Bacteria and Fat: A 'Perfect Storm' for Inflammation

          In this article, scientists from the University of Iowa studied how the interaction between bacteria and fat cells might contribute to diabetes. They experimented this through "immortalizing" fat cells. A normal human body's reaction to an infection or injury is inflammation, which is the connection between fat, bacteria, and diabetes. This occurs because fat cells, or adipocytes, interact with bacterial toxins, which trigger a chronic inflammatory process. This leads to insulin resistance which leads to diabetes. By immortalizing the fat cells, the bacterial toxins would stimulate the adipocytes to release cytokines, which promote inflammation. This builds up continuously dividing, identical cells that can be used for experimentation. In contrast, the primary fat cells, directly taken from fat tissue, quickly stop dividing and can't be used for repeated experiments. 

          The immature precursor fat cells were immortalized by adding in two genes from HPV (the virus that causes cervical cancer). This was added to an exzyme that controls the length of cells' telomeres, which protect chromosome tips on DNA from deterioration. This new experimental "tool" will allow researchers to "investigate the mechanisms of the inflammation and allow [them] to test ways to potentially inhibit the response".

          I found this article very interesting because my Grandfather has diabetes and I'm glad to see that they are finding new ways to investigate and cure diabetes. This method of immortalizing fat cells is very innovative and has a very promising future. Focusing on E. coli and Staphylococcus areus (staph) bacteria allows them to tackle diabetes and obesity, both of which are conditions that affect many Americans today. By promoting chronic inflammation, the staph superantigens may play a role in the development of diabetes. The inflammation would hinder the wound healing in diabetic foot ulcers, which an issue that affects 15-20% of people, including my Grandfather, with diabetes.


http://www.sciencedaily.com/releases/2013/10/131030185153.htm