Intestinal-type and liver-type fatty acid-binding protein in the intestine. Tissue distribution and clinical utility Maurice M.A.L. Pelsers a, *, Zbigniew Namiot b,c , Wojciech Kisielewski c , Andrzej Namiot d , Marcin Januszkiewicz e , Wim T. Hermens f , Jan F.C. Glatz a a Department of Molecular Genetics, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands b Department of Physiology, (District Hospital), Bialystok, Poland c Department of Clinical Pathomorphology (Medical Academy), Bialystok, Poland d Pathology Section, Mental Hospital, Choroszcz, Poland e Department of Surgery (District Hospital), Bialystok, Poland f Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands Received 21 October 2002; accepted 28 May 2003 Abstract Objectives: Intestinal-type fatty acid-binding protein (I-FABP) has been proposed as plasma marker for the detection of acute intestinal injury. However, intestinal mucosa also expresses liver-type FABP (L-FABP). We have investigated the tissue distribution of I-FABP and L-FABP in segments of the human intestine along the duodenal to colonal axis and the potential of both proteins to serve as plasma marker for the diagnosis of intestinal injury. Design and methods: I-FABP and L-FABP were measured with specific immunoassays in autopsy samples of the intestine (duodenum, jejunum, ileum and colon) of 23 subjects and in plasma samples from patients (n = 51) with intestinal and/or hepatic disease. Plasma reference values were established in normal healthy individuals (n = 92). Results: The I-FABP tissue contents in duodenum, jejunum, ileum, proximal colon and distal colon amounted to 2.22, 4.79, 1.04, 0.27 and 0.25 g/g ww, respectively. L-FABP tissue contents were markedly higher, amounting to 124 and 198 g/g ww in duodenum and jejunum, and to 58, 26 and 44 g/g ww in ileum, proximal colon and distal colon, respectively. Elevated plasma levels of both I-FABP and L-FABP were found in patients suffering from intestinal diseases, while only L-FABP was increased in cases of purely hepatocellular injury. Conclusions: I-FABP and L-FABP show a similar pattern of tissue distribution along the duodenal to colonal axis with highest tissue contents found in the jejunum but in each intestinal segment a 40-fold higher content of L-FABP than of I-FABP. Accordingly, besides I-FABP, also L-FABP is a useful plasma marker for the detection of intestinal injury, especially in patients undergoing intestinal surgery. © 2003 The Canadian Society of Clinical Chemists. All rights reserved. Keywords: Intestinal injury; L-FABP; I-FABP; H-FABP; Intestinal tissue content; Reference range; Mesenteric infarction; Ileus 1. Introduction The analysis of specific tissue proteins or enzymes in plasma is a common approach for the detection of tissue necrosis and is widely used for detection of liver, muscle and heart injury [1]. However, for the early detection of intestinal injury due to decreased perfusion of the small bowel, inflammation or rejection, no protein is routinely analyzed. Several studies have investigated the use of bio- chemical markers like hexoaminidase and lactate dehydro- genase [2] or physiologic markers like mucosal pH [3], but these were nonconclusive. By analogy to the use of cyto- plasmic heart-type fatty acid-binding protein (H-FABP) for detection of heart- and muscle injury, the cytoplasmic in- testinal fatty-acid binding protein (I-FABP) is a newly pro- posed marker. I-FABP is part of a family of nine different FABP types, each named after the tissue of its first detection [4,5]. FABPs are 15 kD cytoplasmic proteins, involved in the intracellular buffering and transport of long chain fatty- acids. I-FABP occurs in the enterocytes of small intestine and constitutes 2% of enterocyte protein [5,6]. Several stud- ies have described the use of I-FABP for the detection of rat intestinal injury after acute ischemic diseases [2], rejection * Corresponding author. Fax: +31-43-3884574. E-mail address: maurice.pelsers@gen.unimaas.nl (M.M.A.L. Pelsers). Clinical Biochemistry 36 (2003) 529 –535 0009-9120/03/$ – see front matter © 2003 The Canadian Society of Clinical Chemists. All rights reserved. doi:10.1016/S0009-9120(03)00096-1