How Bacteria and Fat Cells Could Contribute to Type 2 Diabetes
Researchers are exploring how bacteria and fat interact to promote inflammation that could lead to diabetes, type 2. All chronic diseases have an inflammatory component that can be triggered by bacteria, viruses and other environmental factors. According to a new study from University of Iowa investigators, bacteria and fat might create the "perfect storm" for diabetes.
"The idea is that when fat cells (adipocytes) interact with environmental agents -- in this case, bacterial toxins -- they then trigger a chronic inflammatory process," says Patrick Schlievert, Ph.D., UI professor and head of microbiology and co-senior author of the new study in a press release.
Inflammation is a normal response to any infection or stress. Chronic stress can lead to insulin resistance.
Schlievert says there is much interest in the cause of chronic inflammation.
Bacteria and fat a strong dynamic duo that creates inflammation
The study authors noted E. coli that is an intestinal bacterium has been suggested as a cause of diabetes when it triggers fat cells to release cytokines that are inflammatory molecules.
For the current study the investigators looked at how Staphylococcus aureus might do the same thing. Staph as the bacterium is otherwise known is often cultured from diabetic foot wounds. The germ lives are on skin and doesn't cause problems until there is an overgrowth that spawns infection and a common threat to people with diabetes.
The researchers also known that obesity combined with diabetes causes an overgrowth of Staph that releases potentially deadly superantigens that can get in the blood stream to cause sepsis and other serious complications.
Now it's time to get back to E. coli.
The gut bacteria produce a toxin called lipopolysaccharide (LPS). The investigators found Staphylococcus aureus produces high powered antigens that stimulate fat cells to produce cytokine molecules. But that’s not all. Staph combined with LPS from gut bacteria and fat all work together to potentially raise the risk of diabetes.
"The E. coli that resides in our gut produces LPS and every day a small amount of this toxin gets into our circulation, but it is generally cleared from the circulation by the liver. However, people colonized by staph bacteria are also chronically exposed to superantigens, which shut down the LPS detoxification pathway," Schlievert explains.
He adds uncleared LPS in the gut, combined with Staph superantigens may be how the “perfect storm” of inflammation for diabetes occurs.
The researchers tested fat cells in the lab for their discovery that they engineered to keep reproducing. Adipose cells taken from the body quickly stop dividing making it impossible to reproduce study results.
Al Klingelhutz, Ph.D., UI microbiologist and co-senior author of the study said the goal of immortalizing fat cell is to help researchers to find ways to block inflammation that could lead to type 2 diabetes.
Citation: Vu BG, Gourronc FA, Bernlohr DA, Schlievert PM, Klingelhutz AJ (2013) Staphylococcal Superantigens Stimulate Immortalized Human Adipocytes to Produce Chemokines. PLoS ONE 8(10): e77988. doi:10.1371/journal.pone.0077988
October 30, 2013