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Published on: September 25, 2017
Earlier changes in mice after D-galactose treatment were improved by mitochondria derived small peptide MOTS-c
Qingyang Li1, Huanyu Lu2, Guangyu Hu1
1State Key Laboratory of Cancer Biology, Department of Biopharmaceutics, School of Pharmacy, Fourth Military Medical University, Xi'an, 710032, Shaanxi, PR China.
Abstract:
MOTS-c, as a mitochondria derived peptide, exerts benefits for insulin resistance in HFD mice and against various stresses in an AMPK dependent way. Here, in the D-galactose chronic injection models, exogenous MOTS-c was given to determine its direct anti-aging effects. The body weight, insulin sensitivity and blood glucose were determined with mild differences. Tissue morphology analyses disclosed that liver, visceral fat and dermal skin, all displayed aberrant lipid depositions in the D-galactose mice. MOTS-c treatment largely alleviated the lipid accumulations, corresponding with positive changes in mitochondria dynamics, observed in liver transmission electron microscopy and in altered mRNA levels of Drp1 and mitofusins. Notably, the aging phenotypes of small intestine tract were more obvious, including histological defects and lower Ki67 levels, plus with the higher levels of DNA stress, such as P21 and P16, as well as mitochondria dynamics. Collectively, these data provided the direct evidence to support that exogenous givings of MOTS-c prevented abnormal fat accumulations in D-gal mice, putatively via improvement of mitochondria dynamic related pathways.
Insights
Mitochondria-derived peptide MOTS-c (MOTS-c) directly combats aging by reducing fat accumulation and improving mitochondrial function in D-galactose-induced aging models. This peptide shows promise for anti-aging therapies.
Area of Science:
- Biogerontology
- Mitochondrial Biology
- Metabolic Health
Background:
- Mitochondria-derived peptide MOTS-c (MOTS-c) is known to improve insulin resistance and stress responses.
- Aging is associated with metabolic dysfunction and cellular stress.
Purpose of the Study:
- To investigate the direct anti-aging effects of exogenous MOTS-c in a D-galactose-induced chronic aging model.
- To explore the impact of MOTS-c on lipid accumulation, mitochondrial dynamics, and aging phenotypes.
Main Methods:
- Administration of exogenous MOTS-c to D-galactose-treated mice.
- Assessment of body weight, insulin sensitivity, and blood glucose levels.
- Histological analysis of liver, visceral fat, dermal skin, and small intestine.
- Mitochondrial dynamics evaluation using transmission electron microscopy and mRNA analysis (Drp1, mitofusins).
- Analysis of DNA stress markers (P21, P16) and cell proliferation marker (Ki67).
Main Results:
- MOTS-c treatment significantly alleviated aberrant lipid depositions in the liver, visceral fat, and skin of D-galactose mice.
- Improved mitochondrial dynamics were observed in the liver following MOTS-c treatment, evidenced by altered Drp1 and mitofusin mRNA levels.
- MOTS-c mitigated aging phenotypes in the small intestine, including histological defects and reduced Ki67 levels, while also addressing DNA stress markers (P21, P16).
Conclusions:
- Exogenous MOTS-c demonstrates direct anti-aging effects by preventing abnormal fat accumulation in a D-galactose-induced aging model.
- MOTS-c likely exerts its protective effects through the improvement of mitochondria dynamic-related pathways.
- These findings support MOTS-c as a potential therapeutic agent for age-related metabolic and cellular dysfunction.
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