Enterostatin efflux in cat intestinal lymph: relation to lymph flow, hyaluronan and fat absorption. Townsley, M. I., C. Erlanson-Albertsson, A. Ohlsson, C. Rippe, and R. K. Reed. Departments of Physiology, University of South Alabama, USA, and University of Bergen, Norway Department of Medical and Physiological Chemistry, University of Lund, Sweden
APStracts 3:0082G, 1996.
The question addressed in this study was whether enterostatin, the pancreatic procolipase activation peptide, modulates intestinal hyaluronan turnover via lymph. In anesthetized cats, segments of ileum were surgically isolated from the proximal and distal gut, the draining lymphatic cannulated and the segment autoperfused in situ. In several groups, concentrations of immunoreactive enterostatin in lymph were compared to that in plasma at baseline and elevated lymph flow, and both in the absence and presence of fat absorption. The baseline ratio of lymph enterostatin to that in plasma (L/P) in the absence of fat absorption was 1.44+/-0.29, compared to 4.93+/-0.42 following cream feeding (p&LT0.05). In a separate group, when the intes tinal lumen was perfused for 2 h with a mixture of oleic acid and taurocholate, enterostatin L/P doubled compared to baseline. At high lymph flows, enterostatin concentrations fell in all groups, resulting in an L/P of 0.47+/-0.09 (p&LT0.05) in the absence of fat absorption, 0.77+/-0.35 following oleic acid, and 1.26+/-0.13 in the cream-fed group. These changes correlate with the pattern of hyaluronan efflux from the ileum into lymph following fat absorption (Reed et al., Am. J. Physiol. 263:G6-G11, 1992). However, in separate groups when enterostatin was introduced into ileum, either as a close intra-arterial bolus or via the intestinal lumen, there were no resultant changes in efflux of hyaluronan from the intestine into lymph. In conclu sion, despite the fact that delivery of pancreatic exocrine secretions to the ileal lumen was blocked in this model, enterostatin concentration in lymph increased after fat absorption. Nonetheless, it seems clear that enterostatin does not modify intestinal hyaluronan turnover.

Received 19 October 1994; accepted in final form 16 March 1996.
APS Manuscript Number G425-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 23 April 96