When Obesity Doesn’t Always Mean Diabetes: It’s well documented that obesity and diabetes go hand in hand. However a chance encounter with a gene not previously linked to diabetes may have researchers reconsidering what they know, how they apply that knowledge and what it may ultimately mean to overweight patients.
ScienceDaily.com reports, “The chance discovery of a genetic mutation that makes mice enormously fat but protects them from diabetes has given researchers at Boston University School of Medicine, USA, new insights into the cellular mechanisms that link obesity to Type 2 diabetes. Dr Gerald Denis and his colleagues report their findings in the current issue of The Biochemical Journal.”
The gene is known as Brd2 and, “In mice where there had been a single, genetic change in the Brd2 gene, fortuitously reducing its expression, the mice became severely obese — but did not go on to develop Type 2 diabetes. This result was very surprising because in both ‘mice and men’, chronic obesity commonly leads to Type 2 diabetes, with its life-threatening consequences, including heart disease, kidney and nerve damage, osteoporosis, blindness and circulation problems in the feet that can require amputation.”
You need to understand that the ‘fat’ mice would have been comparable to a man weighing 600 pounds. According to ScienceDaily.com the overweight mice, “Exercised at the same levels as normal mice and, in comparison, lived for a surprisingly long time.”
This same report indicates, “There is an urgent need for a much deeper biological understanding of the forces that link obesity and diabetes, in order to design new drugs and therapies for treatment.”
There are some individuals who are obese, yet do not develop diabetes. It is believed that an individual can be overweight and non-diabetic with a correctly functioning metabolism. It is when the metabolism slows down that diabetes can develop. Dr Denis is quoted by ScienceDaily.com as saying, “Studies have shown that these individuals have a reduced ‘inflammatory profile’. Inflammation caused by normal immune cells called macrophages leads to insulin resistance and Type 2 diabetes — this inflammation is typically seen in connection with obesity but it is the inflammation that is a trigger for diabetes, not the obesity itself. The mechanisms that explain this protection from diabetes are not well understood.”
In describing what may be happening in the body of the individual Dr. Denis said, “Much like these protected obese humans, the Brd2-deficient mice have reduced inflammation of fat and never develop failure of the beta cells in the pancreas that is associated with Type 2 diabetes.”
The research on Brd2 was at least partially funded by the National Institutes of Health and Dr Denis was quick to point out, “The strong influence of Brd2 levels on insulin production and action suggest that Brd2 is likely to be a promising target for diabetes treatment, but also imply that overactive Brd2 might cause diabetes. The ways in which Brd2 affects the immune system may also play a part in Type 1 diabetes, further studies to determine this are needed.”
These finding are reported in concert with other studies that are looking to genetic manipulation to turn off genetic triggers that can result in diabetes. Obviously this type of research is not taken lightly and needs additional findings to confirm the true value of the information that may be best described as preliminary.