STARD10, a member of the steroidogenic acute regulatory protein (StAR)-related 
lipid transfer (START) protein family, is highly expressed in the liver and has 
been shown to transfer phosphatidylcholine. Therefore it has been assumed that 
STARD10 may function in the secretion of phospholipids into the bile. To help 
elucidate the physiological role of STARD10, we produced Stard10 knockout mice 
(Stard10(-/-)) and studied their phenotype. Neither liver content nor biliary 
secretion of phosphatidylcholine was altered in Stard10(-/-) mice. Unexpectedly, 
the biliary secretion of bile acids from the liver and the level of 
taurine-conjugated bile acids in the bile were significantly higher in 
Stard10(-/-) mice than wild type (WT) mice. In contrast, the levels of the 
secondary bile acids were lower in the liver of Stard10(-/-) mice, suggesting 
that the enterohepatic cycling is impaired. STARD10 was also expressed in the 
gallbladder and small intestine where the expression level of apical sodium 
dependent bile acid transporter (ASBT) turned out to be markedly lower in 
Stard10(-/-) mice than in WT mice when measured under fed condition. Consistent 
with the above results, the fecal excretion of bile acids was significantly 
increased in Stard10(-/-) mice. Interestingly, PPARα-dependent genes responsible 
for the regulation of bile acid metabolism were down-regulated in the liver of 
Stard10(-/-) mice. The loss of STARD10 impaired the PPARα activity and the 
expression of a PPARα-target gene such as Cyp8b1 in mouse hepatoma cells. These 
results indicate that STARD10 is involved in regulating bile acid metabolism 
through the modulation of PPARα-mediated mechanism.