A new study from the United States has shown a link between regularly consuming a high-fat diet and molecular activity that can be responsible for the onset and severity of type 2 diabetes.
The research on both mice and humans, which was published in the journal Nature Medicine, found a pathway that is activated in pancreatic beta cells, which then leads to metabolic defects in other organs and tissues, such as the adipose (fat), liver and muscle, which leads to diabetes.
Pancreatic beta cells check the levels of glucose in the blood, if the glucose gets too high, beta cells absorb the extra glucose and secrete insulin as a response. The insulin then stimulates other cells to take glucose, which produces energy. For this new pathway, high amounts of fat were seen to interfere with two key factors that switch genes on and off.
When mice without these factors were fed a high-fat diet, their beta cells were not able to sense and respond to glucose, and preservation of one of the functions helped block the onset of diabetes, even for animals that were obese.
Jamey D. Marth, who led the research, commented “The observation that beta cell malfunction significantly contributes to multiple disease signs, including insulin resistance, was unexpected. We noted, however, that studies from other laboratories published over the past few decades had alluded to this possibility.”
He added “Now that we know more fully how states of over-nutrition can lead to type 2 diabetes, we can see more clearly how to intervene.”

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