A new study recently published in the journal FASEB provides evidence that both Type 1 and Type 2 diabetes share a similar cause that differs only in the rate at which either disease occurs. In the study, researchers found that human amylin, a hormone long associated with Type 2 diabetes, accumulates in toxic clumps that destroy the beta cells of the pancreas responsible for producing insulin. This causes progressively worse pancreas function, leading to failure, that ultimately culminates in either form of diabetes(1). Let's take a closer look at the findings.
When you eat a meal, insulin is secreted to help control the level of glucose in the blood by making cells in the body take in glucose. At the same time, the hormone amylin is also secreted to help insulin regulate blood glucose by slowing gastric emptying, reducing digestive enzymes, and causing you to feel full. When a person secretes more amylin than they can break down, clumps of the protein form on the pancreas negatively impacting beta cell function and causing cell death, thus decreasing insulin production.
In this study, researchers took mice and inserted copies of the human amylin gene, making them either homozygous or hemizygous. Mice who were homozygous for human amylin received two copies of the gene while mice who were hemizygous only received one copy. Mice who had two copies of the gene experienced higher levels of amylin, rapid destruction of the pancreas, high levels of insulin, a shortened stage of prediabetes, and juvenile-onset, or Type 1, diabetes. The mice that had one copy of the gene experienced lower levels of amylin and a more prolonged period of prediabetes, which led to adult-onset, or Type 2, diabetes.
If we look at this in concert with the research on leptin resistance that shows it to precede insulin resistance, we get an interesting picture. Leptin is another hormone that signals you to stop eating and is secreted by fat cells. People with leptin resistance produce a lot of leptin, but the cells in the hypothalamus that help regulate food intake don't respond to it. As a result, people with leptin resistance don't get the "full" signal and continue to eat when they don't need to. At some point, this may cause them to overproduce amylin causing the toxic clumps associated with Diabetes. Of course, this is an extreme simplification of a complex topic that needs further study, but it does paint a picture that both could be prevented or reversed. In addition, this study was done in mice so further studies in humans are needed.
Bonus nerd info: Interestingly enough, amylin shares a common effect on cells with amyloid beta, the protein associated with Alzheimer's disease. Both cause dysfunction of the mitochondria and an increase in free radical production due to interference in the activity of complex IV in the mitochondria. The end result of high free radical production...cell death. These mechanisms only differ in where the cells they affect are found, amyloid beta in the brain and amylin in the pancreas(2).
