The Micellar Hypothesis of Fat Absorption: Must It Be Revisited?

Publisher Website
Google Scholar
Abstract
In 1962, Hofman & BorgstroUm (1, 2) applied the then available knowledge of detergent chemistry to the problem of the physicochemical status of intestinal content during digestion of fat. In vitro studies indicated that the products of pancreatic lipolysis of triglyceride fat–mainly 2-mono-glyceride and fatty acid–form mixed micelles with bile salts in an isotropic (optically clear) solution. Ultracentrifugation of intestinal content after a fatty meal fed to man yielded an oil phase and a clear aqueous phase. The former contained mostly unchanged triglyceride and some diglyceride, the latter mainly fatty acid and mono-glyceride. It was concluded that intestinal content during digestion is a detergent solution above its critical micellar concentration (CMC). The results were consistent with the hypothesis that intestinal lipids, during fat digestion, are partitioned between a micellar and an oil phase and that absorption of dietary lipid takes place from a micellar solution containing chiefly fatty acid and 2-monoglyceride (2). Evidence for the last part of this series of events, the uptake of micellar lipid by the enterocyte, was later obtained by in vitro studies using intestinal sacs and brush border preparations (3). In these experiments micellar monoolein and oleic acid were taken up in parallel. It was later shown, both in vitro and in vivo (4, 5), that components other than monoolein/ oleic acid in micellar solution are taken up to a different extent and at different rates, suggesting that micellar lipids are not absorbed as intact aggregates. The results of studies by Simmonds (6) and Westergaard & Dietschy (7) indicated that lipids in general were taken up by diffusion of a monomolecular dispersion of lipids in the aqueous phase rather than through direct transfer of lipid molecules from the mixed micelles to the brush border membrane of the mucosal epithelial cell and that the importance of the mixed lipid– bile salt micelle was to ‘increase the pressure-head for diffusion’ (6) or to ‘overcome the resistance of the unstirred water-layer adjacent to the enterocyte membrane’ (7). For references, see the comprehensive review by Thomson & Dietschy (8).