Choline-specific phosphodiesterase that hydrolyzes sphingomyelin releasing the ceramide and phosphocholine and therefore is involved in sphingomyelin digestion, ceramide formation, and fatty acid (FA) absorption in the gastrointestinal tract (PubMed:21177474). Has also phospholipase C activity and can also cleave phosphocholine from palmitoyl lyso-phosphatidylcholine and platelet-activating factor (PAF) leading to its inactivation. Does not have nucleotide pyrophosphatase activity (By similarity). May promote cholesterol absorption by affecting the levels of sphingomyelin derived from either diet or endogenous sources, in the intestinal lumen (PubMed:24650549). a sphingomyelin + H2O = an N-acylsphing-4-enine + H(+) + phosphocholine a 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine + H2O = a 1-O-alkyl-2-acetyl-sn-glycerol + H(+) + phosphocholine 1-O-octadecyl-2-acetyl-sn-glycero-3-phosphocholine + H2O = 1-O-octadecyl-2-acetyl-sn-glycerol + H(+) + phosphocholine 1-hexadecanoyl-sn-glycero-3-phosphocholine + H2O = 1-hexadecanoyl-sn-glycerol + H(+) + phosphocholine The catalytic domain is released into the extracellular medium when cells are treated with trypsin. Localized at the surface of the microvillar membrane in small intestine enterocytes, and in endosome-like structures situated beneath the microvillar membrane, and in Golgi complex. Expressed in liver and small intestine. N-glycosylated; required for activity and transport to the plasma membrane. Mutant mice are born at the expected Mendelian rate, are viable and fertile, are grown normally without obvious abnormalities. Mice shown signs of hypertrophy of the intestinal epithelium, as the widths of the villi and crypts, as well as the thickness of muscle layer under the crypts appear increased. However, no spontaneous tumorigenesis either in the small intestine or in the colon is identifiedknockout mice up to the age of 10 months.