Finding. Pemafibrate writes only where PPARα sits, and after an oral dose that is mostly liver and jejunum. Lasserre, Guillou, Piccinin and colleagues treat wild-type and whole-body PPARα-knockout littermates with 0.1 mg/kg pemafibrate daily for 14 days and sequence liver, jejunum, kidney, soleus, and brown adipose. The knockout has no differentially expressed genes. The wild-type response is tissue-specific. Liver induces fatty-acid metabolism, mitochondrial function, and energy-production genes. Jejunum turns on lipid programs plus its own homeostasis set. Kidney, soleus, and brown fat barely answer.
Why this paper matters
Selective PPARα modulators are marketed as cleaner fibrates. Someone still has to say which organs actually transcribe. This atlas says oral pemafibrate is a hepato-intestinal writer, and the hepatic page includes mitochondria. That is useful both to people who want a mitochondrial gene list and to people who need to stop claiming a whole-body brown-fat effect from this dose.
The zero-DEG knockout is the selectivity result. It is rarer than press-release selectivity.
What they actually measured
Five-organ RNA-seq, one dose, two weeks, males, littermate knockouts. Tissue ranking by magnitude. Liver mitochondrial-function language is transcriptional.
How to read the score
High 70s. Real PPARα-mitochondrial hepatic module, clean genetic off switch. Not a flux paper.
Caveats
No Seahorse. No female mice. BAT silence could be a timing or dose issue. Do not convert a gene list into a claim that pemafibrate treats mitochondrial disease.
What to do with it
Pull the liver mitochondrial and FAO gene lists as a PPARα-positive control set. If you study intestinal PPARα, the jejunum track is the extrahepatic prize. Ignore soleus and BAT for this regimen.