Contributes to the transcriptional repression of cholesterol 7-alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid synthesis. Probably inactive as a glycosidase. Increases the ability of FGFR1 and FGFR4 to bind FGF21. Interacts with FGF19; this interaction is direct. Interacts (via C-terminus) with FGF21; this interaction is direct (By similarity). Interacts with FGFR1 and FGFR4. Present in liver, muscle and white adipose tissue, but not in kidney (at protein level). Expressed in liver and pancreas, and at lower levels in skin, stomach, skeletal muscle, small intestine and lung. Expression starts at 10.5 dpc in hepatocytes. Expressed in the acinar cells of the pancreas and cervical brown adipose tissue at 15.5 dpc. Expressed in white adipose tissue at 19.5 dpc. Up-regulated during preadipocyte differentiation into adipocytes (at protein level). Contains 2 glycosyl hydrolase 1 regions. However, the first region lacks the essential Glu active site residue at position 241, and the second one lacks the essential Glu active site residue at position 887. These domains are therefore predicted to be inactive. Mice are viable and fertile, but have an altered bile metabolism: they have increased CYP7A1 levels, secrete more bile acids and are resistant to cholesterol gallstone formation. Belongs to the glycosyl hydrolase 1 family. Klotho subfamily.