Sponsored Post: Fat Metabolism and MOTS-c Peptide Investigations
Studies suggest that the mitochondria-derived peptide MOTS-c may increase physical output capacity, reduce fat storage and insulin resistance, and potentially slow the progression of disease manifestation and spread, including osteoporosis.
MOTS-c Peptide
MOTS-c belongs to the family of mitochondrial-derived peptides (MDPs) and is a small peptide encoded in the mitochondrial genome. It was recently put forth by the scientific community that MDPs are bioactive hormones with what is believed to be crucial functions in mitochondrial communication and energy management. New studies have suggested that many mitochondrial DNA methyltransferases (MDPs) may also be active in the cell nucleus and that some may even enter the bloodstream to induce systemic impact. The recently discovered MDP MOTS-c has been linked to mechanisms that contribute to disease states, including osteoporosis, as well as more possible general functions in metabolism, weight management, physical exertion, and lifespan. MOTS-c is a real natural hormone since it has been detected both in cell nuclei and the bloodstream. Researchers have focused heavily on the peptide in the past five years due to its proposed research applications.
MOTS-c Peptide and Muscle Metabolism
Research suggests the MOTS-c peptide may improve muscle glucose uptake and alleviate age-related insulin resistance in rats. This is hypothesized to be achieved by increasing the expression of glucose transporters in response to AMPK activation in skeletal muscle. It is worth noting that this activation occurs apart from the insulin route, providing an alternate strategy for increasing muscle glucose uptake when insulin is either inefficient or unavailable. Consequently, functional insulin resistance may be reduced, muscle function may be improved, and muscle development may be accelerated.
MOTS-c Peptide and Fat Metabolism
Studies in mice have suggested that decreased estrogen levels may cause abnormal adipose tissue to accumulate fat and become dysfunctional. Diabetes is more likely to develop in such a research model due to insulin resistance. However, it has been hypothesized that giving mice MOTS-c peptide may improve brown fat function and decrease fatty tissue growth. Also, the peptide appears to have the potential to stop insulin resistance in its tracks by halting adipose inflammation and adipose malfunction.
At least some of MOTS-c’s possible impact on fat metabolism seems to be mediated via AMPK activation. Findings imply that this route may trigger the glucose and fatty acids absorption by cells for metabolism during periods of low cellular energy. Ketogenic diets may stimulate this system to boost fat metabolism and prevent muscle loss. Investigations purport that MOTS-c may inhibit the adenine nucleotide exchange factor (AICAR) and stimulate the AMP-activated protein kinase (AMPK).
Recent studies have purported that MOTS-c may go from mitochondria to the nucleus, where it may influence gene expression. Data suggests that MOTS-c may control nuclear genes involved in glucose restriction and antioxidant responses during metabolic stress.
Mice studies purport that MOTS-c may be crucial in regulating sphingolipid, monoacylglycerol, and dicarboxylate metabolism, particularly, researchers suggest, in cases of obesity. Scientists propose that MOTS-c seems to inhibit fat storage by modulating these pathways and promoting beta-oxidation. It is quite likely that MOTS-c’s activity in the nucleus may mediate some of these impacts.
The new concept concerning fat deposition and insulin resistance that has emerged due to MOTS-c research is achieving popularity in the scientific community and may provide a novel way to intervene in the pathophysiology of obesity and diabetes. Lack of fat oxidation may come from mitochondrial dysregulation of fat metabolism. Increased amounts of circulating fat may induce an increase in insulin production. This action may result in increased fat storage and a shift in homeostasis as the metabolism adjusts to (and develops resistance to) persistently elevated insulin levels.
MOTS-c Peptide and Insulin Receptivity
MOTS-c may solely be linked to insulin sensitivity in non-obese research models, as suggested by studies that measured the protein in both insulin-sensitive and insulin-resistant research models. In other words, MOTS-c seems to have a role in the onset of insulin resistance but not in its maintenance. Researchers propose that variations in MOTS-c levels may serve as an early warning indication of possible insulin insensitivity in lean models at risk for developing diabetes. Research suggests that MOTS-c supplementation may prevent insulin resistance and subsequent diabetes in this scenario. Studies in mice have suggested some encouraging results, but additional research is required to understand the full breadth of MOTS-c potential in insulin control.
MOTS-c Peptide and Osteoporosis
It has been hypothesized that osteoblasts may use MOTS-c throughout the type I collagen production process. Cell line studies of osteoblasts purport that MOTS-c may control the TGF-beta/SMAD pathway critical for osteoblast survival. It has also been proposed that MOTS-c may enhance type I collagen production and, by extension, bone strength and integrity by boosting the survival of osteoblasts.
More studies on osteoporosis have suggested that MOTS-c, via the same TGF-beta/SMAD pathway, may encourage the development of bone marrow stem cells. Scientists speculate that this may have prompted more bone production (osteogenesis). Therefore, MOTS-c for sale is suggested to not only potentially safeguard osteoblasts but also support their survival and encourage their formation from stem cells.
References
[i] C. Lee, K. H. Kim, and P. Cohen, “MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism,” Free Radic. Biol. Med., vol. 100, pp. 182–187, Nov. 2016. [PMC]
[ii] H. Lu et al., “MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction,” J. Mol. Med. Berl. Ger., vol. 97, no. 4, pp. 473–485, Apr. 2019. [PubMed]
[iii] K. H. Kim, J. M. Son, B. A. Benayoun, and C. Lee, “The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress,” Cell Metab., vol. 28, no. 3, pp. 516-524.e7, Sep. 2018. [PMC]
[iv] S.-J. Kim et al., “The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity,” Physiol. Rep., vol. 7, no. 13, p. e14171, Jul. 2019. [PubMed]
[v] R. Crescenzo, F. Bianco, A. Mazzoli, A. Giacco, G. Liverini, and S. Iossa, “A possible link between hepatic mitochondrial dysfunction and diet-induced insulin resistance,” Eur. J. Nutr., vol. 55, no. 1, pp. 1–6, Feb. 2016. [BMJ]
[vi] L. R. Cataldo, R. Fernández-Verdejo, J. L. Santos, and J. E. Galgani, “Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals,” J. Investig. Med., vol. 66, no. 6, pp. 1019–1022, Aug. 2018. [PubMed]
[vii] N. Che et al., “MOTS-c improves osteoporosis by promoting the synthesis of type I collagen in osteoblasts via TGF-β/SMAD signaling pathway,” Eur. Rev. Med. Pharmacol. Sci., vol. 23, no. 8, pp. 3183–3189, Apr. 2019. [PubMed]
[viii] B.-T. Hu and W.-Z. Chen, “MOTS-c improves osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via TGF-β/Smad pathway,” Eur. Rev. Med. Pharmacol. Sci., vol. 22, no. 21, pp. 7156–7163, Nov. 2018. [PubMed]
[ix] N. Fuku et al., “The mitochondrial-derived peptide MOTS-c: A player in exceptional longevity?,” Aging Cell, vol. 14, Aug. 2015. [Research Gate]
[x] Q. Qin et al., “Downregulation of circulating MOTS-c levels in patients with coronary endothelial dysfunction,” Int. J. Cardiol., vol. 254, pp. 23–27, 01 2018. [PubMed]
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