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 Turnover of Plasma Glucose and Free Fatty Acids in Vivo after Portacaval Anastomosis and Chronic Underfeeding in the Rat

1981 ◽  
Vol 60 (1) ◽  
pp. 87-93 ◽  
Author(s):  
G. S. Sarna ◽  
V. J. Cunningham ◽  
Sheron Tucker ◽  
Jill E. Cremer
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Intravenous Injection ◽  
Plasma Glucose ◽  
Plasma Free Fatty Acid ◽  
Portacaval Anastomosis ◽  
Single Intravenous Injection

1. The metabolic status of rats after end-to-side portacaval anastomosis and the extent to which this differs from sham-operated animals, both fed and pair-fed, was investigated. 2. The body weights of sham-operated pair-fed rats consistently matched the weights of animals with a portacaval anastomosis at different times after the operation, whereas liver weights were significantly reduced in anastomosed animals as compared with the other groups. 3. Plasma glucose, insulin and the irreversible disposal rates for plasma glucose (determined by single intravenous injection of [6-3H]glucose) were similarly and significantly reduced for animals with a portacaval anastomosis and sham-operated pair-fed animals as compared with sham-operated fed control rats. 4. In contrast, plasma free fatty acid levels were significantly higher in animals with a portacaval anastomosis as compared with both sham-operated fed control and sham-operated pair-fed groups of animals. Turnover of plasma free fatty acids was measured in vivo by single intravenous injection of [1-14C]palmitic acid. The raised levels of plasma free fatty acids in animals with a portacaval anastomosis were principally due to reduced clearance and not to an increase in lipolysis. 5. Plasma β-hydroxybutyrate levels were similar in sham-operated fed control rats and animals with a portacaval anastomosis. Pair-fed values were three to four times greater than sham-operated fed control values and after portacaval anastomosis and increased further after a period of 24 h fasting. Values obtained for anastomosed animals increased only marginally after 24 h fasting and were significantly lower than pair-fed-animal values. 6. The rat with an end-to-side portacaval anastomosis may be characterized to be in a metabolic state equivalent to a chronically underfed animal in terms of reduced glucose turnover and plasma insulin concentrations but differs in respect to plasma free fatty acid turnover and plasma β-hydroxybutyrate concentrations.

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.

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.

Turnover of free fatty acids during recovery from exercise

1975 ◽  
Vol 39 (2) ◽  
pp. 247-250 ◽  
Author(s):  
L. Hagenfeldt ◽  
J. Wahren
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Specific Activity ◽  
Plasma Free Fatty Acid ◽  
Plasma Pool ◽  
Arterial Concentration ◽  
Fractional Turnover

The turnover of plasma free fatty acid (FFA) was studied during the recovery from exercise with the aid of a continuous infusion of 14C-labeled oleic acid. Arterial FFA reached a maximum of twice the exercise value after 6 min of recovery and was still 75% above the basal level after 20 min. Within 2 min after exercise, plasma radioactivity had increased and the specific activity of plasma oleic acid had fallen. The rate of uptake of FFA from the plasma pool rsoe by 40% during the first minutes after exercise. The rate of release of FFA to the plasma pool showed a peak 2 min after exercise and was thereafter about 40 mumol/min lower than the rate of uptake. The fractional turnover of FFA decreased to resting levels within 5–10 min after exercise. It is concluded that the postexercise peak in arterial FFA is a consequence of augmented release of FFA into the plasma pool above the level during exercise, possibly related to the release of sympathetic vasoconstrictor tone. As a consequence, the rate of removal of FFA rises at the end of exercise and remains augmented above the basal level for as long as the arterial concentration is increased.

Effect of increased plasma free fatty acid concentrations on muscle metabolism in exercising men

1991 ◽  
Vol 70 (1) ◽  
pp. 194-201 ◽  
Author(s):  
M. Hargreaves ◽  
B. Kiens ◽  
E. A. Richter
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Carbohydrate Metabolism ◽  
Ketone Bodies ◽  
Plasma Concentrations ◽  
Plasma Free Fatty Acid ◽  
Substrate Utilization ◽  
Moderate Intensity

The effect of increasing plasma concentrations of free fatty acids on substrate utilization in muscle during exercise was investigated in 11 healthy young males. One hour of dynamic knee extension at 80% of knee-extensor maximal work capacity was performed first with one leg and then with the other leg during infusion of Intralipid and heparin. Substrate utilization was assessed from arterial and femoral venous blood sampling as well as from muscle biopsies. Intralipid infusion increased mean plasma free fatty acid concentrations from 0.54 +/- 0.08 to 1.12 +/- 0.09 (SE) mM. Thigh glucose uptake during rest, exercise, and recovery was decreased by 64, 33, and 42%, respectively, by Intralipid, whereas muscle glycogen breakdown and release of lactate, pyruvate, and citrate were unaffected. Concentrations of glucose, glucose 6-phosphate, and lactate in muscle before and at termination of exercise were unaffected by Intralipid. During exercise, net leg uptake of plasma free fatty acids was not measurably increased by Intralipid, whereas uptake of ketone bodies was. Local respiratory quotient across the leg was not changed by Intralipid (control 0.87 +/- 0.02, Intralipid 0.86 +/- 0.02). Arterial concentrations of insulin, norepinephrine, and epinephrine were similar in the two trials. It is concluded that at rest and during exercise at a moderate intensity (requiring approximately equal contributions from fat and carbohydrate metabolism), muscle carbohydrate metabolism is affected only with regard to uptake of glucose when plasma concentrations of lipid and lipid metabolites are increased. This effect may be by direct inhibition of glucose transport rather than by the classic glucose-fatty acid cycle.

The Effects of Cold and Prostaglandin E1 on Lipid Mobilization in the Chicken

1971 ◽  
Vol 49 (5) ◽  
pp. 394-398 ◽  
Author(s):  
W. D. Wagner ◽  
R. A. Peterson ◽  
R. J. Cenedella
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Cold Exposure ◽  
Prostaglandin E1 ◽  
Plasma Free Fatty Acid ◽  
Prostaglandin E ◽  
Elevated Plasma ◽  
Lower Plasma ◽  
Lipid Mobilization ◽  
Plasma Ffa

Plasma free fatty acid (FFA) levels and the effects of prostaglandin E1 (PGE1) were studied in cold-acclimated and cold-exposed chickens and compared to controls. Chickens cold-acclimated at 4–7 or 8–11 °C for 4 weeks had significantly elevated plasma FFA when compared to the controls at 19–21 °C. Although PGE1 had no effect on the basal level of FFA of controls, a significantly lower plasma FFA was seen after injection of either 10 or 30 μg PGE1/kg in cold-acclimated chickens. Chickens cold-exposed to 2–3 °C for 4 h demonstrated significant elevations of plasma FFA when compared to controls. Only 30 μg PGE1/kg significantly depressed the plasma FFA in the cold-exposed birds. No inhibition of basal FFA release was seen in control animals. From these experiments, it is concluded that chickens mobilize FFA extensively under cold-exposure and that this stimulated lipolysis is inhibited by PGE1.

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.

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.

Sign in / Sign up

Export Citation Format

Share Document