loss of beta cell number and function. Based on the role of insulin and glucagon in glucose regulation.
The terminal effect of insulin on blood glucose
The drugs designed for diabetes target the secretion of insulin or depression of glucagon to maintain the glucose level within the acceptable range After subcutaneous insulin injection, the period it takes for the insulin to be absorbed and start lowering the blood glucose is the onset time.
For some time, the total insulin activity will increase and cause blood glucose to decrease. As more of the insulin is absorbed and starts to be effective.
The total insulin activity gets higher and reaches its maximum (the peak activity time), corresponding to the minimal
blood sugar level. As the insulin is metabolised by the body, the total
insulin activity decreases and the blood glucose starts to increase
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