Klotho beta/KLB iis a divergent structural member of the glycosidase I superfamily, is expressed primarily in the liver and pancreas, with lower expression in adipose tissue . Like Klotho, Klotho beta facilitates binding between FGF19 subfamily members and their receptors via formation of a ternary complex . The Klotho beta mediated interaction of human FGF19 (mouse FGF15) with FGF Receptor 4 in the liver negatively regulates bile acid synthesis by controlling the secretion of two key bile acid synthase genes, cholesterol 7-alpha hydroxylase (Cyp7a1) and sterol 12-alpha hydroxylase (Cyp8b1) . Klotho beta is also a cofactor for the interaction of FGF21 with FGF Receptor 1c in adipocytes, which allows FGF21 to stimulate GLUT1 expression, upregulating adipocyte insulin-dependent glucose uptake . Since Klotho-related proteins lack critical active site Glu residues present in beta -glycosidases, it was initially unclear whether they were functional enzymes . However, glucuronidase activity has since been demonstrated for Klotho, indicating that physiologically relevant enzymatic activity for Klotho beta is also possible .