UBCO researchers suggest something as simple as regular walks can help people living with Type 2 diabetes control inflammation.
Researchers from UBC Okanagan are looking at how exercise can help balance the immune system and reduce chronic inflammation—a known contributor to the development and progression of various chronic diseases.
Associate Professor Dr. Jonathan Little, and postdoctoral researcher Dr. Hashim Islam, both with UBC Okanagan’s School of Health and Exercise Sciences, are studying how chronic inflammation can create an imbalance that prevents a person’s immune system from protecting them. And how exercise might be the answer.
The immune system, explains Dr. Islam, is critical for preventing infections, removing pathogens and repairing damaged tissues during recovery from an illness or injury. But when immune cells become overactivated, they can overproduce and release small hormone-like molecules called pro-inflammatory cytokines.
An over-abundance of those cytokines can impair the normal function of vital tissues and organs in the body, Dr. Islam explains. This means a person might be susceptible to a number of diseases including Type 2 diabetes.
“This persistent state of immune cell overactivation is known as chronic inflammation and is linked to the development and progression of various long-lasting illnesses that are commonly found in modern society. These include cardiovascular diseases such as hypertension or stroke and Type 2 diabetes—and we’re particularly interested in studying the Type 2 diabetes aspect,” says Dr. Islam.
Lifestyle factors such as imbalanced nutrition, weight gain, obesity and physical inactivity can aggravate chronic inflammation, adds Dr. Little. These conditions increase a person’s chance of getting various cardiometabolic diseases. On the other hand, exercise and diet-induced weight loss are effective for reducing chronic inflammation in the body and lowering the risk of developing cardiometabolic disease.
The researchers are specifically looking at interleukin 10, a molecule that normally acts to inhibit inflammation. Earlier research, in collaboration with colleagues at UBC’s Vancouver campus, demonstrated that immune cells isolated from people with Type 2 diabetes were less responsive to the anti-inflammatory actions of interleukin 10—something that typically acts as a brake or fire extinguisher to prevent immune cell overaction.
The inability of interleukin-10 to inhibit inflammation was linked to elevated blood sugar levels, suggesting that interventions that normalize blood glucose levels may be effective for restoring anti-inflammatory cytokine action in people with Type 2 diabetes.
“Chronic inflammation is when there is an imbalance of pro- and anti-inflammatory molecules in your body. We use the example of a slow-burning flame, or a brake, in the context of chronic disease,” explains Dr. Little. “Most people study the pro-inflammatory molecules and how to reduce them—which is similar to taking the fuel off the fire. Our work, which is quite novel, is looking at how to make anti-inflammatory molecules like interleukin-10—similar to a fire extinguisher—work better and stop the inflammation.”
Dr. Islam is further exploring the mechanisms that may explain why and when interleukin-10 is not working well to inhibit inflammation for people with Type 2 diabetes. His goal is to implement a practical lifestyle intervention that will involve short, frequent bouts of activity—post-meal walking or exercise snacking—throughout the day to improve blood glucose and restore the anti-inflammatory actions of interleukin-10.
“This approach has demonstrated glucose-lowering benefits in people with Type 2 diabetes,” says Dr. Islam. “Given the earlier-identified link between hyperglycemia and impaired interleukin-10 action, this may be a viable non-pharmacological strategy to restore anti-inflammatory cytokine action in people with Type 2 diabetes.”
The research was covered in a recent review article published in the Journal of Physiology and is funded by a Michael Smith Foundation for Health Research Trainee Award and a Killam Accelerator Research Fellowship.
