New study suggests inflammation may not be cause of obesity-type 2 diabetes link

For years, it has been assumed that obesity led to type 2 diabetes by causing inflammation, which was thought to change the way the body reacts to the effects of insulin. However, a new study suggests that this hypothesis may need an update.

Researchers from Children’s Hospital Boston reported in the journal Nature Medicine that inflammation actually activates two different proteins that play key roles in stablizing blood sugar levels. Without the presence of inflammation, these proteins remain dormant.

The findings suggest an important new role for inflammation in the body. Rather than being the cause of health problems like type 2 diabetes, heart disease and certain cancers, it may actually be a helpful reaction to other conditions in the body that are the real cause of disease.

In previous research, the team showed that a protein called XBP1 plays a central role in the healthy function of cells. However, in obese mice, the protein ceases to function. When it is artificially turned back on, blood sugar levels improve. In the current study, the researchers showed that a second protein, p38 MAPK, is important for facilitating the function of XBP1, despite the fact that it is a marker of inflammation.

"This finding is completely contrary to the general dogma in the diabetes field that low-grade inflammation in obesity causes insulin resistance and type 2 diabetes," said lead researcher Umut Ozcan, MD. "For 20 years, this inflammation has been seen as detrimental, whereas it is actually beneficial."

Aside from suggesting a new function of inflammation, Ozcan said the findings could lead to the development of new medications that boost the activation levels of these proteins. This could represent an effective way of controlling blood sugar levels.

Most importantly, results from this study could change the way medicine views inflammation and understands how obesity leads to the development of type 2 diabetes. For years, studies have focused on searching for ways to control inflammation as a potential means to prevent type 2 diabetes in obese individuals. Yet, these findings suggest these approaches may be counter-productive.

While obesity is a well-established risk factor for type 2 diabetes, science has to this point been unable to observe the molecular cause of this association. While inflammation had long been viewed as one potential, the findings suggest the relationship may be more complicated.