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Features

Stress Causes Insulin-Producing Cells to Go Inactive

features-diabetesTwenty-five million Americans, or 8.3 percent of our population, suffer from diabetes. Due to the recent obesity epidemic, nearly two million new cases of diabetes were diagnosed in people aged 20 years and older in 2010, according to the American Diabetes Foundation.

Researchers from Columbia University have proposed a new hypothesis that may change our understanding of the cause of diabetes, and if tested positively, may allow for better treatment options for the millions suffering from diabetes in the near future.

The body’s blood sugar level, commonly reported as the serum glucose concentration, becomes elevated after we eat food, especially that high in carbohydrates. The digestive system breaks down the large complex carbohydrates, polysaccharides, down into disaccharides and eventually into monosaccharides, the most common being glucose. The hormone insulin allows our cells to take up the blood sugar glucose to metabolize it for energy, store it as short term energy reserve known as glycogen, or as fat, the long term energy reserve – depending on our physiological conditions at the time.

In the most common form of diabetes, known as Type 2 diabetes mellitus, the body has either an inability to produce enough insulin or it ignores insulin itself. A lack of insulin therefore does not allow cells to take up glucose from the blood, so the cells cannot metabolize glucose for energy. Barring glucose from entering cells causes the blood to quickly get very concentrated with glucose in a condition known as hyperglycemia.

Hyperglycemia disrupts the osmotic pressure gradient in our blood and leads to a wide gamut of complications, the most common being high blood pressure due to the high solute concentration in the blood. Other complications that may arise include lethargy, heart disease, stroke, blindness, kidney disease and neuropathy, according to the American Diabetes Foundation.

The traditional model of thinking about the cause of Type 2 diabetes mellitus is that the beta cells of the pancreas, which produce insulin, die off and can no longer produce insulin. Researchers Chutima Talchai and Domenico Accili of Columbia University have posed a new hypothesis for the causality of this disease.

After the beta cells are overworked from producing as much insulin as they could under the stressed conditions created by hyperglycemia, the beta cells revert to a nascent state where they do not produce insulin, unlike the traditional model where the beta cells would die off completely.

Omkaran Menon, junior chemistry major, thinks this research “can shed light on so many other things as well. If we can trick the beta cells to start functioning again, who’s to say that other cells in the body couldn’t be tricked into functioning again?”

Alex Ferrara, a fourth year clinical lab sciences major, thought the research to “not only be interesting but informative as well as it describes the variant processes taking place at the cellular level for patients with Type 2 diabetes mellitus. It is crucial to continue this endeavor as it may potentially help cure these people considering that millions are suffering with the disease.”

If it works, this hypothesis may turn the tables on how physicians will treat diabetes in the near future. By focusing treatment on relieving stress on the beta cells rather than on making them produce as much insulin as they can, the beta cells may recuperate forward into their functioning state and begin producing insulin once again and return serum glucose concentrations back to their homeostatic levels.

What exactly is causing these beta cells to de-differentiate and what might be done to get them to begin producing insulin again, said Dr. Dennis Rhoads, professor of biology at the University. These are key questions that need to be answered.

To study what was going on in the molecular scale, Dr. Accili investigated the role played by a protein called FOXO1, which seems to disappear as beta cells stop producing insulin.

In the report that was recently published in the peer-reviewed journal Cell, Dr. Accili and Dr. Talchai genetically engineered mice that lacked the FOXO1 protein and subjected the mice to different forms of stress – “pregnancy for the females, aging for the males” – and the mice went on to develop hyperglycemia, and decreased insulin secretion, the most common signs of Type 2 diabetes mellitus, according to the New York Times.

The beta cells in these studies did not die but dedifferentiated to a nascent state; some even resembled alpha cells which make the hormone glucagon involved in releasing glucose from the cell into the bloodstream.

“We propose that dedifferentiation trumps endocrine cell death in the natural history of beta cell failure and suggest that treatment of beta cell dysfunction should restore differentiation, rather than promoting beta cell replication,” said Dr. Accili and Dr. Talchai in their paper published in Cell.

“Nothing ventured, nothing gained,” said Nick Kulka, a junior biology major. “If this works then maybe this research can be applied to help researchers work with other diseases to open new doors, paving the way for new ways of thinking.”

IMAGE TAKEN from diabetes.org

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