Mode of action of choline. II. The fate of intravenously administered labelled fatty acids in choline-deficient rats

1969 ◽  
Vol 47 (2) ◽  
pp. 207-218 ◽  
Author(s):  
A. Chalvardjian
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Total Phospholipid ◽  
Hepatic Triglyceride ◽  
Rat Serum ◽  
Short Period ◽  
Time Periods ◽  
Phospholipid Pool ◽  
Fatty Acid Pool

Two groups of rats (200 g, male) were fed, respectively, a choline-deficient and a choline-supplemented diet for 3 days. On the 3rd day each rat was injected intravenously with rat serum containing 9,10-3H-palmitate and 18-14C-stearate. The fate of the labelled fatty acids was followed in the triglycerides and phospholipids of liver and serum for time periods ranging from 1 min to 6 h. When compared to the choline-supplemented controls, the livers in the choline-deficient rats were fatty and were characterized by: (1) an increased hepatic triglyceride pool, (2) a decrease in turnover of hepatic triglycerides with sequestration of fatty acids and decrease in their recycling, (3) an increase in the hepatic free fatty acid pool and total phospholipid pool, the latter reflecting the net result of synthesis and transport, (4) a decrease in the early and rapid turnover of the phosphatidylcholine pool, (5) a decrease in turnover of the phosphatidylethanolamine pool, (6) a decrease in transport of triglycerides and phospholipids from liver to serum, and consequently, (7) a decrease in triglyceride and phospholipid pools in serum. These results confirm previous observations that, although an impairment of transport of both triglycerides and phospholipids from liver to serum exists in choline-deficient rats, the hepatic accumulation of triglycerides is far greater than that of phospholipids. This effect is due to the presence of a potential triglyceride pool in liver that can accommodate large amounts of triglyceride within a short period of time.

Differential Mobilization of Essential Fatty Acids into the Serum Free Fatty Acid Pool in Response to Glucose Ingestion

1989 ◽  
pp. 385-387
Author(s):  
Stephen C. Cunnane ◽  
T. M. S. Wolever ◽  
J. K. Armstrong ◽  
D. J. A. Jenkins
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Essential Fatty Acids ◽  
Serum Free Fatty Acid ◽  
Serum Free ◽  
Acid Pool ◽  
Glucose Ingestion ◽  
Fatty Acid Pool

Lipids of antibiotic-sensitive and -resistant strains of Pseudomonas aeruginosa

1971 ◽  
Vol 17 (11) ◽  
pp. 1357-1365 ◽  
Author(s):  
E. A. Anderes ◽  
W. E. Sandine ◽  
P. R. Elliker
Keyword(s):  
Fatty Acids ◽  
Pseudomonas Aeruginosa ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Total Lipid ◽  
Total Phospholipid ◽  
Lipid Production ◽  
Ammonium Compound ◽  
Free Lipid ◽  
Resistant Cells

From a population of cells of Pseudomonas aeruginosa sensitive to 33 parts per million (ppm) of quaternary ammonium compound (QAC) and to 0.1 mg/ml of chloramphenicol (CAP), pure strains resistant to 750 ppm and 2.5 mg/ml of these antibacterial substances were isolated. Lipids from the sensitive and resistant cells grown under various conditions were extracted and characterized. Increased lipid biosynthesis was investigated as a possible factor in the resistance of this bacterium to CAP and QAC.Resistant cells grown in medium containing 207 ppm QAC at 25C averaged 77% more total lipid than sensitive cells. Resistant cells grown in the absence of QAC at 25C retained their resistance and averaged 27% more total lipid than sensitive cells. Cells grown at 32C in the presence of QAC contained 8% more total lipid than sensitive cells but less than cells grown at 25C under the same conditions. There was no increased lipid production by QAC-resistant cells grown at 37C in a Fermacell fermentor. Cells grown in CAP-containing medium (2.5 mg/ml) at 25C developed 28% more total lipid than sensitive cells grown in antibiotic-free medium.Gas–liquid chromatograms of the phospholipid, free fatty acid, and triglyceride fractions of the various cell types indicated that the same fatty acids were present. There was a 10% increase of the C18:1 fatty acid in both the phospholipid and free fatty acid fractions of the free lipids of cells grown in a Fermacell fermentor in the presence of CAP or QAC. However, there was no compensatory decrease in any single fatty acid, but rather a general decrease.Sensitive P. aeruginosa contained 14% free lipid and 3% to 6% bound lipid. The major phospholipid was phosphatidyl ethanolamine, which constituted 59% of the total phospholipid fraction of the sensitive cells. Analysis of fatty acids revealed that C16 amounted to 34%, C18:1 19%, and C16:1 and C18 each about 5% of the total present. These four fatty acids accounted for 63% of the free lipid present in the sensitive cells.

The subcellular distribution of free fatty acids released during post-decapitative ischemia in rat cerebral cortex

1985 ◽  
Vol 63 (11) ◽  
pp. 1183-1188 ◽  
Author(s):  
R. Roy Baker ◽  
Zou Dao Loh
Keyword(s):  
Fatty Acids ◽  
Cerebral Cortex ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Subcellular Distribution ◽  
Phospholipase A ◽  
C Cells ◽  
Acid Pool ◽  
Fatty Acid Pool

After periods of 5 and 30 min following decapitation, rat cerebral cortices were removed and subcellular fractions were prepared. Fractions P1A (large myelin), P1B (nuclei), P1C (cells and debris), P2A (small myelin), P2B (synaptosomes), P2C (mitochondria), and P3 (microsomes) were isolated. Free fatty acid levels of 1.0 and 1.4 μmol/g tissue were found in the homogenates at the early and late times of ischemia. In the 30-min samples, P1A, P1C, and P2A had relatively high specific contents of total free fatty acids in comparison with other subfractions. At this time P2C was relatively enriched in arachidonate, P1A and P2A were enriched in palmitate, and P2B and P3 were enriched in stearate in comparison with the homogenate. P2C had the highest ratio of polyunsaturates/saturates in its free fatty acid pool. Comparing the 5- and 30-min samples, a large increase in the quantity of free fatty acids was found in fractions P1A and P2A, so that at the later time P1A + P2A contained 60 mol% of the free fatty acid in the total subfractions derived from cerebral cortex. In comparison with the homogenate, the lack of accumulation of free fatty acids in certain membranes known to possess phospholipase activities (e.g., phospholipase A2 in P2C) and the buildup of free fatty acids in P1A and P2A led to the hypothesis that free fatty acids may be migrating outwards from intracellular sites of production and accumulating in the multilamellar structure of myelin.

Chylomicron triglyceride metabolism in resting and exercising fed dogs

1982 ◽  
Vol 52 (4) ◽  
pp. 815-820 ◽  
Author(s):  
R. L. Terjung ◽  
L. Budohoski ◽  
K. Nazar ◽  
A. Kobryn ◽  
H. Kaciuba-Uscilko
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Corn Oil ◽  
Removal Rate ◽  
Moderate Intensity ◽  
Beta Oxidation ◽  
Fed State ◽  
Acid Pool ◽  
Fatty Acid Pool

The turnover of circulating triglycerides (TG) was determined in dogs during rest, following ingestion of food that included corn oil, and in the final period of a 1-h treadmill exercise of moderate intensity (72–84 m/min). In all cases the loss of [14C]TG from the plasma followed a first-order process. The fractional removal rate constant at rest was 26.5 +/- 1.9% (SE) n = 10) of the circulating pool size per minute, and it was increased slightly to 33.8 +/- 3.6% (n = 7) per minute during exercise. The uptake of plasma TG-derived fatty acids (5 min postinjection) was increased (P less than 0.05) in working muscle, whereas the TG uptake in fat tended to decrease. Further, the percent of TG-derived fatty acids found in the muscle's acylglyceride pool was less (90.0 +/- 3.6 vs. 53.5 +/- 1.8%), while that in the muscle's free fatty acid pool was greater (12.3 +/- 36.1 +/- 4.7%) in working compared with resting muscle. Thus the fourfold greater quantity of plasma TG-derived fatty acids found in the working muscle's free fatty acid pool could account for the entire increased TG uptake caused by exercise. This suggests that, in the fed state, circulating TG could represent a potential source of fatty acids for beta-oxidation in working muscle. However, the importance of plasma TG-derived fatty acids as an energy substrate during muscle use in a postprandial state has yet to be determined quantitatively.

THE EFFECT OF FREE FATTY ACIDS ON RESIN UPTAKE OF TRI-IODOTHYRONINE FROM HUMAN, RAT, RABBIT AND GUINEA-PIG SERUM AND HUMAN SERUM ALBUMIN

1969 ◽  
Vol 45 (4) ◽  
pp. 489-493 ◽  
Author(s):  
P. W. NATHANIELSZ
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Human Serum Albumin ◽  
Guinea Pig ◽  
Serum Albumin ◽  
Free Fatty Acids ◽  
Human Serum ◽  
Rat Serum ◽  
Pig Serum

SUMMARY Recently changes in plasma free fatty acids have been suggested as a possible regulator of the levels of free thyroxine in the plasma. Oleic acid has been shown to displace tri-iodothyronine from human serum, human serum albumin, rat serum, rabbit serum and guinea-pig serum. The extent of the displacement, much greater from human serum albumin than from whole serum, suggests that free fatty acid does not affect the globulin binding site. It would also appear that, in the rat, all the binding sites are sensitive to free fatty acids and hence there is probably only albumin binding in this species. The results with rabbit and guinea-pig serum were intermediate to those with human and rat serum. A significant rise in resin uptake of tri-iodothyronine in vitro occurred with an increase of free fatty acid level of 0·5 m-equiv./l., well within the physiological range.

scholarly journals Insulin-independent regulation of hepatic triglyceride synthesis by fatty acids

2015 ◽  
Vol 112 (4) ◽  
pp. 1143-1148 ◽  
Author(s):  
Daniel F. Vatner ◽  
Sachin K. Majumdar ◽  
Naoki Kumashiro ◽  
Max C. Petersen ◽  
Yasmeen Rahimi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Insulin Signaling ◽  
Plasma Fatty Acid ◽  
Hepatic Triglyceride ◽  
Triglyceride Synthesis ◽  
Hepatic Glucose ◽  
Acid Esterification ◽  
Fatty Acid Esterification

A central paradox in type 2 diabetes is the apparent selective nature of hepatic insulin resistance—wherein insulin fails to suppress hepatic glucose production yet continues to stimulate lipogenesis, resulting in hyperglycemia, hyperlipidemia, and hepatic steatosis. Although efforts to explain this have focused on finding a branch point in insulin signaling where hepatic glucose and lipid metabolism diverge, we hypothesized that hepatic triglyceride synthesis could be driven by substrate, independent of changes in hepatic insulin signaling. We tested this hypothesis in rats by infusing [U-13C] palmitate to measure rates of fatty acid esterification into hepatic triglyceride while varying plasma fatty acid and insulin concentrations independently. These experiments were performed in normal rats, high fat-fed insulin-resistant rats, and insulin receptor 2′-O-methoxyethyl chimeric antisense oligonucleotide-treated rats. Rates of fatty acid esterification into hepatic triglyceride were found to be dependent on plasma fatty acid infusion rates, independent of changes in plasma insulin concentrations and independent of hepatocellular insulin signaling. Taken together, these results obviate a paradox of selective insulin resistance, because the major source of hepatic lipid synthesis, esterification of preformed fatty acids, is primarily dependent on substrate delivery and largely independent of hepatic insulin action.

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

Effect of glucose concentration in the growth medium on the synthesis of fatty acids by the yeast Candida bogoriensis

1982 ◽  
Vol 28 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Adrian J. Cutler ◽  
Robley J. Light
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Yeast Extract ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Glucose Medium ◽  
Triglyceride Fraction ◽  
Low Glucose ◽  
Stimulation Of

The yeast Candida bogoriensis produced large quantities of an extracellular glycolipid, the diacetyl sophoroside of 13-hydroxydocosanoic acid, when grown on a standard glucose rich medium (3% glucose, 0.15% yeast extract), but not when grown on a low glucose medium (0.5% glucose, 0.4% yeast extract) (A. J. Cutler and R. J. Light. 1979. J. Biol. Chem. 254: 1944–1950). Glucose levels also affected the quantity and distribution of the free fatty acid and triglyceride fractions synthesized by this organism. Cells grown on the low glucose medium contained palmitate and stearate as the major fatty acids in these two fractions, and a 3-h incubation with [1-14C]acetate led primarily to the labeling of these two acids. Cells grown on the standard enriched glucose medium contained relatively less stearate and more behenate than the low glucose grown cells, and the incorporation of [1-14C]acetate into stearate was decreased, while that into behenate was increased.Supplementation of low glucose grown cells with glucose led to a rapid stimulation of fatty acid synthesis, primarily palmitate and stearate in the free fatty acid fraction and stearate in the triglyceride fraction. Total triglyceride began to increase a few hours after supplementation, but synthesis of the extracellular glycolipid, and hence 13-hydroxydocosanoic acid, did not occur until 12–24 h after supplementation. The stimulation by glucose of long chain fatty acid synthesis in C. bogoriensis was therefore a process distinct from the glucose stimulation of palmitate and stearate synthesis, though the two events may be causally related.

scholarly journals Lipolysis and the Free Fatty Acid Pool in Seedlings

1964 ◽  
Vol 39 (6) ◽  
pp. 880-883 ◽  
Author(s):  
Allen J. St. Angelo ◽  
Aaron M. Altschul
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Acid Pool ◽  
Fatty Acid Pool

scholarly journals Free Fatty acids receptors (FFAR2 and FFAR3) control cell proliferation by regulating cellular glucose uptake

2019 ◽  
Author(s):  
Mohammad Aziz ◽  
Saeed Al Mahri ◽  
Amal Alghamdi ◽  
Maaged AlAkiel ◽  
Monira Al Aujan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Fatty Acids ◽  
Cell Proliferation ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Microarray Data ◽  
Free Fatty Acid Receptors

Abstract Background Colorectal cancer is a worldwide problem which has been associated with changes in diet and lifestyle pattern. As a result of colonic fermentation of dietary fibres, short chain free fatty acids are generated which activate Free Fatty Acid Receptors 2 and 3 (FFAR2 and FFAR3). FFAR2 and FFAR3 genes are abundantly expressed in colonic epithelium and play an important role in the metabolic homeostasis of colonic epithelial cells. Earlier studies point to the involvement of FFAR2 in colorectal carcinogenesis. Methods Transcriptome analysis console was used to analyse microarray data from patients and cell lines. We employed shRNA mediated down regulation of FFAR2 and FFAR3 genes which was assessed using qRT-PCR. Assays for glucose uptake and cAMP generation was done along with immunofluorescence studies. For measuring cell proliferation, we employed real time electrical impedance based assay available from xCelligence. Results Microarray data analysis of colorectal cancer patient samples showed a significant down regulation of FFAR2 gene expression. This prompted us to study the FFAR2 in colorectal cancer. Since, FFAR3 shares significant structural and functional homology with FFAR2, we knocked down both these receptors in colorectal cancer cell line HCT 116. These modified cell lines exhibited higher proliferation rate and were found to have increased glucose uptake as well as increased level of GLUT1. Since, FFAR2 and FFAR3 signal through G protein subunit (Gαi), knockdown of these receptors was associated with increased cAMP. Inhibition of PKA did not alter the growth and proliferation of these cells indicating a mechanism independent of cAMP/PKA pathway. Conclusion: Our results suggest role of FFAR2/FFAR3 genes in increased proliferation of colon cancer cells via enhanced glucose uptake and exclude the role of protein kinase A mediated cAMP signalling. Alternate pathways could be involved that would ultimately result in increased cell proliferation as a result of down regulated FFAR2/FFAR3 genes. This study paves the way to understand the mechanism of action of short chain free fatty acid receptors in colorectal cancer.

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