ArticlePhysiological reports2019
The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity.
Article in Physiological reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Pooled it
- Effects of fecal microbiota transplant on DNA methylation in subjects with metabolic syndrome.Gut microbesTrial
- Article
- Modelling 16/8 intermittent fasting and breakfast-skipping in mouse adipocytes 3T3-L1 in vitro: a transcriptomics study.Journal, genetic engineering & biotechnology · 2026Article
- MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia.Frontiers in medicine · 2026Article
- MENTSH: A novel mitochondrial microprotein linked to a SNP associated with type 2 diabetes.Theranostics · 2026Article
- MOTS-c modulates pancreatic islet function in rats and pigs in vitro.Histochemistry and cell biology · 2025Article
- The correlation between mitochondrial derived peptide (MDP) and metabolic states: a systematic review and meta-analysis.Diabetology & metabolic syndrome · 2024Review
- MOTS-c regulates pancreatic alpha and beta cell functions in vitro.Histochemistry and cell biology · 2024Article
- Mitochondrial-derived microprotein MOTS-c attenuates immobilization-induced skeletal muscle atrophy by suppressing lipid infiltration.American journal of physiology. Endocrinology and metabolism · 2024Article
- Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives.Peptides · 2024Review
- Comparative Analysis of Biomarkers in Type 2 Diabetes Patients With and Without Comorbidities: Insights Into the Role of Hypertension and Cardiovascular Disease.Biomarker insights · 2024Article
- The role of MOTS-c-mediated antioxidant defense in aerobic exercise alleviating diabetic myocardial injury.Scientific reports · 2023Article
- Preconception and developmental DEHP exposure alter liver metabolism in a sex-dependent manner in adult mouse offspring.Toxicology · 2023Article
- Effects of intracerebroventricular MOTS-c infusion on thyroid hormones and uncoupling proteins.Biologia futura · 2023Article
- Mitochondrial Open Reading Frame of the 12S rRNA Type-c: Potential Therapeutic Candidate in Retinal Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging.Journal of translational medicine · 2023Review
- MOTS-c Functionally Prevents Metabolic Disorders.Metabolites · 2023Review
- MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases.International journal of molecular sciences · 2022Review
- Racial differences in circulating mitochondria-derived peptides may contribute to prostate cancer health disparities.The Prostate · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
MOTS-c is an exercise mimetic and improves insulin sensitivity in aged and diet-induced obese mice. Although plasma markers are good markers for the metabolic condition, whether MOTS-c changes plasma markers in diet-induced obese mice has not been examined. Here, we used an unbiased metabolomics approach to examine the effect of MOTS-c on plasma markers of metabolic dysfunction. We found that three pathways - sphingolipid metabolism, monoacylglycerol metabolism, and dicarboxylate metabolism - were reduced in MOTS-c-injected mice. Interestingly, these pathways are upregulated in obese and T2D models. MOTS-c improves insulin sensitivity and increases beta-oxidation to prevent fat accumulation in DIO mice through these pathways. These results provide us a better understanding of the mechanism of how MOTS-c improves insulin sensitivity and reduces the body weight and fatty liver and opens a new venue for further study.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.