Scientists Discover How a Fatty Diet Can Cause Type II Diabetes

Doctors have long been aware that a fatty diet can bring about Type II diabetes, but American scientists say they have now discovered how this works.  After experiments on mice and on human cells, they discovered how fat in the blood interferes with the functioning of insulin to control blood sugar levels, which may bring better, more effective treatment a step nearer.

Obesity and a high consumption of fat are known factors in the development of Type II diabetes, and the worsening obesity crisis has seen diabetes cases double in the last 30 years.  In the US,  there are now 25.8 million people with diabetes and a further 79 million with pre-diabetes.  Many more with minimal symptoms may go undetected.

Type II diabetes occurs when the body’s cells stop responding normally to the production of insulin, which is created in the beta cells in the pancreas.  When blood sugar levels rise after a meal, the cells respond by releasing insulin into the bloodstream to stimulate the tissues to take up glucose from the blood.  The cells then store the glucose for their own use when they need energy, and the level of sugar in the blood falls again to normal.

In a diabetic person, the cells have lost the ability to respond effectively to this message.  The glucose therefore remains in the blood and can rise to high levels, causing long-term damage to cells and organs and often leading to serious complications.

Scientists are still trying to find out why the cells lose their ability to respond to insulin, but this latest study, published in Nature Medicine journal, may point the way to the solution.  DiabetesUKhas said the research is interesting and worthy of further work.

The team at theUniversityofCaliforniaand the Sanford-Burnham Medical Research Institute reported that they had identified the way in which fat prevents the insulin response by interfering with a key protein.  The enzyme GnT-4a is vital to the beta cells’ ability to monitor glucose levels in the blood and react.  A fatty diet leads to high levels of fatty acids in the blood, which in turn suppresses the production of this enzyme, leading to diabetes.

The mice used in the experiments were fed a fatty diet and had high levels of fat in their bloodstream.  Scientists found this caused beta cells to malfunction by suppressing GnT-4a, which caused the beta cells to become “blind” to blood sugar levels.  The mice then showed symptoms of Type II diabetes.

The tests were also carried out on human pancreas cells, and the results were the same.

Study leader Dr. Jamey Martin reported that the significance of beta cell malfunction in insulin resistance and other symptoms of diabetes could lead the way to more effective treatments for the disease.  Artificially boosting GnT-4a levels in a patient could prevent them from developing Type II diabetes.  Beta cell gene therapy or drug therapy could prevent the suppression of the enzyme by the fat, he said.

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