Health x Wellness
Anti-inflammatory “switch” could treat diabetes, or even ageing itself.
We all know that inflammation is our body’s way of fighting internal biological threats, but when it gets out of control, it can lead to a host of other problems that would certainly be detrimental to an individual.
However, your days of struggling with your body’s overly enthusiastic immune system might just come to an end as researchers at UC Berkeley have recently identified a molecular “switch” that could effectively turn off that reaction. In fact this discovery could potentially lead to a reversal of ageing-associated conditions.
In a study that was done on mice, what the UC Berkeley researchers discovered was something called the NLRP3 inflammasome – an immune protein responsible for detecting potential threats to the body. If something invasive is detected, the protein launches an inflammation response. In normal circumstances, the immune response would be regarded as a standard and beneficial function; however, the body sometimes stays in this state for too long, and chronic inflammation ensues, leading to other chronic conditions such as diabetes and multiple sclerosis.
But from the study, the researchers discovered a way to “deactivate” THE NLRP3 inflammasome, through a process known as deacetylation. By studying the mice and immune cells called macrophages, the research team realised that a specific protein known as SIRT2 is responsible for deacetylating the NLRP3 inflammasome. Mice that were bred with the inability to produce SIRT2 exhibited more signs of inflammation than the control group. The test mice also had higher insulin resistance, a condition associated with type 2 diabetes.
The researchers also studied two groups of older mice whose immune systems were “tweaked” to have either the acetylated or deacetylated version of the NLRP3 inflammasome. The “deacetylated” group had better insulin resistance after six weeks in comparison to the control group of “acetylated” mice.
“I think this finding has very important implications in treating major human chronic diseases,” Danica Chen, senior author of the study said. “It’s also a timely question to ask, because in the past year, many promising Alzheimer’s disease trials ended in failure. One possible explanation is that treatment starts too late, and it has gone to the point of no return. So, I think it’s more urgent than ever to understand the reversibility of ageing-related conditions and use that knowledge to aid a drug development for aging-related diseases.”
The study was published in the journal Cell Metabolism
