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Intestinal lipid metabolism is altered in Liver Fatty Acid‐Binding Protein‐null mice (LFABP‐/‐)
Author(s) -
Lagakos William S,
Storch Judith,
Zhou Yin Xiu,
Mandap Bernadette,
Binas Bert
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb35
Subject(s) - lipid metabolism , intestinal mucosa , metabolism , small intestine , monoacylglycerol lipase , medicine , biochemistry , triglyceride , biology , chemistry , endocrinology , cholesterol , endocannabinoid system , receptor
LFABP is expressed at high levels in the mammalian small intestine and binds the products of dietary triacylglycerol (TG) digestion, fatty acids (FA) and monoacylglycerol (MG). The precise role of intestinal LFABP in processing these diet‐derived lipids is unknown. We investigated the acute metabolism of FA and MG in wild‐type (WT) and LFABP −/− small intestinal mucosa in vivo . Two minutes after intraduodenal administration of [ 14 C]‐oleate, mucosal [ 14 C] was recovered primarily in TG, with no difference between WT and LFABP −/− . After intraduodenal [ 3 H]‐monoolein administration, however, [ 3 H] recovery in phospholipids (PL) and diacylglycerol was significantly increased ( p<0.05 ) while recovery in TG tended to be lower in LFABP −/− . [ 3 H] recovery was also increased in the MG fraction which may reflect slower assimilation of newly arrived MG ( P<0.05 ). Food deprivation increased [ 14 C]‐oleate oxidation in WT and LFABP −/− mucosa, although this was markedly attenuated in LFABP −/− ( P<0.01 ). Interestingly, the total FA oxidative capacity is unchanged in LFABP −/− intestinal mucosa homogenates in vitro , implying that the FA oxidation defect is mediated by alterations in substrate availability. Mucosal lipid analysis showed that LFABP‐ablation caused a significant increase in TG and PL content, and reduced cholesterol and FA content ( P<0.05 ). Overall, the results suggest that LFABP may be involved in the acute trafficking of FA to oxidative pathways, and the incorporation of MG, but perhaps not FA, into complex lipids. Supported by a grant from NIDDK (JS).