Free Fatty Acid Mobilization Research Articles

Effects of thyroid hormones on adenyl cyclase in adipose tissue and on free fatty acid mobilization.

Effects of thyroid hormones on adenyl cyclase in adipose tissue and on free fatty acid mobilization.

Mobilization of plasma free fatty acids during the growth of various experimental tumors

Several tumors of mice and rats including Ehrlich-carcinoma, Sarcoma 180, Yoshida H 130, Walker carcinosarcoma, T 8 uterine epithelioma, and Flexner-Jobling carcinoma, induced an increase in plasma FFA. Walker carcinosarcoma induced a strong mobilization of FFA which depleted the stores of triglycerides in the adipose tissue. This effect was not due to the reduction of food intake shown by Walker-bearing animals. It is suggested that Walker tumor was producing factors able to mobilize lipids from adipose tissue.

Effect of nicotinic acid on plasma lipids in patients with hyperlipoproteinemia during the first week of treatment

Thirteen patients with hyperlipoproteinemia were treated with nicotinic acid. The fasting plasma lipid level was followed before treatment and daily during the first 5 days of treatment with 1 g of nicotinic acid three times a day. After treatment for 1 day the average triglyceride level was significantly reduced, whilst the cholesterol concentration was unaffected. The triglycerides then remained fairly stable at this new level. The cholesterol level, however, was not significantly reduced until the 4th and 5th days of treatment. The concentration of phospholipids behaved in a similar way to that of cholesterol. These findings suggest that the concentration of the triglyceride-rich very low density lipoproteins (VLDLP) is reduced after 1 day's treatment, whereas the level of the cholesterol and phospholipid-rich low density lipoproteins (LDLP) is not lowered until the 4th to 5th days. This type of lipoprotein change was confirmed by analysis of plasma lipoproteins, separated in the preparative ultracentrifuge, from a case of essential hypercholesterolemia. The following working hypothesis for the action of nicotinic acid on plasma lipids is suggested. Nicotinic acid inhibits mobilization of free fatty acids from adipose tissue. This reduces the uptake of free fatty acids in the liver, which is followed in turn by decreased hepatic formation of VLDLP. The consequences would be reduced conversion of VLDLP to LDLP and, eventually, diminution of the LDLP level in plasma; thus plasma cholesterol and phospholipids would be lowered. Further work is required to confirm this hypothesis and to determine whether nicotinic acid has other effects on fatty acid transport than that of inhibiting lipolysis in adipose tissue.

Hepatic triglyceride secretion in relation to lipogenesis and free fatty acid mobilization in fasted and glucose-refed rats

Plasma triglyceride concentrations were significantly lowered by a single feeding of glucose to rats that had been fasted for 22 hr. Three feedings of glucose produced a similar effect. In the glucose-refed animals mobilization of free fatty acids from adipose tissue was impaired more rapidly than hepatic lipogenesis was restored from its low fasting level. These effects of glucose were shown by both a 50% fall in plasma free fatty acid concentration and an 84% decrease in free fatty acid release by isolated epididymal fat pads within 30 min after a single refeeding of glucose. Hepatic lipogenesis from either acetate-1-(14)C or glucose-U-(14)C was not restored even after glucose had been fed three times at hourly intervals. Triton-induced hypertriglyceridemia was used to measure the hepatic triglyceride secretory rate; it was found that glucose refeeding decreased this rate in all but one of several experiments. This decreased secretion rate was sufficient to account for the nearly complete disappearance of triglyceride in very low density lipoproteins (d < 1.019) that occurred within 1 hr after a single glucose intubation.

Metabolic Effects of Actinomycin in Rats.

SummaryIn hypophysectomized rats fasting reduced the metabolism of glucose in adipose tissue and diaphragm muscle in vitro and increased the mobilization of free fatty acids and glycerol. Hepatic and cardiac glycogen were also reduced. Treatment with actinomycin D reversed these effects, and caused a substantial increase in glucose utilization by adipose tissue. Actinomycin partially prevented the increased lipolysis caused by fasting in normal rats, but failed to reduce the lipolysis evoked by epinephrine or corticotropin.

Quantitative aspects of free fatty acid metabolism in the fasted rat

Palmitate-1-(14)C was injected intravenously into unanesthetized, fasted rats. Disappearance of tracer from plasma free fatty acids was studied. A large component of free fatty acid (FFA) recycling was directly demonstrated by reinjection experiments. The latter studies also indicated the existence of an unidentified, rapidly turning over polar lipid in plasma which was synthesized from palmitate-(14)C. The appearance of (14)C in hepatic and extrahepatic triglycerides, in other esters, and in respired CO(2) was also followed. The data were analyzed using a multicompartmental model and a digital computer. Only a small fraction of the triglycerides formed in liver was derived directly from plasma free fatty acids. The major portion of net triglyceride formation appeared to be by way of an intermediate nontriglyceride ester pool which turned over relatively slowly compared to plasma free fatty acids. Initial approximations are as follows ( micromoles of fatty acid per min per 100 g body weight): net free fatty acid mobilization (irreversible disposal) = 2.4; hepatic triglyceride formation directly from plasma free fatty acid = 0.1; total hepatic lipid formation from plasma free fatty acids = 0.5; oxidation of free fatty acids to CO(2) = 0.8; percentage of respired CO(2) from direct oxidation of fatty acids = 12%; extrahepatic triglyceride formation directly from fatty acids = 0.4; total extrahepatic lipid formed directly from fatty acids = 1.2.

In Vivo and In Vitro Manifestations of Adrenergic Blockade inBordetella pertussis-vaccinated Mice

The in vivo metabolic events which follow the administration of epinephrine, norepinephrine, or isoproterenol were examined in normal, Bordetella pertussis-vaccinated, and alpha and beta adrenergically blocked mice. The normal hyperglycemic response to epinephrine was suppressed in all experimental groups. The pertussis-sensitized and beta-blocked animals produced similar split patterns of altered response not duplicated by the alpha-blocking compounds. Those catecholamines that normally increase free fatty acids and lactic acid in the circulation failed to do so in the pertussis-sensitized and beta-blocked animals; the inhibition of free fatty acid mobilization was also demonstrated with adipose tissue incubated in vitro. An extract of the pertussis organism added to incubation media prevented the catecholamine-induced free fatty acid response. The epinephrine-stabilizing effect of bovine serum albumin (Cohn-fraction V) was observed. The results of these studies further emphasize a correlation between pertussis-sensitized and beta-adrenergically blocked mice.

Exercise, adrenergic blockage, and free fatty acid mobilization.

Exercise, adrenergic blockage, and free fatty acid mobilization.

Regular, Filter-Tip, and Modified Cigarettes

A recent report from the Roswell Park Memorial Institute, at Buffalo, 1,2 stated that filter-tip cigarettes did not effectively remove tars and nicotine from cigarette smoke. The study was based on an analysis of the tar and nicotine content of the smoke of nine brands of filter-tip cigarettes, and it was concluded that filters did not protect the smoker against the health hazards of smoking. We have previously investigated certain biochemical and pharmacological effects of cigarette smoking 3-6 and felt it would be of interest to determine the influence of filters and other cigarette modifications on these effects. This report presents the results of a comparative study of the effect on nicotine excretion, free fatty acid (FFA) mobilization, and catecholamine excretion of regular and filter-tip cigarettes, pipe tobacco cigarettes, and lettuce leaf cigarettes. Method of Study.— Six normal men, ages 28 to 45, participated in this study. All were habitual

Concentrations of glycerides and phospholipids in rat heart and gastrocnemius muscles. Effects of alloxan-diabetes and perfusion.

1. Methods are described for the extraction of lipid and assay of mono-, di- and tri-glyceride glycerol and phospholipid phosphorus in rat heart and gastrocnemius muscles. 2. In hearts from normal animals, concentrations found were: monoglyceride, 0.6; diglyceride, 0.1; triglyceride, 12.6mumoles of glyceride glycerol/g. of dry muscle; phospholipid, 171mug.atoms of phospholipid phosphorus/g. of dry muscle. Concentrations of glycerides in gastrocnemius muscle were similar to heart muscle but those of phospholipids were lower (64mug.atoms of phospholipid phosphorus/g. of dry muscle). 3. Alloxan-diabetes increased the concentration of triglyceride in the muscles twofold. This increase was shown to be dependent in the heart on the availability of growth hormone and cortisol but not on the availability of dietary lipid. Total glyceride in the heart was increased after 48 and 72hr. starvation but not after 96hr. Changes in glyceride concentration seen in starvation and diabetes were not associated with significant changes in phospholipid concentration. It is suggested that mobilization of free fatty acids in diabetes leads to the synthesis of additional glyceride in muscle. 4. The possible contribution of glyceride fatty acid in the heart to respiration during perfusion has been calculated from the net loss of glyceride during perfusion, and also from the relative rates of lipolysis and esterification and compared with oxidation of fatty acid required for the balance of oxygen consumption (oxygen not utilized in the oxidation of glucose or glycogen glucose). In the normal or diabetic heart perfused with glucose and insulin the breakdown of glyceride can account for the balance of oxygen consumption. In the normal heart perfused without substrate the balance of oxygen consumption is not entirely accounted for by the breakdown of glyceride.

Hyperlipemia in acute pancreatitis: Metabolic studies in a patient and demonstration of abnormal lipoprotein-triglyceride complexes resistant to the action of lipoprotein lipase

A patient with acute pancreatitis and transient hyperlipemia is described. During the episode of pancreatitis the presence of plasma lipoprotein-triglyceride complexes with abnormal physical properties and chemical composition was demonstrated. In a polyvinylpyrrolidone (PVP) gradient column the behavior of these complexes was different from the behavior of fat particles of normal serums. In addition, they were characterized by a higher proportion of all lipoprotein constituents, with the exception of triglyceride; by a fatty acid composition similar to that of adipose tissue; and by unusual resistance to the action of postheparin lipoprotein lipase. The possibility that acute pancreatitis could produce augmented mobilization of free fatty acids or of triglyceride-lipoprotein complexes from adipose tissue is considered.

Effect of glucocorticoid hormones on fatty acid mobilization and re-esterification in rat adipose tissue.

1. The effect of dexamethasone and cortisol on fatty acid mobilization and re-esterification has been studied in intact adipose tissue and isolated fat cells of the rat. 2. Dexamethasone added in vitro inhibited both the re-esterification of mobilized free fatty acids and the esterification of palmitate in the medium. 3. Under several conditions (low concentrations of dexamethasone, cortisol at a high concentration, with tissue from starved animals), steroid-induced release of free fatty acids could be accounted for by decreased re-esterification only, overall lipolytic activity remaining unmodified. At higher concentrations of dexamethasone, however, stimulation of lipolytic activity also occurred. 4. Decreased re-esterification produced by dexamethasone was observed in the total absence of glucose from the incubation medium. Further, dexamethasone stimulated the disappearance of prelabelled [(14)C]glycogen from the tissue. 5. The evidence presented suggests that mobilization of free fatty acids induced by glucocorticoid hormones under physiological conditions is primarily due to a decrease of the re-esterification rate rather than to lipase activation.

Incorporation of [ 14C 6]glucose and [9,10- 3H]palmitic acid in vitro into lipids of adipose tissue from essential fatty acid-deficient rats

The simultaneous incorporation of labelled glucose and palmitic acid into lipids has been investigated in vitro in epididymal fat pads of rats fed essential fatty acid-deficient diet, in order to obtain information on possible metabolic differences brought about by essential fatty acid-deficiency in adipose tissue. It has been found that the incorporation of both precursors, but especially of glucose, is greater into adipose tissue lipids (mostly triglycerides) in rats fed essential fatty acid-deficient diet than in controls, indicating a greater triglyceride synthesis in these animals. Lipid synthesis in the adipose tissue of essential fatty acid-deficient animals, however, does not seem to differ qualitatively from that of controls. The distribution of radioactivity among the lipid components suggests that no change in the metabolic utilization of essential fatty acids for the synthesis of neutral lipids occurs. Also the incorporation of palmitic acid and glucose into glycerides is similarly affected in control and essential fatty acid-deficient animals during fasting or nicotinic acid or theophylline treatment. It may be concluded that the increased free fatty acid mobilization in essential fatty acid-deficient rats is not a consequence of decreased triglyceride synthesis. On the other hand, the enhanced lipolysis observed is related to the increased synthesis of triglycerides in adipose tissue. The relationship between these observations and the role of prostaglandins, which are synthesized from essential fatty acids in adipose tissue, is discussed.

Free Fatty Acid Mobilization

Free Fatty Acid Mobilization

The effect of prostaglandin E1 on free fatty acid mobilization and transport

The effect of prostaglandin E1 on free fatty acid mobilization and transport

Beta adrenergic stimulation of insulin release in man.

Normal men and women were infused with the π-adrenergic receptor stimulator, isoproterenol (isopropylnorepinephrine, Isuprel). At a low dose (2 μg./min.), immunoreactive insulin (IRI) and free fatty acid (FFA) concentrations rose without a measurable change in plasma glucose. The rise in IRI was not blocked by pretreatment with nicotinic acid to prevent FFA mobilization by isoproterenol. Higher doses of isoproterenol (6 μg./min.) caused larger increments of IRI and FFA concentrations but also elevated plasma glucose. All effects of isoproterenol were the β-adrenergic receptor DlocKing agent y propranolol. Propranolol had no effect on glycogenolysis or IRI stimulation by glucagon. It is concluded that isoprotenol inereases IRI levll by direet seimnlation of β-adrenergic receptors. The ability of glucagon to stimulate the pancreatic islet and to elevate IRI appears to be mediated by a different mechanism.

Comparison of heparin-released and epinephrine-sensitive lipases in rat adipose tissue.

ARTICLESComparison of heparin-released and epinephrine-sensitive lipases in rat adipose tissueSJ Ho, RJ Ho, and HC MengSJ Ho, RJ Ho, and HC MengPublished Online:01 Feb 1967https://doi.org/10.1152/ajplegacy.1967.212.2.284MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAn in situ perfusion protocol of rat epididymal adipose tissue useful in metabolic studiesJournal of Lipid Research, Vol. 46, No. 8Regulation of lipoprotein lipase in different rat tissuesMetabolism, Vol. 37, No. 6Blood Vessel ProteoglycansEstablished cell lines from rat adipose tissue that secrete lipoprotein lipaseIn Vitro, Vol. 19, No. 5Tissue lipoprotein lipase activity and its action in lipoprotein metabolismInternational Journal of Biochemistry, Vol. 13, No. 5Effects of metabolic inhibitors on the synthesis and release of lipoprotein lipase in cultured cells derived from the stromal-vascular fraction of rat adipose tissueBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 618, No. 1A comparison of molecular properties of hepatic triglyceride lipase and lipoprotein lipase from human post-heparin plasma.Journal of Biological Chemistry, Vol. 253, No. 9Glyceride metabolism in the myopathic hamsterLipids, Vol. 12, No. 7Lipoprotein Lipase and Lipid Metabolism in Mammary GlandJournal of Dairy Science, Vol. 60, No. 4Effect of reflex stimuli on vascular resistance and glycerol release in in vivo dog subcutaneous adipose tissuePflügers Archiv, Vol. 369, No. 1Role of capillary endothelium in the clearance of chylomicrons. A model for lipid transport from blood by lateral diffusion in cell membranes.Circulation Research, Vol. 39, No. 2Hydrolysis of chylomicron phosphatidylcholine in vitro by lipoprotein lipase, phospholipase a2 and phospholipase CBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 431, No. 3Metabolismus der LipoproteinePhysiologic Implications of the Interaction between Lipoprotein Lipase and Some Sulfated GlycosaminoglycansCholesterol esterase in rat adipose tissue and its activation by cyclic adenosine 3':5'-monophosphate-dependent protein kinase.Journal of Biological Chemistry, Vol. 250, No. 12Chemistry and Pharmacology of HeparinJournal of Pharmaceutical Sciences, Vol. 62, No. 4Uptake of blood triglyceride by various tissuesLipids, Vol. 7, No. 8Biochemische Grundlagen der gest�rten Wechselbeziehungen zwischen Kohlenhydrat- und Fettstoffwechsel bei Diabetes mellitusKlinische Wochenschrift, Vol. 48, No. 19Lipoprotein Lipase of the Bovine Mammary GlandJournal of Dairy Science, Vol. 53, No. 10Adipose tissue dynamics and regulation, revisitedThe mechanism of heparin stimulation of rat adipocyte lipoprotein lipaseJournal of Lipid Research, Vol. 10, No. 4Degradation of (131I) insulin and inhibition of post-heparin lipolytic activity by collagenaseLife Sciences, Vol. 7, No. 24The mobilization of free fatty acids from rabbit adipose tissue in situ19 July 2012 | British Journal of Pharmacology, Vol. 34, No. 3Die physiologische Rolle des FettgewebesKlinische Wochenschrift, Vol. 45, No. 18 More from this issue > Volume 212Issue 2February 1967Pages 284-290 Copyright & PermissionsCopyright © 1967 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1967.212.2.284PubMed6018008History Published online 1 February 1967 Published in print 1 February 1967 Metrics

Tissue lipoprotein lipase in normal individuals and in individuals with exogenous hypertriglyceridemia and the relationship of this enzyme to assimilation of fat.

Lipoprotein lipase activity (LLA) was measured in the adipose tissue of six healthy subjects and five members of a family in whom the trait for familial exogenous hypertriglyceridemia was segregating. The lipase activity measured was characteristic of lipoprotein lipase: increased by feeding, dependent on the presence of serum, and inhibited by sodium chloride and protamine sulfate. When compared with lipase activity in healthy individuals, LLA was grossly deficient in two siblings with postabsorptive chylomicronemia and was intermediate in both parents and one sibling, who had normal postabsorptive triglycerides. These findings are compatible with autosomal recessive inheritance. The hormone-sensitive lipolytic enzyme responsible for mobilization of free fatty acids from adipose storage was normal in the hyperlipemic subjects. After a 104-g fat meal, the serum triglyceride increased more in subjects heterozygotic for LLA deficiency than in the healthy subjects, and there was a relatively greater increase in chylomicrons and very low density lipoproteins in the affected individuals. These observations demonstrate the physiologic importance of lipoprotein lipase in removal of these lipoprotein groups and further clarify the differences between endogenous and exogenous hypertriglyceridemia.

Metabolic effects of isoproterenol and propranolol in normal subjects before, during and after triiodothyronine-induced hypermetabolism.

SummaryEffective beta adrenergic receptor blockade was produced in 8 normal men before, during and after a 14-day period of triiodothyronine-induced hypermetabolism. Triiodothyronine did not augment the increases in plasma levels of free fatty acids during infusions of graded doses of isopro-terenol. The increments in plasma FFA during isoproterenol administration were significantly attenuated by propranolol in the hy-permetabolic period as well as during the initial and final control periods. Neither isoproterenol nor propranolol produced any appreciable changes in blood glucose in any period. The results also suggest that beta adrenergic receptors may mediate the effects of isoproterenol upon free fatty acid mobilization but do not suggest a similar receptor role for regulation of blood sugar levels.

Plasma Free Fatty Acids in Mental Patients before and after Intravenous Administration of Insulin

Farstad, M. Plasma Free Fatty Acids in Mental Patients before and after Intravenous Administration of Insulin. Scand. J. din. Lab. Invest. 19, 101–105, 1967. Prolonged insulin-induced hypoglycemia in mental patients was accompanied by increased levels of blood glucose and plasma free fatty acids in the fasting state, and by a reduced ability to increase the plasma free fatty acids during the posthypoglycemic phase.Myristic and oleic acids disappeared to a greater extent than the total fraction of free fatty acids during the initial hypoglycemia, whereas the disappearance of linoleic and arachidonic acids was less than the disappearance of the total fraction. The two latter acids were mobilized only to a slight degree during the post-hypoglycemic phase while myristic and oleic acids were mobilized at a higher degree than the total free fatty acid fraction.Differences in the post-hypoglycemic mobilization of the individual free fatty acids in patients with a prolonged hypoglycemia were probably due to a reduced release of fatty acids from the fat depots in these patients.