Browse evidence-based analysis of health-related claims and assertions
Apelin turns on genes that help build more mitochondria in muscles, improving energy production.
Descriptive
Apelin lowers blood fat levels and helps mice process sugar better, improving overall metabolic health.
Apelin's benefits for fat burning and mitochondria in muscles only work when AMPK is active, as shown in genetically modified mice.
Mechanistic
Apelin activates a key energy-sensing enzyme in muscles, which helps reduce fat buildup and improve metabolism.
Apelin-treated mice burn more fat for energy during active periods compared to placebo-treated mice, shown by their breathing patterns.
Apelin reduces harmful fat byproducts in muscles, which helps muscles take up more glucose in response to insulin.
Apelin makes mouse muscles produce more mitochondria, the cell's energy factories, leading to better fat-burning capacity.
Apelin helps mouse muscles use oxygen more efficiently for energy production, especially when using fat as fuel.
Apelin-treated mice burn fat more completely in their muscles compared to placebo-treated mice, reducing harmful fat byproducts.
Giving apelin to obese, insulin-resistant mice for a month helps them lose body fat and lowers their blood sugar levels compared to mice given a placebo.
Obese mice treated with MOTS-c had lower levels of ANGPTL4 in their muscles, which may help prevent fat buildup.
Quantitative
MOTS-c treatment in obese mice reduced the activity of a liver enzyme called Por by half, which may affect fat metabolism.
MOTS-c injections in obese mice lowered sebacate, a dicarboxylic acid, by 42% compared to untreated mice.
Obese mice given MOTS-c had lower levels of suberate, a dicarboxylic acid, by 40% compared to untreated mice.
MOTS-c injections in obese mice reduced a type of fat molecule called 2-oleoylglycerol by about 32% compared to untreated mice.
Obese mice treated with MOTS-c had lower levels of a specific sphingolipid called palmitoyl sphingomyelin, which is associated with insulin resistance.
MOTS-c injections in obese mice lowered a specific blood fat molecule called sphingosine 1-phosphate by about 14% compared to untreated mice.
Obese mice given MOTS-c injections for three days had lower blood sugar levels than mice that didn't receive the treatment.
When PGC-1α is increased in muscle cells, they break down a specific type of fat (lignoceric acid) more efficiently using both peroxisomes and mitochondria. This finding is from the abstract summary - full study details were not available
Increasing PGC-1α in muscle cells leads to higher levels of mRNA for breaking down fats in peroxisomes. This finding is from the abstract summary - full study details were not available
When muscle cells in a lab have more PGC-1α protein, they show higher levels of PMP70, which is a protein involved in peroxisome function. This finding is from the abstract summary - full study details were not available
In immobilized mice, higher levels of MOTS-c in the muscles were linked to better muscle mass retention.
Correlational
MOTS-c lowered levels of myostatin, a protein that inhibits muscle growth, in the muscles of immobilized mice.
MOTS-c reduced the amount of fatty acids in the muscles of immobilized mice, which may prevent harmful fat buildup.