MOTS-c A True Anti-Aging Peptide
MOTS-c is a naturally occurring mitochondrial derived peptide which declines with age. The mitochondria, which are present in all of our cells, are responsible for the conversion of energy-storing molecules, such as ATP, for optimum cellular functioning and metabolism.
Aging is characterized by the gradual loss of metabolic balance, muscle loss and generally diminished physical capacities. Improved mitochondrial fitness and enhanced physical capabilities aid healthy aging. Since MOTS-C levels are diminished with advancing age, its administration therapeutically can help with age-related conditions.
Research has shown that MOTS-C may have beneficial effects on a great number of conditions such as diabetes, cardiovascular disease, osteoporosis, obesity and dementia-Alzheimer’s disease.
Replenishing diminished MOTS-c levels may help slow down the aging process and therefore it should be considered is a true anti-aging peptide.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9570330/
MOTS-c can be used clinically for the wide variety of health conditions in which fatigue is a significant symptom.
The biological effects of MOTS-c, are due to its signaling effects regulating mitochondrial bioenergetics and metabolism. MOTS-c triggers the activation of AMPK, a key regulator of cellular metabolism. MOTS-C is an important regulator for energy balance and the metabolism of amino acids, carbohydrates, and lipids and effects glucose regulation and it can improve insulin resistance.
While the process of aging is linked to several different factors, it is clear that advancing age itself is the biggest risk factor for chronic diseases and functional impairments that limit life expectancy. MOTS-c levels in individuals in their seventies is 20% lower than for those in their twenties. MOTS-c exists in metabolic pathways along with age-modifiers such as NAD+, another metabolic cofactor which is also a critical modulator of cell signaling. Both of these diminish with age. It is thus felt that maintaining NAD+ levels in conjunction with maintaining MOTS-c
levels could postpone age-related disorders and possibly increase longevity.
Effects on Diabetes
The complications of diabetes are a leading cause of death in the U.S. and throughout the world. Oxidative stress is a critical factor in the development, progression, and consequences of diabetes. MOTS-c might mitigate against this oxidative stress. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6640593/
Mitochondrial dysfunction is linked to Type 2 diabetes and its complications. In one study of 225 normal and pre-diabetic patients, MOTS-c levels were shown to be significantly lower in Type 2 diabetes than in non-diabetics. Study have revealed that MOTS-c administration improves blood glucose levels and insulin sensitivity.
Cardiovascular Diseases
Cardiovascular disease refers to functional and structural abnormalities of the coronary vessels, a leading cause of death worldwide, particularly affecting elderly populations.
Endothelial cells provide the inner lining of blood vessels. Endothelial dysfunction is a hallmark of CVD, and is characterized by inflammation and a reduced capacity for vasodilation, the expansion of a blood vessel which allows for optimum blood flow. Research has shown a correlation between reduced MOTS-c levels and coronary endothelial dysfunction in patients who were studied.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8396025/
Vascular calcification (VC) is the abnormal deposition of calcium crystal deposits in arterial walls. It has been shown experimentally that MOTS-c therapy may protect against vascular calcification, which is consistent with the beneficial effect of MOTS-c against both oxidative stress and development of heart muscle contractile dysfunction. An important area of ongoing research is to identify non-invasive blood-based biomarkers for the early diagnosis and prognosis of many diseases. Studies support the notion that MOTS-c could be an early predictor of coronary atherosclerosis and a possible marker cardiometabolic dysfunction.
Post-Menopausal Disorders
Post menopausal women have an increased risk of obesity, and impaired insulin secretion and sensitivity. In obesity, fat excess impairs adipose function and increases systemic inflammation. Administration of MOTS-c activated AMPK might mitigate against fat deposition, restore energy, and improve insulin sensitivity.
Osteoporosis
Low bone mass and altered bone microarchitecture leads to excess risk of fractures in those with osteoporosis. The imbalance between synthesis and absorption of bone related minerals and Type I collagen, is crucial in Osteoporosis. Type I collagen makes up over 80% of bone organic matter. Cells treated with MOTS-c show enhancement of the mechanisms, by which the bone forming cells called osteoblasts produce more type I collagen. Bone mesenchymal stem cells also have their development enhanced via treatment with MOTS-c.
https://pubmed.ncbi.nlm.nih.gov/31081069/
Postmenopausal osteoporosis causes bone resorption due to estrogen deprivation. It appears that MOTS-c may be a promising osteoporosis treatment since it enhances bone density, and cell quantity via a variety of mechanisms.
Alzheimer’s Disease
Aging is a major risk factor associated with Alzheimer’s disease (AD). Damaged mitochondria produce reactive free radicals, which cause oxidative stress, cell death and cognitive impairments in AD. Research has shown that MOTS-c therapy increased the formation of object and location recognition memories by activating AMPK, and acting to decrease proinflammatory cytokine production.
https://pubmed.ncbi.nlm.nih.gov/33861582/
MOTS-c in Relation to Muscle Homeostasis and Physical Activity
Mitochondria supply more energy to the muscles during exercise by communicating exercise-induced signals to other organs. MOTS-c administration and exercise training have an additive effect. MOTS-c treatment activates skeletal muscle AMPK, a well-known exercise regulator. Exercise is known to reduce the incidence of Type 2 diabetes and cardiovascular disease. It appears that MOTS-c therapy and regular aerobic exercise may reduce diabetic heart dysfunction through similar mechanisms.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8969227/
With advancing age there is an accumulation of DNA mutations, and resultant metabolic dysfunction, which are both inherent involved in the aging process. These mitochondrial genetic changes may contribute to the age-dependent decrease in MOTS-c levels. Given that aging is associated with a decline of mitochondrial functions along with the development of aging-related diseases, and given that the tissue and circulating levels of MOTS-c fall with age, it is compelling to hypothesize that declining MOTS-c levels are also related to age-related metabolic deterioration.
MOTS-c and other age-modifiers such as NAD+ share metabolic pathways. NAD+ also declines with age. Increasing its levels can also improve age-related disorders. This suggests that co-administration of these age modifiers may ad further clinical benefit. More clinical research is needed to refine therapeutic approaches based on the naturally produced peptides which decline with age.