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MOTS-c: Insulin Resistance Studies

Animal studies have suggested that the mitochondrial-derived peptide MOTS-c may increase metabolic balance and lifespan, decrease body fat, and prevent diabetes. Researchers have speculated that mitochondrial-derived peptides (MDPs), of which this short peptide is a part, may serve a crucial role in mitochondrial signaling and energy regulation.

New studies indicate that many MDPs may function inside the nucleus of a cell. Animal studies have ascertained that many of them are absorbed by the body and have widespread impacts.


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One of the recently discovered MDPs is called the MOTS-c peptide. It has been linked to processes that contribute to illnesses like diabetes and osteoporosis as well as to metabolic processes, lifespan, exercise ability, weight control, and disease risk. Over the past five years, extensive studies have been conducted on the potential of the MOTS c peptide.

MOTS-c Peptide: What is it?

The 16-amino acid peptide MOTS-c has been hypothesized to improve metabolic homeostasis and performance in experimental animals. This includes the body’s ability to use glucose as fuel.

MOTS-c Peptide Research

Recently published work from the University of Southern California [i] suggested that MOTS-C may have protected insulin-producing pancreas cells from being destroyed by the immune system. Consequently, it was speculated to protect rodents from developing type 1 diabetes in the study.

Many subjects have type 1 diabetes, an inflammatory disorder. The body’s defense system targets insulin-producing pancreatic cells. It has been theorized in recent studies that the peptide MOTS-c may help regulatory T-cells, which are immunological cells that determine which cells are part of the animal test subjects’ tissues and dampen killer T-cell activation.

“We can avoid the development of type 1 diabetes in rodent models,” said Changhan David Lee, co-corresponding research author.

Another key finding from this research was that skeletal muscle is the MOTS’s preferred site of action. Without raising insulin levels in the tissues of the animal subjects, it has been hypothesized to increase glucose absorption in muscle cells and improve insulin sensitivity by stimulating the AMPK pathway.

MOTS-c Peptide Properties

To sum up, here are the hypothesized properties of MOTS c peptide that have been suggested through rodent studies:

  • It may prevent insulin intolerance.
  • It may increase metabolic adaptability
  • It may aid in the process of dropping pounds
  • It may aid in maintaining optimal mitochondrial activity
  • It may improve the capacity for physical activity
  • It may facilitate a more stable blood sugar level
  • It may be useful in the context of osteoporosis 

MOTS-c Peptide and Diabetes

Additional mouse studies suggest the centrality of MOTS-c in the etiology of insulin sensitivity, corroborating the findings of the USC study.

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Experts speculate the peptide could effectively track slender rodents at risk for developing diabetes. Alterations in MOTS-c levels, they hypothesize, might be an indicator of a change in insulin sensitivity.

While studies in rodent models have purported some encouraging results, more clinical trials are needed to fully grasp the impact of MOTS-c.

MOTS-c Peptide and Weight

Thanks to research conducted at the USC Leonard Davis School of Gerontology, MOTS-c hormone has been indicated to combat the weight increase associated with a high-fat diet for a while [ii].

Research suggests that MOTS-c has recently been identified as a peptide. In animal studies, researchers were ecstatic to learn that it may effectively target muscle tissue and reverse insulin resistance from a high-fat diet.

The researchers gave MOTS-c to rodents that had been given a high-fat diet, which leads to obesity and insulin intolerance, to study the impacts. 

MOTS-c Peptide and Fat 

This study also ascertained that MOTS-c might play an important role in regulating monoacylglycerol, sphingolipid, and dicarboxylate biosynthesis. MOTS-c has been hypothesized to have aided in weight reduction in experimental animals by inhibiting fat buildup via these mechanisms.

Many researchers have begun to draw connections between MOTS-c and weight reduction. Research suggests that increased circulating fat causes an animal’s body to raise insulin levels to eliminate lipids from circulation. According to research, this may be caused by a disruption of fat metabolism in mitochondria, resulting in a fat combustion shortage. The animal’s body becomes insulin-resistant and begins storing more fat.

MOTS-c Peptide and the Heart

Research examining MOTS-c levels in animals having cardiac angiography has found that those with lower levels of MOTS-c in circulation have higher levels of endothelial cell malfunction.

Plaque development, blood pressure, and blood coagulation can all be controlled, to varying degrees, by endothelial cells. Additional rodent studies indicate that MOTS-c may sensitize endothelium cells, speculated to enhance endothelial and blood artery function.

While mitochondria-derived peptides like MOTS-s have been asserted to improve cardiac health, they are hardly unique. From what researchers can tell, at least three MDPs may protect heart cells from the damaging effects of inflammation and stress. So, scientists think that MDP dysfunction contributes to the development of arterial illness.

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References

[i] Kong, Byung Soo, Se Hee Min, Changhan Lee, and Young Min Cho. “Mitochondrial-Encoded MOTS-c Prevents Pancreatic Islet Destruction in Autoimmune Diabetes.” Cell Reports 36, no. 4 (July 2021): 109447. doi:10.1016/j.celrep.2021.109447

[ii] Lee, Changhan, Kyung Hwa Kim, and Pinchas Cohen. “MOTS-c: A Novel Mitochondrial-Derived Peptide Regulating Muscle and Fat Metabolism.” Free Radical Biology and Medicine 100 (November 2016): 182–187. doi:10.1016/j.freeradbiomed.2016.05.015.

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Ifiokobong Ibanga

Ifiokobong Ibanga is the founder of InfoGuideNIgeria.com. You can get in touch with him on Instagram @ifiokobong. If you need a personal assistance on this topic, kindly send a message. Much Love!

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