Type 2 Diabetes May Be Transmissable

Preliminary findings in a research project have found that type 2 diabetes may be transmissable. Transmission would be through what's called a "misfolding of islet amyloid polypeptide protein" (IAPP), which is the way some other relatively rare diseases like mad cow disease are distributed. Findings were published in the journal Experimental Medicine.

The research was conducted by a team at the McGovern Medical School in Texas, a part of the University of Texas Health Science Center.

The research is based on previous findings that type 2 diabetes patients have IAPP accumulations in their pancreas.

That knowledge led to the researchers to wonder if a misfolding of the IAPP in pancreatic islets might have something to do with diabetes' spread. When pancreatic beta cells secret insulin, they also secrete IAPP as a peptide hormone. The effects of an overabundance of IAPP in type 2 diabetes is not well understood, but it's believed that these hormones can damage cells, slowing insulin production.

The research hypothesis was that the IAPP abundance could be causing insulin production slow-downs by misfolding. Diseases such as "mad cow" and Creutzfeldt-Jakob disease all spread this way and are classified as "prion disease" after the prion proteins that are accumulated as a result. Prions are normal in the body and are part of the natural proteins occurring in the body's cells, but when they form abnormally, they tend to misalign and accumulate.

Prion diseases are most commonly known in their neurodegenerative conditions such as Alzheimer's and Parkinson's. It's when the misfolded prions trigger other cells to also misfold (or "seed") that the disease can be spread to cells that do not have the problem - including cells of other organisms.

The spreading of prion diseases is relatively complex and rare and usually happens only when misfolded prions come in contact with tissues directly. But the theory that the scientists are chasing is that type 2 diabetes could be a prion disease that can spread in that way.

The team tested the theory by using mice whose pancreases were modified to express human IAPP. When misfolded IAPP was injected into those mice, it triggered aggregates in the mices' pancreases and within weeks, the mice developed type 2 diabetes symptoms. Further examination in vitro of human IAPP found similar results.

The authors caution against jumping to conclusions from these preliminary results, but believe they may be on track to understanding why some patients with no history of diabetes will contract type 2 after organ transplants.

Source: MedicalNewsToday.com