Amylin, or islet amyloid polypeptide (IAPP) plays an important role in glycemic regulation. It helps you feel satiated and slows gastric emptying. Irregular levels of amylin can affect both Type 1 and Type 2 diabetes. Amylin and its co-secretion insulin are instrumental in controlling blood glucose, as well as appetite and weight. This article will provide an overview of how amylin works, the roles it plays, and how we use its analog, pramlintide, to aid in regaining balance.
Amylin is a peptide made up of 37 amino acids – the building blocks of the body. Amylin is secreted by the pancreatic beta-cells, which also secrete insulin at the same time, in response to nutrient intake. This secretion is released in a ratio of 100 to 1 (insulin to amylin). Amylin and insulin work together to regulate nutrient levels in the blood.
Amylin promotes the feeling of satiety by slowing gastric emptying. It also prevents spikes in blood glucose levels after meals. Altogether, these effects help regulate the blood sugar, which is important for normal bodily function. When blood sugar levels are outside of the normal range, it can indicate a medical condition, like diabetes.
When amylin is out of balance, we primarily see issues with diabetes. People with Type 1 diabetes are deficient in amylin, while people in the early stages of Type 2 diabetes have elevated levels of the peptide. It’s worth noting, too, that Type 2 diabetes is characterized by hyperinsulinemia – elevated levels of insulin. However, as time goes on, people in the later stages of Type 2 diabetes experience deficiencies in amylin secretion.
Although early research seemed to show that amylin inhibits insulin secretion leading to insulin resistance and the development of Type 2 diabetes, a body of more recent research suggests otherwise. We now know that amylin is an active pancreatic islet hormone – it works alongside insulin and glucagon to maintain glucose balance. Since amylin influences gastric emptying, it regulates the rate at which glucose flows into circulation. As a result, amylin controls how quickly glucose from our meals enters our systems and limits its release as well as hepatic glucose production. In all, it’s clear that amylin works with insulin to control blood sugar.
It’s also worth noting that we sometimes see increased levels of amylin in the plasma outside of people with diabetes. This includes people with obesity and those with impaired glucose tolerance. Pregnant women with normal glucose tolerance and those with gestational diabetes also sometimes have higher levels of plasma amylin.
Additionally, epidemiological studies have shown a clear link between metabolic disorders and neurodegenerative disorders. In particular, these studies have established a connection between Type 2 diabetes and Alzheimer’s disease. With this in mind, researchers believe that amylin could have a key role in acting as the interface between these two types of disorders.
In theory, amylin replacement could help improve glycemic control for diabetic people. Unfortunately, human amylin has certain properties that make it cluster and form amyloid fibers that may cause the destruction of beta cells in Type 2 diabetes. Since we need beta cells to make insulin, using amylin as a medication would be harmful.
Instead, scientists have developed a stable analog – pramlintide. Pramlintide has similar pharmacokinetic and pharmacodynamic properties to amylin, as well as similar actions. About 5,000 patients have been treated with pramlintide across a number of clinical trials. Thanks to these tests, we know that pramlintide is both safe and effective.
Further research is needed to understand whether adjusting amylin levels could aid in treating Alzheimer’s disease. Researchers do know that both amylin and beta-amyloids are prone to forming amyloid plaque and cytotoxic effects. Amylin can form these plaques in pancreatic islet cells as well as the central nervous system (CNS). In the CNS, it can co-localize with beta-amyloid plaques in some Alzheimer’s disease patients. With this knowledge, researchers theorize that amylin could be a second amyloid in neurodegenerative disorders.
Additionally, we may be able to learn something from where and when these plaques form. There’s some evidence that early processes of amyloid formation in the CNS could be related to hyperamylasemia conditions. Meanwhile, late stages of central amyloid pathologies are likely related to hypoamylinemic conditions. In short, we need to study and learn more about these relationships to potentially establish amylin-based treatment interventions. These advancements could aid in treatments for neurodegenerative disorders, as well as their metabolic comorbidities.
Ultimately, amylin is a key peptide that helps maintain a healthy appetite and normal blood sugar in the average person. People with diabetes have an imbalance in insulin as well as amylin. Though more research is needed, amylin nd its analog could potentially aid in treating multiple conditions.
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