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Enterostatin efflux in cat intestinal lymph: relation to lymph flow, hyaluronan, and fat absorption
M I Townsley1, C Erlanson-Albertsson, A Ohlsson
1Department of Physiology, University of South Alabama, Mobile 36688, USA.
Insights
Enterostatin, a peptide from pancreatic procolipase, increases in intestinal lymph after fat absorption. However, this study found enterostatin does not alter intestinal hyaluronan turnover, despite its elevated lymph levels.
Area of Science:
- Gastroenterology
- Physiology
- Molecular Biology
Background:
- Enterostatin is the activation peptide of pancreatic procolipase.
- Hyaluronan turnover is a key process in intestinal function.
- The role of enterostatin in intestinal hyaluronan metabolism via lymph was previously unclear.
Purpose of the Study:
- To investigate whether enterostatin modulates intestinal hyaluronan turnover through lymphatic transport.
- To determine the relationship between fat absorption, enterostatin levels in lymph, and hyaluronan efflux.
Main Methods:
- Surgical isolation of feline ileal segments with cannulated lymphatic drainage.
- In situ autoperfusion of isolated ileal segments.
- Measurement of immunoreactive enterostatin concentrations in lymph and plasma under various conditions (baseline, fat absorption, high lymph flow).
- Intestinal lumen perfusion with oleic acid and taurocholate.
- Introduction of enterostatin into the ileum via intra-arterial bolus or lumen perfusion.
Main Results:
- Enterostatin concentration in lymph significantly increased after cream feeding and oleic acid perfusion, with lymph/plasma ratios rising from baseline.
- At high lymph flows, enterostatin concentrations decreased, altering the lymph/plasma ratio.
- Despite increased enterostatin levels in lymph post-fat absorption, direct administration of enterostatin into the ileum did not alter hyaluronan efflux into the lymph.
Conclusions:
- Enterostatin concentration in intestinal lymph increases following fat absorption, even when pancreatic secretions are blocked.
- Enterostatin does not appear to modify intestinal hyaluronan turnover or its efflux into the lymph.
- The observed correlation between hyaluronan efflux and fat absorption is likely independent of enterostatin's direct action on hyaluronan metabolism.
Abstract:
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 was cannulated, and the segment was autoperfused in situ. In several groups, concentrations of immunoreactive enterostatin in lymph were compared with that in plasma at baseline and elevated lymph flow and 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 with 4.93 +/- 0.42 after cream feeding (P < 0.05). In a separate group, when the intestinal lumen was perfused for 2 h with a mixture of oleic acid and taurocholate, enterostatin L/P doubled compared with baseline. At high lymph flows, enterostatin concentrations fell in all groups, resulting in an L/P of 0.47 +/- 0.09 (P < 0.05) in the absence of fat absorption, 0.77 +/- 0.35 after 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 after fat absorption [R.K. Reed, M.I Townsley, V.H. Pitts, T.C. Laurent, and A.E. Taylor. Am. J. Physiol, 263 (Gastrointest. Liver Physiol. 26): 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 conclusion, 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.
