Inhibition of β‐Glucuronidase by Casein Hydrolysate Formula

Author:

Gourley Glenn R.1,Kreamer Bill L.1,Cohnen Monika2

Affiliation:

1. Department of Pediatrics and the Waisman Center on Mental Retardation and Human Development University of Wisconsin Medical School Madison Wisconsin U.S.A.

2. Justus‐Liebig Universität Giessen Germany

Abstract

Background:A casein hydrolysate infant formula has been shown to be associated with lower levels of neonatal jaundice than are standard infant formulas. Because β‐glucuronidase is related to neonatal jaundice, this study examined the effect of a casein hydrolysate formula on β‐glucuronidase.Methods:β‐glucuronidase activity was measured with or without added dietary components. The β‐glucuronidase sources used were meconium, breast milk, and the purified bovine liver enzyme. The dietary components assayed for their effect on β‐glucuronidase activity included casein hydrolysate formula (Nutramigen), whey‐predominant formula (Enfamil), breast milk, enzymatically hydrolyzed casein, and other constituents of the casein hydrolysate formula. Stool samples of 6‐day‐old infants, who were exclusively fed one of the two formulas or breast milk, were also assayed for inhibition of β‐glucuronidase.Results:Only Nutramigen, enzymatically hydrolyzed casein, and stool from Nutramigen‐fed infants consistently demonstrated significant inhibition of β‐glucuronidase activity, ranging from 45% to 85% of that in controls. The inhibition of β‐glucuronidase in purified bovine liver demonstrates a dose response in a pH range from 4 to 7.3.Conclusions:Hydrolyzed casein contains a β‐glucuronidase inhibitor that, in casein hydrolysate‐fed infants, persists after passage through the digestive tract. These data are consistent with the possibility that inhibition of β‐glucuronidase is a mechanism by which infants fed casein hydrolysate have lower jaundice levels than infants fed routine formulas or breast milk. Further study of this mechanism is needed.

Funder

National Institutes of Health

Waisman Center

Publisher

Wiley

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