Apelin makes mouse muscles produce more mitochondria, the cell's energy factories, leading to better fat-burning capacity.
Scientific Claim
Chronic apelin treatment (0.1 μmol/kg/day intraperitoneally for 4 weeks) in high-fat diet-induced insulin-resistant mice is associated with increased mitochondrial biogenesis, including higher mtDNA content (n=4 per group, P ≤ 0.01) and elevated citrate synthase activity (2.91 vs 2.62 μmol/min/mg protein, P < 0.001).
Original Statement
“The mtDNA–to–nuclear DNA ratio was significantly higher in soleus muscle of apelin-treated mice than in PBS-treated mice (Fig. 4D). Moreover, the electron microscopy demonstrated that apelin treatment significantly increased the density of intramyofibrillar (IMF) mitochondria (Fig. 4E). Citrate synthase activity, a quantitative marker of mitochondria content, was also found in muscle homogenates of apelin-treated mice compared with control (2.62 ± 0.02 vs. 2.91 ± 0.07 μmol/min/mg proteins, n = 7–9; P < 0.001).”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The claim uses 'associated with' which correctly reflects the associative nature of the study design, avoiding causal language.
Evidence from Studies
Supporting (1)
Apelin Treatment Increases Complete Fatty Acid Oxidation, Mitochondrial Oxidative Capacity, and Biogenesis in Muscle of Insulin-Resistant Mice