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