Studies on the uptake of fatty acids by brush border membranes of the rabbit intestine

1985 ◽  
Vol 63 (4) ◽  
pp. 249-256 ◽  
Author(s):  
P. Proulx ◽  
H. Aubry ◽  
I. Brglez ◽  
D. G. Williamson
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Bile Salt ◽  
Chain Length ◽  
Brush Border ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Egg Lecithin

Initial studies revealed that the uptake of palmitic acid and oleic acid into brush border membranes was similar when these were isolated from either whole small intestine, jejunum, or ileum. The uptake of these fatty acids was somewhat lower with membranes obtained from duodenum. Subsequent studies, all with membranes obtained from whole intestine, indicated an increase in binding with chain length of fatty acid of up to 16 carbons. Unsaturation decreased this uptake somewhat. Taurocholate and 1-palmitoyl lysolecithin had a moderate stimulatory effect on the binding of oleic acid and palmitic acid at concentrations of 10 and 0.5 mM, respectively, and inhibited at higher concentrations. Addition of 1.4 mM egg lecithin to the fatty acid – bile salt micelles, such that the lecithin – bile salt ratio was 0.2, decreased the uptake of fatty acids generally, but did not significantly affect the pattern of binding by membrane fractions isolated from different segments nor did it change the pattern of labelling when fatty acid chain length and unsaturation were varied. At lower concentrations, egg lecithin had little effect on the uptake of oleic acid, whereas dipalmitoyl phosphatidylcholine stimulated binding of both palmitic acid and oleic acid over the entire range of concentrations tested. Preincubation of the membranes with this saturated phospholipid stimulated the uptake of oleic acid, and addition of this choline lipid to the oleic acid – bile salt containing micelles did not substantially enhance fatty acid uptake in lipid-treated membranes. The binding of fatty acid was very rapid either in the presence or the absence of Ca2+, such that even in zero-time controls essentially equilibrium bindings were obtained. The presence of Ca2+ stimulated the incorporation substantially. The results as a whole indicate that fatty acid uptake into brush border membrane is very responsive to a variety of conditions which could prevail in the gut during the absorption process.

Palmitic acid uptake by the rat soleus muscle in vitro

2001 ◽  
Vol 79 (4) ◽  
pp. 419-424 ◽  
Author(s):  
M Górecka ◽  
M Synak ◽  
L Budohoski ◽  
J Langfort ◽  
S Moskalewski ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Soleus Muscle ◽  
Fatty Acid Uptake ◽  
Cellular Fatty Acid ◽  
Acid Uptake ◽  
Acid Complex ◽  
Rat Soleus Muscle

The rate of fatty acid uptake, oxidation, and deposition in skeletal muscles in relation to total and unbound to albumin fatty acids concentration in the medium were investigated in the incubated rat soleus muscle. An immunohistochemical technique was applied to demonstrate whether the albumin-bound fatty acid complex from the medium penetrates well within all areas of the muscle strips. It was found that the percentage of incorporation of palmitic acid into intramuscular lipids was fairly constant, independently of the fatty acid concentration in the medium, and amounted to 63–72% for triacylglycerols, 7–12% for diacylglycerols-monoacylglycerols, and 19–26% for phospholipids. Both palmitic acid incorporation into the muscle triacylglycerol stores and its oxidation to CO2closely correlated with an increase in both total and unbound to albumin fatty acid concentrations in the incubation medium. Under conditions of increased total but constant unbound to albumin palmitic acid concentrations, the incorporation of palmitic acid into triacylglycerols and its oxidation to CO2were also increased, but to a lower extent. This supports the hypothesis that the cellular fatty acid metabolism depends not only on the availability of fatty acids unbound to albumin, but also on the availability of fatty acids complexed to albumin.Key words: skeletal muscle, fatty acids, triacylglycerols, phospholipids.

scholarly journals Myo-inositol alters 13C-labeled fatty acid metabolism in human placental explants

2019 ◽  
Vol 243 (1) ◽  
pp. 73-84 ◽  
Author(s):  
Oliver C Watkins ◽  
Mohammed Omedul Islam ◽  
Preben Selvam ◽  
Reshma Appukuttan Pillai ◽  
Amaury Cazenave-Gassiot ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Docosahexaenoic Acid ◽  
Palmitic Acid ◽  
Acid Metabolism ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Liquid Chromatography Mass Spectrometry ◽  
Acid Processing ◽  
Clinical Consequences

We postulate that myo-inositol, a proposed intervention for gestational diabetes, affects transplacental lipid supply to the fetus. We investigated the effect of myo-inositol on fatty acid processing in human placental explants from uncomplicated pregnancies. Explants were incubated with 13C-labeled palmitic acid, 13C-oleic acid and 13C-docosahexaenoic acid across a range of myo-inositol concentrations for 24 h and 48 h. The incorporation of labeled fatty acids into individual lipids was quantified by liquid chromatography mass spectrometry. At 24 h, myo-inositol increased the amount of 13C-palmitic acid and 13C-oleic-acid labeled lipids (median fold change relative to control = 1). Significant effects were seen with 30 µM myo-inositol (physiological) for 13C-palmitic acid-lysophosphatidylcholines (1.26) and 13C-palmitic acid-phosphatidylethanolamines (1.17). At 48 h, myo-inositol addition increased 13C-oleic-acid-lipids but decreased 13C-palmitic acid and 13C-docosahexaenoic-acid lipids. Significant effects were seen with 30 µM myo-inositol for 13C-oleic-acid-phosphatidylcholines (1.25), 13C-oleic-acid-phosphatidylethanolamines (1.37) and 13C-oleic-acid-triacylglycerols (1.32) and with 100 µM myo-inositol for 13C-docosahexaenoic-acid-triacylglycerols (0.78). Lipids labeled with the same 13C-fatty acid showed similar responses when tested at the same time point, suggesting myo-inositol alters upstream processes such as fatty acid uptake or activation. Myo-inositol supplementation may alter placental lipid physiology with unknown clinical consequences.

scholarly journals Lipid Accumulation and Chronic Kidney Disease

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 722 ◽  
Author(s):  
Zhibo Gai ◽  
Tianqi Wang ◽  
Michele Visentin ◽  
Gerd Kullak-Ublick ◽  
Xianjun Fu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Kidney Disease ◽  
Lipid Accumulation ◽  
Scavenger Receptor ◽  
Fatty Acid Uptake ◽  
Lipid Lowering ◽  
Fatty Acid Transport ◽  
Acid Uptake

Obesity and hyperlipidemia are the most prevalent independent risk factors of chronic kidney disease (CKD), suggesting that lipid accumulation in the renal parenchyma is detrimental to renal function. Non-esterified fatty acids (also known as free fatty acids, FFA) are especially harmful to the kidneys. A concerted, increased FFA uptake due to high fat diets, overexpression of fatty acid uptake systems such as the CD36 scavenger receptor and the fatty acid transport proteins, and a reduced β-oxidation rate underlie the intracellular lipid accumulation in non-adipose tissues. FFAs in excess can damage podocytes, proximal tubular epithelial cells and the tubulointerstitial tissue through various mechanisms, in particular by boosting the production of reactive oxygen species (ROS) and lipid peroxidation, promoting mitochondrial damage and tissue inflammation, which result in glomerular and tubular lesions. Not all lipids are bad for the kidneys: polyunsaturated fatty acids (PUFA) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) seem to help lag the progression of chronic kidney disease (CKD). Lifestyle interventions, especially dietary adjustments, and lipid-lowering drugs can contribute to improve the clinical outcome of patients with CKD.

Effect of insulin on free fatty acid uptake by hepatocytes in the duck

1984 ◽  
Vol 102 (3) ◽  
pp. 381-386 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe
Keyword(s):  
Fatty Acids ◽  
Growth Hormone ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Metabolism ◽  
Free Fatty Acids ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Low Doses ◽  
Higher Doses

ABSTRACT To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake. J. Endocr. (1984) 102, 381–386

Isotope tracer measures of meal fatty acid metabolism: reproducibility and effects of the menstrual cycle

2005 ◽  
Vol 288 (3) ◽  
pp. E547-E555 ◽  
Author(s):  
Ana Paola Uranga ◽  
James Levine ◽  
Michael Jensen
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Menstrual Cycle ◽  
Dietary Fat ◽  
Fatty Acid Uptake ◽  
Upper Body ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Lower Body

Oxidation and adipose tissue uptake of dietary fat can be measured by adding fatty acid tracers to meals. These studies were conducted to measure between-study variability of these types of experiments and assess whether dietary fatty acids are handled differently in the follicular vs. luteal phase of the menstrual cycle. Healthy normal-weight men ( n = 12) and women ( n = 12) participated in these studies, which were block randomized to control for study order, isotope ([3H]triolein vs. [14C]triolein), and menstrual cycle. Energy expenditure (indirect calorimetry), meal fatty acid oxidation, and meal fatty acid uptake into upper body and lower body subcutaneous fat (biopsies) 24 h after the experimental meal were measured. A greater portion of meal fatty acids was stored in upper body subcutaneous adipose tissue (24 ± 2 vs. 16 ± 2%, P < 0.005) and lower body fat (12 ± 1 vs. 7 ± 1%, P < 0.005) in women than in men. Meal fatty acid oxidation (3H2O generation) was greater in men than in women (52 ± 3 vs. 45 ± 2%, P = 0.04). Leg adipose tissue uptake of meal fatty acids was 15 ± 2% in the follicular phase of the menstrual cycle and 10 ± 1% in the luteal phase ( P = NS). Variance in meal fatty acid uptake was somewhat ( P = NS) greater in women than in men, although menstrual cycle factors did not contribute significantly. We conclude that leg uptake of dietary fat is slightly more variable in women than in men, but that there are no major effects of menstrual cycle on meal fatty acid disposal.

Effect of surface and intracellular pH on hepatocellular fatty acid uptake

1996 ◽  
Vol 271 (6) ◽  
pp. G1067-G1073
Author(s):  
C. Elsing ◽  
A. Kassner ◽  
W. Stremmel
Keyword(s):  
Fatty Acids ◽  
Plasma Membrane ◽  
Fatty Acid ◽  
Intracellular Ph ◽  
Outer Surface ◽  
Fatty Acid Uptake ◽  
Proton Gradient ◽  
Fatty Acid Transport ◽  
Acid Uptake ◽  
Acid Transport

Fatty acids enter hepatocytes, at least in part, by a carrier-mediated uptake mechanism. The importance of driving forces for fatty acid uptake is still controversial. To evaluate possible driving mechanisms for fatty acid transport across plasma membranes, we examined the role of transmembrane proton gradients on fatty acid influx in primary cultured rat hepatocytes. After hepatocytes were loaded with SNARF-1 acetoxymethyl ester, changes in intracellular pH (pHi) under different experimental conditions were measured and recorded by confocal laser scanning microscopy. Fatty acid transport was increased by 45% during cellular alkalosis, achieved by adding 20 mM NH4Cl to the medium, and a concomitant paracellular acidification was observed. Fatty acid uptake was decreased by 30% during cellular acidosis after withdrawal of NH4Cl from the medium. Cellular acidosis activates the Na+/H+ antiporter to export excessive protons to the outer cell surface. Inhibition of Na+/H+ antiporter activity by amiloride diminishes pHi recovery and thereby accumulation of protons at the outer surface of the plasma membrane. Under these conditions, fatty acid uptake was further inhibited by 57% of control conditions. This suggests stimulation of fatty acid influx by an inwardly directed proton gradient. The accelerating effect of protons at the outer surface of the plasma membrane was confirmed by studies in which pH of the medium was varied at constant pHi. Significantly higher fatty acid influx rates were observed at low buffer pH. Recorded differences in fatty acid uptake appeared to be independent of changes in membrane potential, because BaCl2 did not influence initial uptake velocity during cellular alkalosis and paracellular acidosis. Moreover, addition of oleate-albumin mixtures to the NH4Cl incubation buffer did not change the observed intracellular alkalinization. In contrast, after cells were acid loaded, addition of oleate-albumin solutions to the recovery buffer increased pHi recovery rates from 0.21 +/- 0.02 to 0.36 +/- 0.05 pH units/min (P < 0.05), indicating that fatty acids further stimulate Na+/H+ antiporter activity during pHi recovery from an acid load. It is concluded that carrier-mediated uptake of fatty acids in hepatocytes follows an inwardly directed transmembrane proton gradient and is stimulated by the presence of H+ at the outer surface of the plasma membrane.

scholarly journals Biocatalyst Engineering by Assembly of Fatty Acid Transport and Oxidation Activities for In Vivo Application of Cytochrome P-450BM-3 Monooxygenase

1998 ◽  
Vol 64 (10) ◽  
pp. 3784-3790 ◽  
Author(s):  
Silke Schneider ◽  
Marcel G. Wubbolts ◽  
Dominique Sanglard ◽  
Bernard Witholt
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Coenzyme A ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Uptake System ◽  
Whole Cells ◽  
E Coli ◽  
Cytochrome P 450 ◽  
Long Chain

ABSTRACT The application of whole cells containing cytochrome P-450BM-3 monooxygenase [EC 1.14.14.1 ] for the bioconversion of long-chain saturated fatty acids to ω-1, ω-2, and ω-3 hydroxy fatty acids was investigated. We utilized pentadecanoic acid and studied its conversion to a mixture of 12-, 13-, and 14-hydroxypentadecanoic acids by this monooxygenase. For this purpose,Escherichia coli recombinants containing plasmid pCYP102 producing the fatty acid monooxygenase cytochrome P-450BM-3were used. To overcome inefficient uptake of pentadecanoic acid by intact E. coli cells, we made use of a cloned fatty acid uptake system from Pseudomonas oleovorans which, in contrast to the common FadL fatty acid uptake system of E. coli, does not require coupling by FadD (acyl-coenzyme A synthetase) of the imported fatty acid to coenzyme A. This system fromP. oleovorans is encoded by a gene carried by plasmid pGEc47, which has been shown to effect facilitated uptake of oleic acid in E. coli W3110 (M. Nieboer, Ph.D. thesis, University of Groningen, Groningen, The Netherlands, 1996). By using a double recombinant of E. coli K27, which is a fadDmutant and therefore unable to consume substrates or products via the β-oxidation cycle, a twofold increase in productivity was achieved. Applying cytochrome P-450BM-3 monooxygenase as a biocatalyst in whole cells does not require the exogenous addition of the costly cofactor NADPH. In combination with the coenzyme A-independent fatty acid uptake system from P. oleovorans, cytochrome P-450BM-3 recombinants appear to be useful alternatives to the enzymatic approach for the bioconversion of long-chain fatty acids to subterminal hydroxylated fatty acids.

scholarly journals Effect of fatty acid chain length and saturation on the gastrointestinal handling and metabolic disposal of dietary fatty acids in women

1999 ◽  
Vol 81 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Amanda E. Jones ◽  
Michael Stolinski ◽  
Ruth D. Smith ◽  
Jane L. Murphy ◽  
Stephen A. Wootton
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Stearic Acid ◽  
Palmitic Acid ◽  
Chain Length ◽  
Time Course ◽  
Absorbed Dose ◽  
Dietary Fatty Acids ◽  
Fatty Acid Chain ◽  
Degree Of Unsaturation

The gastrointestinal handling and metabolic disposal of [1-13C]palmitic acid, [1-13C]stearic acid and [1-13C]oleic acid administered within a lipid–casein–glucose–sucrose emulsion were examined in normal healthy women by determining both the amount and nature of the13C label in stool and label excreted on breath as13CO2. The greatest excretion of13C label in stool was in the stearic acid trial (9.2 % of administered dose) whilst comparatively little label was observed in stool in either the palmitic acid (1.2 % of administered dose) or oleic acid (1.9 % of administered dose) trials. In both the palmitic acid and oleic acid trials, all of the label in stool was identified as being present in the form in which it was administered (i.e. [13C]palmitic acid in the palmitic acid trial and [13C]oleic acid in the oleic acid trial). In contrast, only 87 % of the label in the stool in the stearic acid trial was identified as [13C]stearic acid, the remainder was identified as [13C]palmitic acid which may reflect chain shortening of [1-13C]stearic acid within the gastrointestinal tract. Small, but statistically significant, differences were observed in the time course of recovery of13C label on breath over the initial 9 h of the study period (oleic acid = palmitic acid > stearic acid). However, when calculated over the 24 h study period, the recovery of the label as13CO2was similar in all three trials (approximately 25 % of absorbed dose). These results support the view that chain length and degree of unsaturation may influence the gastrointestinal handling and immediate metabolic disposal of these fatty acids even when presented within an emulsion.

scholarly journals Lipid storage by adipose tissue macrophages regulates systemic glucose tolerance

2014 ◽  
Vol 307 (4) ◽  
pp. E374-E383 ◽  
Author(s):  
Myriam Aouadi ◽  
Pranitha Vangala ◽  
Joseph C. Yawe ◽  
Michaela Tencerova ◽  
Sarah M. Nicoloro ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Fatty Acid Uptake ◽  
Foam Cell Formation ◽  
Acid Uptake ◽  
Obese Mice ◽  
Adipose Tissue Macrophages

Proinflammatory pathways in adipose tissue macrophages (ATMs) can impair glucose tolerance in obesity, but ATMs may also be beneficial as repositories for excess lipid that adipocytes are unable to store. To test this hypothesis, we selectively targeted visceral ATMs in obese mice with siRNA against lipoprotein lipase (LPL), leaving macrophages within other organs unaffected. Selective silencing of ATM LPL decreased foam cell formation in visceral adipose tissue of obese mice, consistent with a reduced supply of fatty acids from VLDL hydrolysis. Unexpectedly, silencing LPL also decreased the expression of genes involved in fatty acid uptake (CD36) and esterification in ATMs. This deficit in fatty acid uptake capacity was associated with increased circulating serum free fatty acids. Importantly, ATM LPL silencing also caused a marked increase in circulating fatty acid-binding protein-4, an adipocyte-derived lipid chaperone previously reported to induce liver insulin resistance and glucose intolerance. Consistent with this concept, obese mice with LPL-depleted ATMs exhibited higher hepatic glucose production from pyruvate and glucose intolerance. Silencing CD36 in ATMs also promoted glucose intolerance. Taken together, the data indicate that LPL secreted by ATMs enhances their ability to sequester excess lipid in obese mice, promoting systemic glucose tolerance.

scholarly journals High rates of [1-14C]acetate incorporation into the lipid of isolated spinach chloroplasts

1976 ◽  
Vol 158 (3) ◽  
pp. 593-601 ◽  
Author(s):  
P G Roughan ◽  
C R Slack ◽  
R Holland
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Free Fatty Acids ◽  
Acid Synthesis ◽  
Polar Lipids ◽  
Acetate Incorporation ◽  
Spinach Chloroplasts ◽  
Triton X

Spinach chloroplasts, isolated by techniques yielding preparations with high O2- evolving activity, showed rates of light-dependent acetate incorporation into lipids 3-4 fold higher than any previously reported. Incorporation rates as high as 500 nmol of acetate/h per mg of chlorophyll were measured in buffered sorbitol solutions containing only NaHCO3 and [1-14C]acetate, and as high as 800 nmol/h per mg of chlorophyll when 0.13 mM-Triton X-100 was also included in the reaction media. The fatty acids synthesized were predominantly oleic (70-80% of the total fatty acid radioactivity) and palmitic (20-25%) with only minor amounts (1-5%) of linoleic acid. Linolenic acid synthesis was not detected in the system in vitro. Free fatty acids accounted for 70-90% of the radioactivity incorporated and the remainder was shared fairly evenly between 1,2-diacylglycerols and polar lipids. Oleic acid constituted 80-90% of the free fatty acids synthesized, but the diacylglycerols and polar lipids contained slightly more palmitic acid than oleic acid. Triton X-100 stimulated the synthesis of diacylglycerols 3-6 fold, but stimulated free fatty acid synthesis only 1-1.5-fold. Added glycerol 1-phosphate stimulated both the synthesis of diacylglycerols and palmitic acid relative to oleic acid, but did not increase acetate incorporation into total chloroplast lipids. CoA and ATP, when added separately, stimulated acetate incorporation into chloroplast lipids to variable extents and had no effect on the types of lipid synthesized, but when added together resulted in 34% of the incorporated acetate appearing in long-chain acyl-CoA. Pyruvate was a much less effective precursor of chloroplast fatty acids than was acetate.

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