Linoleic acid absorption in the unaesthetized rat: Mechanism of transport and influence of luminal factors on absorption

Chow, S. L.; Hollander, Daniel

doi:10.1007/bf02533421

Cited by 39 publications

(9 citation statements)

References 25 publications

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“…1) and the absence of an energy requirement suggest that at low luminal concentrations, linoleic acid is absorbed by a facilitated diffusion mechanism, which could be carrier-mediated and does not require energy. These findings are in agreement with previous reports that suggested that at low luminal concentrations (0.04-1.2 mM) linoleic acid was absorbed by a facilitated diffusion mechanism, and at high concentration (2-5mM) by simple diffusion (9,13). A similar, concentrationdependent dual mechanism of transport has previously been reported for other nutrients (14,15) and is probably shared by other long-chain unsaturated fatty acids (16).…”

Section: Linoleic Acid Cholesterol After Resectionsupporting

confidence: 92%

Changes in Uptake of Linoleic Acid and Cholesterol by Jejunal Sacs of Rats in Vitro, after Distal Small-Bowel Resection

Molina¹,

Ruı́z-Gutı́errez²,

Vázquez³

et al. 1990

Scandinavian Journal of Gastroenterology

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Both linoleic acid and cholesterol uptake were studied in small-intestinal sacs of rats in vitro after distal small-bowel resection (DSBR). The relationship between linoleic acid concentration and its absorption was non-linear at low concentrations and became linear at high concentrations in the three groups of animals. These observations indicate that a concentration-dependent dual mechanism of transport is operative in linoleic acid intestinal uptake. Experiments with rotenone and ouabain suggest that a facilitated diffusion is the predominant mechanism of absorption at low concentrations, whereas at high concentrations simple diffusion is predominant. The apparent kinetic constants of linoleic acid uptake (Kd, Kt, and Vmax) increased after DSBR. The uptake of linoleic acid is, however, influenced by the simultaneous presence of linolenic acid, the inhibition constant being decreased after the surgical operation. After the surgical operation an increase of cholesterol uptake was observed, with a parallel enhancement in the apparent mass-transfer coefficient (Kd). Taken together, these results suggest that both organ growth and changes in transport function of the enterocytes appear to be involved in the adaptive response of the bowel to intestinal resection.

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Section: Linoleic Acid Cholesterol After Resectionsupporting

confidence: 92%

Changes in Uptake of Linoleic Acid and Cholesterol by Jejunal Sacs of Rats in Vitro, after Distal Small-Bowel Resection

Molina¹,

Ruı́z-Gutı́errez²,

Vázquez³

et al. 1990

Scandinavian Journal of Gastroenterology

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“…Our data are not necessarily in conflict with those of Chow and Hollander [62] who proposed simple or facilitated diffusion of FA depending on the FA concentration because the kinetics of the flux of FA into caveolae could appear compatible with either interpretation. Further, the saturation kinetics proposed by Murota and Storch to indicate protein mediated absorption [63] could be the result of only a certain amount of FA able to be absorbed by the caveolae.…”

Section: Discussioncontrasting

confidence: 50%

Intestinal caveolin-1 is important for dietary fatty acid absorption

Siddiqi

Sheth

Patel

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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SUMMARY How dietary fatty acids are absorbed into the enterocyte and transported to the ER is not established. We tested the possibility that caveolin-1 containing lipid rafts and endocytic vesicles were involved. Apical brush border membranes took up 15% of albumin bound 3H-oleate whereas brush border membranes from caveolin-1 KO mice took up only 1%. In brush border membranes, the 3H-oleate was in the detergent resistant fraction of an OptiPrep gradient. On OptiPrep gradients of intestinal cytosol, we also found the 3H-oleate in the detergent resistant fraction, separate from OptiPrep gradients spiked with 3H-oleate or 3H-triacylglycerol. Caveolin-1 immuno-depletion of cytosol removed 91% of absorbed 3H-oleate whereas immuno-depletion using IgG, or anti-caveolin-2 or −3 or anti-clathrin antibodies removed 20%. Electron microscopy showed the presence of caveolin-1 containing vesicles in WT mouse cytosol that were 4 fold increased by feeding intestinal sacs 1 mM oleate. No vesicles were seen in caveolin-1 KO mouse cytosol. Caveolin-1 KO mice gained less weight on a 23% fat diet and had increased fat in their stool compared to WT mice. We conclude that dietary fatty acids are absorbed by caveolae in enterocyte brush border membranes, are endocytosed, and transported in cytosol in caveolin-1 containing endocytic vesicles.

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“…Although conflicting results have been reported, deletion of either CD36 or FATP4 alone in mouse intestine does not appear to dramatically alter fatty acid uptake (Goudriaan et al, 2002; Nauli et al, 2006; Shim et al, 2009). Studies utilizing cultured cell systems have supported a passive diffusion model by showing that the rate of fatty acid uptake is linear, protease-resistant, and temperature-independent (Chow and Hollander, 1979; Ling et al, 1989; Trotter et al, 1996). By contrast, others have pointed to a carrier-mediated model based on observations that fatty acid uptake is saturable and competitive with other fatty acids (Ho and Storch, 2001; Murota and Storch, 2005).…”

Section: Introductionmentioning

confidence: 99%

Intestinal Phospholipid Remodeling Is Required for Dietary-Lipid Uptake and Survival on a High-Fat Diet

et al. 2016

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Summary Phospholipids are important determinants of membrane biophysical properties, but the impact of membrane acyl chain composition on dietary lipid absorption is unknown. Here we demonstrate that the LXR-responsive phospholipid-remodeling enzyme Lpcat3 modulates intestinal fatty acid and cholesterol absorption and is required for survival on a high-fat diet. Mice lacking Lpcat3 in the intestine thrive on carbohydrate-based chow, but lose body weight rapidly and become moribund on a triglyceride-rich diet. Lpcat3-dependent incorporation of polyunsaturated fatty acids into phospholipids is required for the efficient transport of dietary lipids into enterocytes. Furthermore, loss of Lpcat3 amplifies the production of gut hormones including GLP-1 and oleoylethanolamide in response to high-fat feeding, contributing to the paradoxical cessation of food intake in the setting of starvation. These results reveal that membrane phospholipid composition is a gating factor in passive lipid absorption, and implicate LXR-Lpcat3 signaling in a gut-brain feedback loop that couples absorption to food intake.

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Linoleic acid absorption in the unaesthetized rat: Mechanism of transport and influence of luminal factors on absorption

Cited by 39 publications

References 25 publications

Changes in Uptake of Linoleic Acid and Cholesterol by Jejunal Sacs of Rats in Vitro, after Distal Small-Bowel Resection

Changes in Uptake of Linoleic Acid and Cholesterol by Jejunal Sacs of Rats in Vitro, after Distal Small-Bowel Resection

Intestinal caveolin-1 is important for dietary fatty acid absorption

Intestinal Phospholipid Remodeling Is Required for Dietary-Lipid Uptake and Survival on a High-Fat Diet

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