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Study addresses role of gene in treating diabetes, liver disease

Staff Writer

Published: Thursday, March 12, 2009

Updated: Sunday, August 30, 2009 02:08

Inhibiting the gene PGC-1b may play an important role in treating non-alcoholic fatty liver disease, type 2 diabetes and insulin resistance caused by an increased consumption of high fructose corn syrup, according to Yale medical researchers in the March issue of Cell Metabolism Journal.

Normally, PGC-1b regulates liver glucose and lipid metabolism while simple sugars are converted into fatty acids in the body, Cell Metabolism reported. However, when the body is introduced to large amounts of high fructose corn syrup, PGC-1b increases the actions of an element binding protein that causes fructose-induced insulin resistance, leading to non-alcoholic fatty liver disease and type 2 diabetes.

The inhibition of the gene PGC-1b, Cell Metabolism stated, prevents fructose-induced insulin resistance from occurring by preventing the complications in the transcription process of the element-binding gene SREBP.

Christie Hust, director of the Texas Tech Diabetes Education Center, said two types of sugars - complex and simple - can affect type 2 diabetes and non-alcoholic fatty liver disease.

According to the Mayo Clinic Web site, non-alcoholic fatty liver disease refers to the accumulation of fat in the liver of people who drink little or no alcohol and is caused by the liver's inability to effectively break down adipose tissue.

The gene PGC-1b is located in liver and fat tissue throughout the body, according to Cell Metabolism, causing increased levels of fat tissue when confronted with large and continuous amounts of high fructose corn syrup.

Non-alcoholic fatty liver disease affects about 29 million Americans and typically does not cause adverse symptoms. However, increased amounts of fat in the liver can cause inflammation, scarring and liver failure in patients, according to the Centers for Disease Control Web site.

The body typically handles sugar by breaking it down into glucose, said Dr. Kelly Bennett, medical director of Tech Student Health Services, which causes the pancreas to release insulin to regulate blood sugar levels.

"The pancreas releases insulin which puts any blood sugar not being used by the body into storage," Bennett said. "When there is a high circulation of insulin due to a breakdown in the process, the fat cells can't take the sugar and people run into a problem."

Patients who have non-alcoholic fatty liver disease do not have to be diabetic to get the disease however, Bennett said.

"Much research is leaning toward the glycemic index," Hust said. "It is a way of evaluating foods according to how quickly they are made into glucose. Foods with a high glycemic index enter the bloodstream rapidly, while low glycemic foods promote a slower release of glucose and insulin. Most of the glycemic index is easy to figure out, but there are times when some of the complex carbohydrates behave more like simple sugars."

Hust said simple sugars are then made into glucose faster which requires a large amount of insulin to be produced to pull the glucose into the cells, which adds to the insulin resistance and high blood sugar levels.

The Tech Diabetes Education Center typically treats older adults and may see one or two college-aged students, she said.

"A lot of our patients do not have health insurance," Hust said. "We operate in an under-served population, and the only Tech students we typically see are the Tech School of Nursing students who work in our clinics."

Bennett said the Student Wellness Center encounters pre-diabetes and fatty liver disease cases throughout the year in patients.

"We see hundreds of cases of pre-diabetes or metabolic syndrome per year," she said. "We probably get 20 or so proven cases of fatty liver per year too. In fact, the CT report another doctor just showed me had fatty liver as an incidental finding on one of our mid-20-year-old patients."

Bennett said although she was unaware of any research relating to the gene PGC-1b at the Tech Health Sciences Center, the center is conducting diabetes and pre-diabetes research in other areas related to prevention.

"Technically everyone can be insulin resistant," Bennett said. "But there are patients who are genetically predisposed, and because they eat and drink things like candy and coke without moderation, their blood sugar increases which can cause problems in them that it wouldn't cause in other people."

Bennett said everyone also maintains a threshold at which they can become insulin resistant if they gain enough weight through eating fatty and sugar-filled foods.

According to the Centers for Disease Control Web site, type 2 diabetes typically is caused by insulin resistance, a disorder that causes cells to use insulin improperly, and accounts for 90 percent to 95 percent of all diagnosed diabetes cases.

Type 2 diabetes can be controlled by monitoring blood glucose levels, following a careful diet, losing excess weight, exercising, and taking oral medication, according to the CDC Web site.

Hust said type 2 diabetes is typically caused by obesity, poor diet and a lack of exercise, which leads to insulin resistance as the pancreas slows down its production of insulin.

The Texas Department of State Health Services Web site stated type 2 diabetes and non-alcoholic fatty liver disease are not reportable; however, diseases such as the flu, anthrax and botulism are reportable.

The Lubbock Health Department only contains information relating to the number of infected cases occurring for reportable disease and therefore does not know the number of type 2 diabetes cases or non-alcoholic fatty liver cases occurring in Lubbock, according to the department's Web site.

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