High-fat diets = no good.
A study published in the journal “Diabetes” describes the research team’s efforts in discovering that high-fat diets activate the gene responsible for the disruption of insulin production in pancreatic beta cells that triggers on the onset of Type 2 diabetes as reported by DiabeticLive.com.
Tampa, FL (PRWEB) September 28, 2011
Study Identifies Possible “Master” Type 2 Diabetes Gene: Australian scientists may have found the answer to reversing Type 2 diabetes. A study published in the journal “Diabetes” describes the research team’s efforts in discovering a that high-fat diets activate the gene responsible for the disruption of insulin production in pancreatic beta cells that triggers on the onset of Type 2 diabetes. The researchers conducted their investigation at the Diabetes and Obesity Research Program at the Garvan Institute of Medical Research in Sydney.
Type 2 diabetes, sometimes called adult onset diabetes because it typically occurs later in life, is caused by both genetic factors and environmental ones such as poor diet, little exercise and being overweight. Production of insulin by the beta cells of the pancreas is reduced drastically in Type 2 diabetics; the lack of insulin causes elevated levels of glucose in the bloodstream. Insulin normally carries that glucose out of the blood and into cells, which use it as energy.
The gene discovered by the Australian research team is known as ld1. It lays dormant in individuals who eat a healthy diet and get regular exercise, but according to the researchers, high-fat diets trigger the gene into activating. Once active, the gene disrupts insulin production in the pancreas, which leads to Type 2 diabetes. Scientists conducted the study on cell cultures and on mice, which are typically used for such investigations since their genetic makeup is similar to that of a human.
According to the researchers’ findings, high-fat diets trigger the activation of the ld1 gene in mice. However, suppressing that gene and feeding mice the same high-fat diet did not result in the development of Type 2 diabetes. They also found that pancreatic tissue taken from diabetic patients shows higher levels of ld1, which is also thought to contribute to the growth of cancer cells.
The team’s next investigation will center on the feasibility of targeting the ld1 gene in therapies intended to reverse Type 2 diabetes. “The drugs could help the beta cells continue to produce insulin and protect them from the effects of a high-fat diet,” said Dr. Laybutt. “So even when you were having this high-fat diet your beta cells would be protected against the normal deterioration that occurs. That’s the potential. You wouldn’t have diabetes anymore because it only occurs when the beta cells fail to secrete enough insulin.”
Even if it is discovered that the gene can be targeted for such therapies, Dr. Laybutt cautions that it would be a “five to 10 year process” in testing the medication for safety before it could be marketed and sold.