出版社:American Society for Biochemistry and Molecular Biology
摘要:FA transport protein 4 (FATP4), one member of a multigene family of FA transporters, was proposed as a major FA transporter in intestinal lipid absorption. Due to the fact that Fatp4 −/− mice die because of a perinatal skin defect, we rescued the skin phenotype using an FATP4 transgene driven by a keratinocyte-specific promoter ( Fatp4 −/− ;Ivl-Fatp4 tg/+ mice) to elucidate the role of intestinal FATP4 in dietary lipid absorption. Fatp4 −/− ;Ivl-Fatp4 tg/+ mice and wild-type littermates displayed indistinguishable food consumption, growth, and weight gain on either low or high fat (Western) diets, with no differences in intestinal triglyceride (TG) absorption or fecal fat losses. Cholesterol absorption and intestinal TG absorption kinetics were indistinguishable between the genotypes, although Western diet fed Fatp4 −/− ;Ivl-Fatp4 tg/+ mice showed a significant increase in enterocyte TG and FA content. There was no compensatory upregulation of other FATP family members or any other FA or cholesterol transporters in Fatp4 −/− ;Ivl-Fatp4 tg/+ mice. Furthermore, although serum cholesterol levels were lower in Fatp4 −/− ;Ivl-Fatp4 tg/+ mice, there was no difference in hepatic VLDL secretion in-vivo or in hepatic lipid content on either a chow or Western diet. Taken together, our studies find no evidence for a physiological role of intestinal FATP4 in dietary lipid absorption in mice.