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7 resourcesThis resource examines how respiratory exchange ratio, heat production, and food intake collectively inform metabolic effects in MOTS-c-treated mice, based strictly on animal research. It details experimental findings, mechanistic insights, and limitations, without extrapolating to human outcomes.
This resource examines how the foundational MOTS-c study applied extracellular acidification rate (ECAR) measurements to assess glycolytic flux in cell models, detailing the methodology, findings, and limitations. It distinguishes in vitro results from broader clinical implications and highlights the mechanistic context of MOTS-c’s metabolic actions.
This resource examines the role of the folic acid rescue test in MOTS-c cellular experiments, focusing on mechanistic findings, experimental design, and the interpretation of results within the context of current peptide research. Evidence is drawn from controlled in vitro studies, with limitations and uncertainties clearly stated.
This resource examines the role of skeletal muscle endpoints in the study of MOTS-c, a mitochondrial-derived peptide, focusing on mechanistic, cellular, and animal model evidence. It details how skeletal muscle measurements inform our understanding of MOTS-c’s metabolic actions, highlights experimental methods, and discusses the limitations and uncertainties of current research.
Mutant and scrambled peptide controls are essential in MOTS-c studies to confirm specificity and rule out non-sequence-dependent effects. This article explains their use, interpretation, and limitations in the context of metabolic research.
Experimental studies of MOTS-c, a mitochondrial-derived peptide, reveal novel mechanisms of mitochondrial-to-cell signaling. This resource reviews the molecular origins, cellular actions, and systemic effects of MOTS-c in laboratory and animal models, highlighting its role in metabolic regulation and the current limitations of the evidence.
Learn what a primary MOTS-c study found about metabolic signaling in cells and mice, including AMPK pathways and limits of translation to people.
