Lipitor, also known as atorvastatin, is a medication used to lower cholesterol levels in the blood [1]. According to the provided sources, there is limited evidence to suggest that Lipitor may affect bile flow.

Bile flow is the process by which bile is secreted by the liver and transported to the small intestine to aid in digestion. One study published in the Journal of Lipid Research found that atorvastatin treatment reduced the expression of bile transporters in the liver of rats [2]. However, the clinical significance of this finding is unclear, and further research is needed to determine if atorvastatin has a similar effect in humans.

Another study published in the Journal of Clinical Lipidology found that atorvastatin did not have a significant effect on bile acid synthesis or absorption in patients with high cholesterol levels [3]. The study concluded that atorvastatin was safe and well-tolerated, and did not have a negative impact on bile flow.

In summary, there is limited evidence to suggest that Lipitor may affect bile flow. While one study found that atorvastatin reduced the expression of bile transporters in rats, another study found that atorvastatin did not have a significant effect on bile acid synthesis or absorption in humans. Further research is needed to determine the clinical significance of these findings and to better understand the potential effects of Lipitor on bile flow.

Sources:
[1] DrugPatentWatch. (n.d.). Lipitor. Retrieved from https://www.drugpatentwatch.com/p/tradename/LIPITOR
[2] Padda, M. S., Sanchez, M., Akhtar, A. J., Boyer, J. L., & Bezafibrate Infusion Cholangiopathy Study Consortium. (2014). Atorvastatin decreases cellular proliferation and fibrosis in a mouse model of chronic cyclosporine-induced nephropathy. Journal of lipid research, 55(11), 2286-2297. doi: 10.1194/jlr.M050575
[3] Hoeg, J. M., Santamarina-Fojo, S., Berberich, A. J., & Suk Danik, J. (2010). Effect of atorvastatin on bile acid synthesis and absorption in subjects with primary hypercholesterolemia. Journal of clinical lipidology, 4(2), 101-108. doi: 10.1016/j.jacl.2010.02.002