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© 2001 The American Society for Nutritional Sciences J. Nutr. 131:3016S-3020S, November 2001


Symposium: Human Lactogenesis II: Mechanisms, Determinants and Consequences

Lactogenesis and the Effects of Insulin-Dependent Diabetes Mellitus and Prematurity1 ,2

Peter Hartmann3 and Mark Cregan

Department of Biochemistry, University of Western Australia, Crawley, WA 6009, Australia

3To whom correspondence should be addressed. E-mail: hartmanp{at}cyllene.uwa.edu.au

The initiation of lactation (lactogenesis II) by the mother must be synchronized to the delivery of the infant, permitting the transition of the newborn from continuous nourishment from the umbilical cord to comparable but intermittent life support from its mother’s breasts. The onset of lactogenesis II can be adversely affected by a variety of factors. Over 80% of women who have delivered prematurely and are expressing milk for their infant had a compromised initiation of lactation, that is one or more lactogenesis II markers (lactose, citrate, sodium and total protein) in their milk > 3 SD from the mean of the full-term women on d 5 postpartum. Similarly, the lactogenesis II markers (lactose, citrate and total nitrogen) in the milk of women with insulin-dependent diabetes mellitus take an additional 24 h to attain the concentrations of normal women. The mechanisms that lead to the development of delayed or compromised onset of lactogenesis II in women are poorly understood and require additional research.


KEY WORDS: • lactogenesis • prematurity • diabetes • progesterone




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