The absorption of short-chain fats by premature infants.

That premature infants commonly exhibit defective fat absorption has been known for many years (Rubner and Langstein, 1915; Muhl, 1923; Tidwell, Holt, Farrow and Neale, 1935). This steatorrhoea is, however, masked and the excess of unabsorbed fat does not separate out in the gross or in microscopically detectable globules. Efforts to compensate for the caloric deficit caused by this unabsorbed fat have followed several lines, such as low-fat feedings (Gordon and McNamara, 1941), homogenization (Morales, Chung, Lewis, Messina and Holt, 1950b) and emulsifying agents (Snyderman, Morales, Chung, Lewis, Messina and Holt, 1953) to facilitate fat absorption and the use of the more readily assimilable unsaturated fats (Tidwell et al., 1935). The present authors have also shown that increasing the fat intake improved absolute absorption (Morales et al., 1950a) and did not produce deleterious effects. A further approach to the problem was suggested by the work of Frazer (1946) which indicated that short-chain fats were absorbed through the portal circulation rather than by the lacteals. It seemed possible that the absorption defect in the premature infant might be confined to the lacteal nmchanism and that portal absorption would be quite normal. In this event the defect in fat absorption could be overcome simply by feeding short-chain fats. Observations of this kind were therefore made, using tributyrin and triacetin to replace butter fat in feeds.