Mitochondrial peptide prevents Type-1 diabetes in mice, study finds

August 16, 2021
A new study of human cells in culture and live mice – by a research team at the University of Southern California (USC) – has shown that injections of an immune cell-regulating peptide can prevent the destruction of insulin-producing pancreatic cells that cause type-1 diabetes. It is very likely that the peptide could later be adapted for treatments for other autoimmune disorders as well. Type-1 diabetes or juvenile diabetes is characterised by the routine self-destruction of hormone-producing cells in specific regions of the pancreas. When immune cells mistakenly destroy healthy pancreatic cells that produce the sugar-regulating hormone insulin, the body will eventually lose the ability to control its blood sugar levels. USC researchers, however, have seen how treatment with a mitochondrial peptide known as MOTS-c prevents the onset of disease. Simply put, MOTS-c supports regulatory T cells, which are crucial to distinguishing between the body’s own cells and foreign pathogens; this reduces the amount of “killer” T cells that are activated to attack the insulin-producing cells. Mice that had been genetically engineered to develop type-1 diabetes were observed to have reduced activation of killer T cells following injections of MOTS-c; a subsequent study of human cells from both diabetic and non-diabetic patients also revealed that MOTS-c treatment reduced the activation of killer T cells. The study of human cells additionally revealed how type-1 diabetes patients have significantly lower levels of MOTS-c circulating in their blood compared to non-diabetic patients, further supplementing the researchers’ hypothesis. Unlike most other proteins which are encoded in the DNA in the nucleus, MOTS-c is encoded in the DNA of mitochondria, the “powerhouses” of cells that convert food to energy. MOTS-c was first thought to play a role only in counteracting diet-induced and age-dependent insulin resistance – effects commonly associated with exercising. “It’s been thought for the longest time that the immune system is exclusively encoded in the nuclear genome,” said USC Associate Professor of Gerontology Changhan David Lee. “Now we’re bringing into play an immune regulator that’s encoded in the mitochondrial genome.” According to Lee, the mitochondrial genome “encodes for previously unknown genes that yield small proteins with multiple physiological roles, including aging, exercise, metabolism, and immunity.” Further studies on the molecular mechanism of mitochondrial-encoded peptides such as MOTS-c may provide “novel therapeutic targets” for various autoimmune conditions.

A new study of human cells in culture and live mice – by a research team at the University of Southern California (USC) – has shown that injections of an immune cell-regulating peptide can prevent the destruction of insulin-producing pancreatic cells that cause type-1 diabetes. It is very likely that the peptide could later be adapted for treatments for other autoimmune disorders as well.

Type-1 diabetes or juvenile diabetes is characterised by the routine self-destruction of hormone-producing cells in specific regions of the pancreas. When immune cells mistakenly destroy healthy pancreatic cells that produce the sugar-regulating hormone insulin, the body will eventually lose the ability to control its blood sugar levels.

Read also: Diabetics could one day use remote-activated insulin-releasing device instead of needles

USC researchers, however, have seen how treatment with a mitochondrial peptide known as MOTS-c prevents the onset of disease. Simply put, MOTS-c supports regulatory T cells, which are crucial to distinguishing between the body’s own cells and foreign pathogens; this reduces the amount of “killer” T cells that are activated to attack the insulin-producing cells.

Mice that had been genetically engineered to develop type-1 diabetes were observed to have reduced activation of killer T cells following injections of MOTS-c; a subsequent study of human cells from both diabetic and non-diabetic patients also revealed that MOTS-c treatment reduced the activation of killer T cells.

The study of human cells additionally revealed how type-1 diabetes patients have significantly lower levels of MOTS-c circulating in their blood compared to non-diabetic patients, further supplementing the researchers’ hypothesis.

Unlike most other proteins which are encoded in the DNA in the nucleus, MOTS-c is encoded in the DNA of mitochondria, the “powerhouses” of cells that convert food to energy. MOTS-c was first thought to play a role only in counteracting diet-induced and age-dependent insulin resistance – effects commonly associated with exercising.

“It’s been thought for the longest time that the immune system is exclusively encoded in the nuclear genome,” said USC Associate Professor of Gerontology Changhan David Lee. “Now we’re bringing into play an immune regulator that’s encoded in the mitochondrial genome.”

According to Lee, the mitochondrial genome “encodes for previously unknown genes that yield small proteins with multiple physiological roles, including aging, exercise, metabolism, and immunity.” Further studies on the molecular mechanism of mitochondrial-encoded peptides such as MOTS-c may provide “novel therapeutic targets” for various autoimmune conditions.

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