Apelin's benefits for fat burning and mitochondria in muscles only work when AMPK is active, as shown in genetically modified mice.
Scientific Claim
Apelin treatment in high-fat diet-induced insulin-resistant mice is associated with improvements in fatty acid oxidation and mitochondrial biogenesis that are linked to AMPK activity, as these effects are absent in mice with muscle-specific inactive AMPK (AMPK-DN model).
Original Statement
“The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.”
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' and 'linked to' 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