The small protein that initially gained attention as an “exercise mimetic” now appears to play a significant role in immune regulation, according to the study’s authors.
A new study found that administering the small protein MOTS-c to type 1 diabetes-prone mice prevented the immune system from destroying insulin-producing pancreatic cells, effectively preventing the onset of the autoimmune disease.
Type 1 diabetes, formerly known as juvenile diabetes, is an autoimmune disease that affects between 5 percent and 10 percent of people with diabetes. In type 1 diabetes, the immune system attacks the pancreas’s islet regions, which are composed of hormone-producing cells.
When immune cells destroy healthy beta cells—pancreatic cells that produce the sugar-regulating hormone insulin—the body loses its ability to produce insulin, regulate blood sugar levels, and utilise sugar properly for energy.
The new study demonstrates how treating mice with MOTS-c promotes the activity of regulatory T cells—immune cells that recognise which cells are their own—and thus reduces the activation of “killer” T cells that attack healthy cells in the pancreatic islets.
In contrast, a subsequent analysis in humans revealed that type 1 diabetes patients had significantly lower MOTS-c levels in their blood than non-diabetic patients, and a study of human cells from both diabetic and non-diabetic patients revealed that MOTS-c treatment decreased “killer” T-cell activation.
MOTS-potential c’s immune-regulating function suggests new therapeutic targets for autoimmune diseases other than type 1 diabetes, says the study.
MOTS-c is one of several newly identified hormones encoded in the DNA of mitochondria, the “powerhouses” of cells that convert food to energy; the majority of other hormones are encoded in the nucleus’s DNA.
“The mitochondrial genome encodes for previously unknown genes that yield small proteins with multiple physiological roles, including aging, exercise, metabolism, and immunity,” the study author points out.
“Further studies on the molecular mechanism of these mitochondrial-encoded peptides are ongoing and may provide novel therapeutic targets for autoimmune conditions, which increases as we age.”
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