Expression of fatty acyl‐CoA binding proteins in colon cells: response to butyrate and transformation

Abstract

Fatty acyl-CoA affect many cellular functions as well as serving as cellular building blocks. Several families of cytosolic fatty acyl-CoA binding proteins may modulate the activities of fatty acyl-CoA. Intestinal enterocytes contain at least three unique families of cytosolic proteins that bind fatty acyl-CoA: acyl-CoA binding protein (ACBP), fatty acid binding proteins (including the liver, L-FABP and intestinal, I-FABP), and sterol carrier protein-2 (SCP-2). Immortalized rat colon epithelial cell lines expressed only ACBP and SCP-2 at levels of 0.75 +/- 0.13 and 0.42 +/- 0.02 ng/microgram protein. Ras and src transformation increased colon cell density and differentially altered ACBP and SCP-2 expression without affecting I-FABP or L-FABP levels. ACBP levels were 1.8-fold and 1.5-fold increased in ras- and src-transformed cells, respectively. In contrast, SCP-2 expression was significantly decreased 55 and 67% in ras- and src-transformed cells, respectively. Butyrate treatment of ras- and src-transformed cells decreased cell proliferation up to 60-85% as compared to 25-30% in control cells. Butyrate treatment decreased ACBP expression in all cell lines but had no effect on the levels of SCP-2, I-FABP, or L-FABP. These studies suggest that the differential expression of ACBP and SCP-2 in rat colonic cell lines, as well as their modulation by butyrate, may be altered by cell transformation.

Structural and functional characterization of a new recombinant histidine-tagged acyl coenzyme A binding protein (ACBP) from mouse

“…These data are in agreement with ACBP gene expression being upregulated by lipogenic transcription factors such as sterolregulatory element binding protein (SREBP) in the liver [35,39] and by PPARγ during adipocyte differentiation from fibroblasts upon insulin stimulation [17,28]. ACBP is also found at abnormally high levels in tumor cells that exhibit very high rates of lipid synthesis as well as proliferation [6,14,16,25,40]. Conversely, ACBP suppression results in reduced cellular growth rates, abnormal fatty acyl-CoA composition, vesicle accumulation, and membrane defects in yeast [13,36]; inhibition of adipocyte differentiation [27]; and lethality in some types of mammalian cells [9].…”

Diazepam-binding inhibitor-derived peptides induce intracellular calcium changes and modulate human neutrophil function

“…In view of the fact that DBI is released from nerve terminals and its fragments can be found in liquor and peripheral blood [33], such peptides may represent novel neuroendocrine mediators linking the central nervous system to the immune system. Moreover, inasmuch as DBI or a protein with an identical amino acid sequence, previously named acyl-CoA binding protein, is also widely distributed in many peripheral organs such as gut and endocrine cells of the pancreatic islets [5,34], liver, kidney [35], adrenals [36], adipose tissue, heart, muscles, and mammary gland [37] of different species, and in circulating mononuclear cells [38], in red blood cells [39], and even in neoplastic cell lines [40], it cannot be excluded that high concentrations of DBI and/or of its processing products may occur locally as the result of leakage from damaged cells during tissue injury. DBI-derived peptides may thus also add to the multiple agents constituting the local microenvironment in inflamed tissues.…”

Metabolomics reveals a novel vitamin E metabolite and attenuated vitamin E metabolism upon PXR activation

“…In a very recent report, Scpx-null mice treated with phytol, a source of BCFA, exhibited a decreased ability to metabolize branched-chain lipids (37). Transcription of Scp2 is positively regulated by the Forkhead transcription factor (Fox)O3a (38), but not regulated through PPARs (39,40). Tocopherol metabolism was not enhanced by clofibrate, an inducer of peroxisomal b-oxidation, in HepG2 cells (30) and urinary CEHC metabolites were not increased in wildtype mice treated with the rodent PPARa agonist, 4-chloro-6-(2,3-xylidino)-pyrimidynylthioacetic acid (Wy-14,643) (data not shown).…”