Keeping Pancreatic ß cells Healthy Is the Key to Stop Type II Diabetes
Type 2 Diabetes Mellitus (T2DM) is a progressive disease caused by specific genetic and environmental factors that induce insulin resistance and beta cell failure. It has been shown that at the time of diagnosis of T2DM, beta cell function is already reduced by approximately 50% and that the reduction of beta cell function appears to start with 10-12 years prior to the appearance of hyperglycemia symptom 1,2. Given that insulin resistance is reversible or can be overcome by increasing blood insulin concentration, these studies imply that the real cause of hyperglycemia or T2DM is beta cell dysfunction 3,4.
Eating Too Sweet Results in Stress on ß cells
While hyperglycemia can be reversed, some of its consequences continue. Studies have shown that constant exposure of beta cells to high plasma glucose causes reduction of insulin gene expression and even worse, beta cell death; this is known as glucotoxicity 5,6,7. High free fatty acid concentration in our blood, no matter directly from fat or converted from sugar in our diets, has similar effects on beta cell function; this is known as lipotoxicity. Several mechanisms have been proposed for glucotoxicity and lipotocixity induced beta-cell dysfunction and death, such as: reactive oxygen species (ROS) production in mitochondria and inflammation, and endoplasmic reticulum stress.