Prevent Obesity To Avoid Treating Diabetes In The Future

Newly diagnosed type 2 diabetics tend to have one thing in common: obesity. Exactly how diet and obesity trigger diabetes has long been the subject of intense scientific research.
A new study published online August 14 in Nature Medicine reveals a pathway that links high-fat
diets to a sequence of molecular events responsible for the onset and severity of diabetes.

WHAT IS DIABETES TYPE 2?

Diabetes mellitus type 2 (also known as type 2 diabetes) is a long term metabolic disorder that is characterized by high blood sugar, insulin resistance, and relative lack of insulin.

 Common symptoms include increased thirst, frequent urination, and unexplained weight loss.
In a further studies, spanning mice and humans a research team at the Center for Nanomedicine, a
collaboration between Sanford-Burnham and the University of California, Santa Barbara, discovered a pathway to disease that is activated in pancreatic beta cells, and then leads to metabolic defects in other organs and tissues, including the liver, muscle and adipose (fat).
Together, this adds up to diabetes.

“We were initially surprised to learn how much the pancreatic beta cell contributes to the onset and severity of diabetes,” says Dr. Jamey Marth, director of the Center for Nanomedicine and senior author of the study. “The observation that beta cell malfunction significantly contributes to multiple disease signs, including insulin resistance, was unexpected.

As he aslo noted, however, that studies from other laboratories published over the past few decades had alluded to this possibility.”
In healthy people, pancreatic beta cells monitor the bloodstream for glucose using glucose
transporters anchored in their cellular membranes.
 When blood glucose is high, such as after a meal, beta cells take in this additional glucose and respond by secreting insulin in a timed and measured response. In turn, insulin stimulates other cells in the body to take up glucose, a nutrient they need to produce energy.

In this newly discovered pathway, high levels of fat were found to interfere with two key transcription factors—proteins that switch genes on and off. These transcription factors, FOXA2
and HNF1A, are normally required for the production of an enzyme called GnT-4a glycosyltransferase that modifies proteins with a particular glycan (polysaccharide or sugar) structure. Proper retention of glucose transporters in the cell membrane depends on this modification, but when FOXA2 and HNF1A aren’t working properly, GnT-4a’s function is greatly diminished.

So a further research was carried out on a mice otherwise fed in a high-fat diet, they found that the animals’ beta cells could not sense and respond to blood glucose.

Preservation of GnT-4a function was able to block the onset of diabetes, even in obese animals. Diminished glucose sensing by beta cells was shown to be an important determinant of disease onset and severity.

Obesity can lead to diabetes because it trigger changes to the body’s metabolism.
These changes cause fat tissue (adipose tissue) to release fat molecules into the blood, which can affect insulin responsive cells and lead to reduced insulin sensitivity.

Symptoms of Obesity:

Urinating often.
Feeling very thirsty.
Feeling very hungry – even though you are
eating.
Extreme fatigue.
Blurry vision.
Cuts/bruises that are slow to heal.
Weight loss – even though you are eating
more (type 1)
Tingling, pain, or numbness in the hands/feet
(type 2).


"PREVENTION IS BETTER THAN CURE."