Enteral feeding and gut atrophy.

Abstract

Because of the hypothesis that enteral feeding prevents intestinal mucosal atrophy and bacterial translocation, when fasting or malnutrition is present, nutrition support by the enteral route is usually preferred, if it is available. If nutrients are provided only parenterally intestinal mucosal mass falls dramatically in rats, but the relevance of this finding to humans has not been documented. This article reviews findings in the last 2 years relating to this dilemma. Most work continues to be done in rats and pigs, two species that demonstrate mucosal atrophy with fasting. The earlier demonstration of effects of administration of hormones and glutamine have been corroborated, but proper controls for hormones (related peptides) or glutamine (most importantly glutamate) have usually not been included. In humans mucosal atrophy does not occur except modestly (approximately 10% decrease in thickness) in some reports during catabolic conditions, such as in critical-care units. Even so, no evidence for reversal by enteral feeding has as yet been provided. On the other hand, evidence for specific gene adaptation with or without mucosal atrophy has begun to appear in animals and humans. The focus on mucosal atrophy has obscured the adaptation that may occur simultaneously to minimize the atrophy. Attention to gene adaptation during fasting and malnutrition may provide evidence, in future, for appropriate therapeutic interventions.