Oxygenating your body's cells can reduce inflammation and insulin resistance

(NaturalNews) For the first time, researchers have uncovered the mechanism by which an unhealthy diet leads to type 2 diabetes, in a study conducted by researchers from the University of California, San Diego, and published in the journal Cell on June 5.

"We've described the etiology of obesity-related diabetes. We've pinpointed the steps, the way the whole thing happens," researcher Jerrold M. Olefsky, MD, said.

How high-fat diets produce inflammation

Diabetes, characterized by high blood sugar levels, is the seventh-leading killer in the United States, responsible for 70,000 deaths per year. It is the leading cause of blindness and kidney failure in adults, a major cause of nerve damage and related amputations and a major risk factor for heart disease and stroke.

Diabetes now affects 8.3 percent of the U.S. population, or more than 25 million people -- a threefold increase since 1980. In addition, another 79 million people are prediabetic, at risk for developing type 2 diabetes.

In type 1 diabetes, the pancreas does not produce sufficient levels of the blood-sugar-regulating hormone insulin. In the case of type 2 diabetes, the body becomes desensitized to insulin.

Research has shown that obesity and poor diet are major risk factors for type 2 diabetes. Studies have suggested that obesity leads to chronic inflammation in the body's adipose (fat) tissues and that this can lead to systemic inflammation throughout the body, which leads to insulin resistance and diabetes. The new study sought to uncover the mechanisms by which this occurs.

Researchers fed mice a high-fat diet and then observed the activity levels of a wide variety of biomarkers. They found that a diet high in saturated fatty acids increased the activity of adenine nucleotide translocase 2 (ANT2), a mitochondrial protein found in the membrane of fat cells. ANT2 is known to play an important role in cellular energy metabolism.

When ANT2 was activated, fat cells began to consume more oxygen within their membranes, leaving less for the rest of the cell. This caused an overall state of inadequate oxygen supply to fat cells (hypoxia). Hypoxia, in turn, caused the deprived fat cells to produce a protective transcription factor called HIF-1alpha.

HIF-1alpha then triggered the release of proteins called chemokines, which alert the immune system when cells are in distress. This led directly to an inflammatory response.

While inflammation is part of a healthy immune response, chronic inflammation has been linked to a number of diseases. Indeed, the researchers found that, when the diet high in saturated fat was maintained over time, the resulting chronic inflammation led to obesity and insulin resistance, as well as inflammation of other bodily tissues.

The study was funded by the American Diabetes Association, the National Institute of Aging, the National Institute of Child Health and Human Development, the National Institutes of Health and the Wellcome Trust.

Implications for prevention?

"The research is in mice, but the evidence suggests that the processes are comparable in humans and these findings are important to not just understanding how diabetes begins, but how better to treat and prevent it," Olefsky said.

The researchers expressed hope that inhibiting the activity of either ANT2 or HIF-1alpha could hinder or even reverse the cellular damage caused by a high-fat diet in prediabetics. Promisingly, they found that mice who had been genetically engineered to have fat cells without HIF-1alpha seemed immune to the inflammation and insulin resistance typically caused by a high-fat diet.

By uncovering the physiological mechanisms by which a high-fat diet leads to diabetes, the study also emphasizes the most effective means of preventing (and sometimes even treating) the disease: improving your diet and exercise habits.

Sources for this article include:

http://www.newswise.com

http://ucsdnews.ucsd.edu

http://health.ucsd.edu

http://www.naturalnews.com

http://science.naturalnews.com

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