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

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.

1981 ◽  
Vol 61 (4) ◽  
pp. 919-924 ◽  
Author(s):  
A. D. GRAHAM ◽  
G. D. PHILLIPS

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.


1961 ◽  
Vol 200 (5) ◽  
pp. 1095-1098 ◽  
Author(s):  
Frank J. Hohenleitner ◽  
John J. Spitzer

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.


1973 ◽  
Vol 134 (2) ◽  
pp. 499-506 ◽  
Author(s):  
Oliver E. Owen ◽  
Helene Markus ◽  
Stuart Sarshik ◽  
Maria Mozzoli

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.


1962 ◽  
Vol 203 (2) ◽  
pp. 311-315 ◽  
Author(s):  
P. T. Bodel ◽  
D. Rubinstein ◽  
E. E. McGarry ◽  
J. C. Beck

Human and rat diaphragm and rat gastrocnemius muscle oxidize and esterify palmitate-1-C14. Incorporation of C14 was found to be in proportion to the palmitate present in the medium over a range of concentrations from 0.8 to 2.9 µEq/ml. Fasting increased C14O2 production but had no effect on esterification. Iodoacetate or an atmosphere of nitrogen inhibited esterification of palmitate but increased the amount of free fatty acid in the tissue. Insulin increased esterification, and this was enhanced by the addition of glucose. Glucose and insulin exerted a sparing action on the oxidation of glycerides by a tissue previously charged with palmitate-1-C14. Growth hormone administered in vivo over a period of 1 week or in vitro during incubation had no effect on esterification or metabolism of palmitate-1-C14.


1975 ◽  
Vol 39 (2) ◽  
pp. 247-250 ◽  
Author(s):  
L. Hagenfeldt ◽  
J. Wahren

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.


1975 ◽  
Vol 229 (2) ◽  
pp. 255-259 ◽  
Author(s):  
RB Dunn ◽  
JB Critz

These experiments were designed to determine: 1) if lactate can be extracted from the arterial blood and utilized by resting skeletal muscle of the dog, and 2) if lactate uptake or production by skeletal muscle is influenced by the level of circulating free fatty acids. Skeletal muscle arteriovenous differences in lactate were measured at several arterial lactate and free fatty acid concentrations. With sodium pentobarbital anesthesia and a low concentration of free fatty acids, arterial lactate concentrations of 1-2 mM were associated with extraction of lactate; however, when circulating free fatty acids were elevated (greater than 1 mM), no extraction of lactate occurred at these lactate concentrations. The relationship between arterial free fatty acids and uptake or release of lactate demonstrated in these in vivo studies suggest that the inhibition of free fatty acid release from adipose tissue that occurs when the arterial lactate concentration increases may function facilitate the metabolism of lactate by skeletal muscle.


1991 ◽  
Vol 70 (1) ◽  
pp. 194-201 ◽  
Author(s):  
M. Hargreaves ◽  
B. Kiens ◽  
E. A. Richter

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.


1984 ◽  
Vol 102 (3) ◽  
pp. 381-386 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe

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


1997 ◽  
Vol 273 (1) ◽  
pp. G184-G190 ◽  
Author(s):  
M. Saghir ◽  
J. Werner ◽  
M. Laposata

Fatty acid ethyl esters (FAEE), esterification products of fatty acids and ethanol, are in use as fatty acid supplements, but they also have been implicated as toxic mediators of ethanol ingestion. We hypothesized that hydrolysis of orally ingested FAEE occurs in the gastrointestinal (GI) tract and in the blood to explain their apparent lack of toxicity. To study the in vivo inactivation of FAEE by hydrolysis to free fatty acids and ethanol, we assessed the hydrolysis of FAEE administered as an oil directly into the rat stomach and when injected within the core of low-density lipoprotein particles into the circulation of rats. Our studies demonstrate that FAEE are rapidly degraded to free fatty acids and ethanol in the GI tract at the level of the duodenum with limited hydrolysis in the stomach. In addition, FAEE are rapidly degraded in the circulation, with a half-life of only 58 s. Thus the degradation of FAEE in the GI tract and in the blood provides an explanation for the apparent lack of toxicity of orally ingested FAEE.


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