Reaction of Free Fatty Acids with Protein in Cod Muscle Frozen and Stored at −29 C after Aging in Ice

1969 ◽  
Vol 26 (10) ◽  
pp. 2727-2736 ◽  
Author(s):  
Margaret L. Anderson ◽  
Elinor M. Ravesi
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Complex Formation ◽  
Free Fatty Acids ◽  
Phase Contrast ◽  
Reaction Rate ◽  
Frozen Storage ◽  
Phase Contrast Micrographs ◽  
Protein Extractability

Freezing and holding cod muscle in the frozen state favored the association process that involves protein–free fatty acid (FFA) complex formation and begins during aging in ice. Changes in protein extractability, in ultracentrifugal patterns of protein extracted, and in phase contrast micrographs of inextractable muscle fragments were followed in muscle that had been aged in ice to produce various contents of FFA and then frozen and held at −29 C. After 11 months, these changes, which took place largely during the first week of storage, were comparable with those that occur when the FFA are formed during frozen storage. The results were consistent with a reaction rate that was greater at −29 C than at temperatures a few degrees above 0 C.

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

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.

Epinephrine-insulin antagonism on free fatty acid release

1961 ◽  
Vol 201 (5) ◽  
pp. 815-818 ◽  
Author(s):  
John J. Spitzer ◽  
William T. McElroy
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Blood Sugar ◽  
Drug Administration ◽  
Hepatic Uptake ◽  
Fatty Acid Release ◽  
Plasma Ffa ◽  
Acid Release

The effects of epinephrine or norepinephrine were studied in dogs receiving insulin plus glucose prior to and during administration of the amine. Epinephrine caused a significantly smaller elevation of free fatty acids (FFA) with than without insulin plus glucose administration. Blood sugar responses were quantitatively similar. Epinephrine increased both hepatic uptake of FFA and hepatic release of glucose; these changes were similar to the ones found previously in dogs not receiving insulin plus glucose. The action of norepinephrine on elevating plasma FFA was only slightly and not significantly affected by the administration of insulin plus glucose. When the order of drug administration was reversed, infusion of insulin plus glucose lowered plasma FFA levels and hepatic FFA uptake in animals already receiving either epinephrine or nonepinephrine.

Changes in plasma free fatty acid concentrations on passage through the dog kidney

1961 ◽  
Vol 200 (5) ◽  
pp. 1095-1098 ◽  
Author(s):  
Frank J. Hohenleitner ◽  
John J. Spitzer
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Renal Plasma Flow ◽  
Plasma Free Fatty Acid ◽  
Systemic Artery ◽  
Arterial Concentration ◽  
Dog Kidney ◽  
Anesthetized Dogs

To measure the renal removal of free fatty acids from the plasma, simultaneous determinations of this metabolite were performed in a systemic artery and a renal vein in the anesthetized dogs. Renal plasma flow was also determined by the PAH method, and the renal uptake of free fatty acids was calculated. Concentrations of free fatty acids in renal venous plasma were usually lower than the arterial concentrations. The arteriovenous differences were statistically highly significant. The results also suggested that the degree of free fatty acid removal was proportional to the arterial concentration of this metabolite.

Free fatty acid concentration and composition in arterial blood

1962 ◽  
Vol 203 (2) ◽  
pp. 306-310 ◽  
Author(s):  
Martin E. Rothlin ◽  
Christine B. Rothlin ◽  
Vernon E. Wendt
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Free Fatty Acid Concentration ◽  
Arterial Blood ◽  
Arterial Concentration ◽  
The Subject ◽  
Palmitic Acids

The effect of the administration of norepinephrine, glucose and insulin, pentobarbital, and Hypertensin on the arterial concentration and composition of plasma free fatty acids (FFA) has been studied in man and dog. With a rise of the FFA concentration as produced by norepinephrine, the contribution of oleic acid to the total FFA increased, while that of stearic and palmitic acids decreased. The reverse changes in the FFA composition were observed when their arterial level fell under the influence of other agents studied. The FFA composition was dependent on the FFA concentration in arterial blood, but not on the experimental condition of the subject or animal at the time of analysis. At high FFA levels, the FFA composition approached that of depot fat.

scholarly journals Article Commentary: A Role for IR-β in the Free Fatty Acid Mediated Development of Hepatic Insulin Resistance?

2009 ◽  
Vol 2 ◽  
pp. BCI.S2996
Author(s):  
Samit Shah ◽  
Arthur G. Cox
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Pi3k Pathway ◽  
Hepatic Insulin Resistance ◽  
Hamster Model ◽  
High Concentrations ◽  
Nfκb Pathway

Several studies have been conducted to elucidate the role of free fatty acids (FFAs) in the pathogenesis of type 2 diabetes, but the exact molecular mechanism by which FFAs alter glucose metabolism in the liver is still not completely understood. 1 – 4 In a recent publication, Ragheb and coworkers have examined the effect of free fatty acid (FFA) treatment on insulin signaling and insulin resistance by using immunoprecipitation and immunoblotting to study the effect of high concentrations of insulin and FFAs on insulin receptor-beta (IR-β) and downstream elements in the PI3K pathway using the fructose-fed hamster model. 5 Their results clearly show that free fatty acids have an insignificant effect on IR-β and supports previous findings that FFAs lead to insulin resistance in the liver via the PKC-NFκB pathway. 2 , 3

Changes in free fatty acids during the ripening of Idiazabal cheese: influence of brining time and smoking

1994 ◽  
Vol 61 (2) ◽  
pp. 281-288 ◽  
Author(s):  
Ana I. Nájera ◽  
Luis J. R. Barron ◽  
Yolanda Barcina
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Free Fatty Acid Content ◽  
Acid Content ◽  
Lipolytic Activity ◽  
Fatty Acid Content ◽  
Ripening Period ◽  
Cheese Ripening

SummaryThe effect of brining time and smoking on the free fatty acid content of Idiazabal cheese during ripening was examined. The main free fatty acids considered underwent at least some increase during the first stage of ripening before day 90 and tended to level off around a constant value towards the end of the ripening period. There were significant differences in free fatty acid levels during ripening among cheeses with different brining times and between smoked and unsmoked cheeses. Brining time and smoking exerted marked effects on lipolytic activity during cheese ripening, depending upon the free fatty acid involved and ripening time. In general, brining and smoking led to increases in free fatty acid levels at the end of the ripening period; the different behaviour of butyric acid may be due to a specific lipolytic activity.

scholarly journals Relationship between plasma and muscle concentrations of ketone bodies and free fatty acids in fed, starved and alloxan-diabetic states

1973 ◽  
Vol 134 (2) ◽  
pp. 499-506 ◽  
Author(s):  
Oliver E. Owen ◽  
Helene Markus ◽  
Stuart Sarshik ◽  
Maria Mozzoli
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Plasma Glucose ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Water Concentration ◽  
Diabetic Rats ◽  
Muscle Membrane

1. Concentrations of ketone bodies, free fatty acids and chloride in fed, 24–120h-starved and alloxan-diabetic rats were determined in plasma and striated muscle. Plasma glucose concentrations were also measured in these groups of animals. 2. Intracellular metabolite concentrations were calculated by using chloride as an endogenous marker of extracellular space. 3. The mean intracellular ketone-body concentrations (±s.e.m.) were 0.17±0.02, 0.76±0.11 and 2.82±0.50μmol/ml of water in fed, 48h-starved and alloxan-diabetic rats, respectively. Mean (intracellular water concentration)/(plasma water concentration) ratios were 0.47, 0.30 and 0.32 in fed, 48h-starved and alloxan-diabetic rats respectively. The relationship between ketone-body concentrations in the plasma and intracellular compartments appeared to follow an asymptotic pattern. 4. Only intracellular 3-hydroxybutyrate concentrations rose during starvation whereas concentrations of both 3-hydroxybutyrate and acetoacetate were elevated in the alloxan-diabetic state. 5. During starvation plasma glucose concentrations were lowest at 48h, and increased with further starvation. 6. There was no significant difference in the muscle intracellular free fatty acid concentrations of fed, starved and alloxan-diabetic rats. Mean free fatty acid intramuscular concentrations (±s.e.m.) were 0.81±0.08, 0.98±0.21 and 0.91±0.10μmol/ml in fed, 48h-starved and alloxan-diabetic states. 7. The intracellular ketosis of starvation and the stability of free fatty acid intracellular concentrations suggests that neither muscle membrane permeability nor concentrations of free fatty acids per se are major factors in limiting ketone-body oxidation in these states.

PLASMA GLUCOSE, LACTATE AND FREE FATTY ACID RESPONSES TO ADRENALINE IN CHRONICALLY WARM- AND COLD-EXPOSED SHEEP

1981 ◽  
Vol 61 (4) ◽  
pp. 919-924 ◽  
Author(s):  
A. D. GRAHAM ◽  
G. D. PHILLIPS
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Cold Exposure ◽  
Plasma Glucose ◽  
Plasma Free Fatty Acid ◽  
Temperature Treatment ◽  
Glucose Response ◽  
Adrenaline Infusion

The effects of chronic cold exposure, fasting, or both on the plasma metabolite responses to jugular infusions of adrenaline were studied in eight five-mo-old wether lambs. Following maintenance at 20–22 °C or −4 to 10 °C for 2–3 wk the sheep received adrenaline infusions (0.15 μg∙kg−1∙min−1) for 75 min prior to and following a 72-h fast. Plasma samples collected at intervals of 10–15 min before and during adrenaline infusion were analyzed for glucose, lactate and total free fatty acids. Chronic cold exposure had no effect on the pre-infusion plasma glucose, lactate or free fatty acid concentrations. Fasting decreased plasma glucose and lactate and increased plasma free fatty acid concentrations. The plasma glucose response to adrenaline was greater (P < 0.01) in cold- than warm-exposed sheep and fasting depressed this response to a greater extent in the cold-exposed sheep. The plasma lactate response to adrenaline was not influenced by temperature treatment or fasting. Both groups of fasted sheep showed a large increase in plasma free fatty acids during adrenaline infusion but when fed the response was minimal.

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.

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