Type 2 diabetes is a well-known metabolic disorder that affects millions of people worldwide. While we know its symptoms, risk factors, and treatments, we still don’t know exactly how it develops. In essence, it is a well-known condition with a little-known cause.
Till date, what we know about type 2 diabetes is it occurs when the cells fail to utilize a glucose-metabolizing hormone insulin. This is called insulin resistance (IR). Over time, the beta cells of pancreas begin to produce less insulin. As a result, the blood glucose levels rise.
How A New Study Might Change Everything We Know About Type 2 Diabetes
In 2015, a study published in Clinical Interventions in Aging found that the beta cells, along with insulin, also secrete another hormone Human islet amyloid polypeptide (h-IAPP). H-IAPP is thought to be the main cause behind the aggregation of proteins in the beta cells. The toxic aggregate then destroys the beta cells causing a dysfunctional insulin secretion.
In line with the older study, a new study attempted to explore why the protein aggregates were toxic for the beta cells. During the study that involved mice, the researchers found that protein misfolding could probably be killing the insulin-secreting beta cells. In fact, the misfolded proteins show elicit abnormal physiological functions and are known as prions. Did you know mad cow (Bovine spongiform encephalopathy) is a prion disease?
In a normal condition, the proteins that have a physiological role can change their shape through a process called folding. When the folding process goes wrong and the proteins cannot function normally, it is called misfolding.
Thus, the study suggests Type 2 diabetes could be caused by protein misfolding similar to that in mad cow disease.
What It Means For The Future of Type 2 Diabetes
Maybe it’s time the researchers start taking a new route to find a cure for type 2 diabetes. New roads often lead to new destinations.
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