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PubMed1984

In vivo evidence for alpha 2-adrenergic-dependent inhibition of lipid mobilization in the rabbit.

Both alpha- and beta-agonists were infused i.v. in unanesthetized rabbits. The alpha-adrenergic effect on lipid mobilization was investigated by comparing the modifications of blood glycerol levels induced by clonidine (alpha 2-agonist) and amidephrine (alpha 1-agonist) alone or in combination with isoprenaline (beta-agonist). Clonidine (2 micrograms X kg-1 X min-1) was found to significantly reduce the basal or isoprenaline-stimulated glycerol levels whereas amidephrine (10 micrograms X kg-1 X min-1) was without any effect. Plasma IRI levels were also reduced by clonidine. The results suggest that the reduction of lipid mobilization produced by clonidine could have been the consequence of the stimulation of the alpha 2-adrenergic antilipolytic receptors previously shown to be present in isolated fat cell membranes.

Adrenergic alpha-Agonists↗
PubMed2001

Improved analysis of 1H-MR spectra in the presence of mobile lipids.

Focal brain lesions can be associated with proton magnetic resonance spectra (1H-MRS)-detectable mobile lipids, reflecting severe tissue degradation and necrosis. However, advanced fitting procedures, such as the LCModel, fail to adequately fit spectra in the presence of lipid resonances. To overcome this, different approaches to generate lipid model spectra were compared using a phantom, real in vivo data, and simulated data. Twenty-six in vivo short-echo time (TE) 1H-MRS from 21 malignant gliomas, four infections, and one ischemia were analyzed to evaluate the performance of the modified LCModel fit. Adding simulated aliphatic resonances at 1.3 and 0.9 ppm improved the overall fitting quality remarkably and allowed good separation of lactate and alanine. Also, a better differentiation of glioblastomas and anaplastic gliomas was achieved. In conclusion, we propose a simple way to efficiently include lipid resonances in the LCModel, allowing a better fit of in vivo short-TE 1H-MRS, and demonstrate the diagnostic potential of quantitative assessment of mobile lipids in brain tumors.

Alanine↗
PubMed2005

Atrial natriuretic peptide stimulates lipid mobilization during repeated bouts of endurance exercise.

Atrial natriuretic peptide (ANP) controls lipolysis in human adipocytes. Lipid mobilization is increased during repeated bouts of exercise, but the underlying mechanisms involved in this process have not yet been delineated. The relative involvement of catecholamine- and ANP-dependent pathways in the control of lipid mobilization during repeated bouts of exercise was thus investigated in subcutaneous adipose tissue (SCAT) by microdialysis. The study was performed in healthy males. Subjects performed two 45-min exercise bouts (E1 and E2) at 50% of their maximal oxygen uptake separated by a 60-min rest period. Extracellular glycerol concentration (EGC), reflecting SCAT lipolysis, was measured in a control probe perfused with Ringer solution and in two other probes perfused with either Ringer plus phentolamine (alpha(1/2)-AR antagonist) or Ringer plus both phentolamine and propranolol (beta-AR antagonist). Plasma epinephrine, plasma glycerol, and EGC were 1.7-, 1.6-, and 1.2-fold higher in E2 than in E1, respectively. Phentolamine potentiated exercise-induced EGC increase during E2 only. Propranolol reduced the lipolytic rate during both E1 and E2 compared with the probe with phentolamine. Plasma ANP concentration increased more during E2 than during E1 and was correlated with the increase in EGC in the probe containing phentolamine plus propranolol. The results suggest that ANP is involved in the control of lipolysis during exercise and that it contributes to stimulation of lipolysis during repeated bouts of exercise.

Adipose Tissue↗
PubMed1994

Mobile lipids and metabolic heterogeneity of brain tumours as detectable by ex vivo 1H MR spectroscopy.

To examine metabolic heterogeneity in primary brain tumour, multiple biopsies (one to five per tumour) from four benign meningiomas, five acoustic schwannomas, eleven glial tumours and five medulloblastomas were each subdivided into one to five samples (total = 194) and investigated using ex vivo 360 MHz 1H MR spectroscopy with histopathological correlation. Low amounts of mobile lipids were detected in meningothelial meningiomas and medulloblastomas, high amounts in some or all samples of all other tumours. The differences in non-lipid metabolites between different tumour types were less marked, with the exception of the medulloblastomas, which had high amounts of N-acetyl aspartate and cholines. The amount of mobile lipid correlated with Antoni type B areas in schwannomas and necrosis in a high grade giant cell tumour. The amount of lipid varied significantly from sample to sample in a grade 2 astrocytoma and grade 4 astrocytoma samples with 0-5% necrosis but did not correlate with the site in the tumour or histopathological characteristics. The metabolic heterogeneity occurred on a spatial scale at least as small as the size of the MR samples, i.e., < or = 60 mg. These results suggest that the detection of metabolic heterogeneity and mobile lipids may have importance for the design of clinical studies.

Astrocytoma↗
PubMed1999

Subcellular localization studies indicate that lipoxygenases 1 to 6 are not involved in lipid mobilization during soybean germination

Soybean (Glycine max) lipoxygenase (LOX) has been proposed to be involved in reserve lipid mobilization during germination. Here, subcellular fractionation studies show that LOX1, -2, -3, -4, -5, and -6 isozymes were associated with the soluble fraction but not with purified oil bodies. The purified oil bodies contained small amounts of LOX1 (<0.01% total activity), which apparently is an artifact of the purification process. Immunogold labeling indicated that, in cotyledon parenchyma cells of LOX wild-type seeds that had soaked and germinated for 4 d, the majority of LOX protein was present in the cytoplasm. In 4-d-germinated cotyledons of a LOX1/2/3 triple null mutant (L0), a small amount of label was found in the cytoplasm. In epidermal cells, LOX appeared in vacuoles of both wild-type and L0 germinated seeds. No LOXs cross-reacting with seed LOX antibodies were found to be associated with the cell wall, plasma membrane, oil bodies, or mitochondria. Lipid analysis showed that degradation rates of total lipids and triacylglycerols between the wild type and L0 were not significantly different. These results suggest that LOX1, -2, -3, -4, -5, and -6 are not directly involved in reserve lipid mobilization during soybean germination.

Journal Article↗
PubMed1999

Mobile lipids in rat brain slices observed by gradient-enhanced NMR.

Short-echo gradient-enhanced nuclear magnetic resonance (NMR) spectroscopy was utilized to identify mobile lipids in perfused neonate and juvenile rat brain slices. Lipid signals were present at low levels within 1 hr of tissue preparation and increased with time under standard perfusion conditions and in the presence of high phosphocreatine and low lactate levels. Both one- and two-dimensional NMR spectra demonstrate peaks consistent with the generation of free fatty acids or neutral lipids following tissue trauma. The present work demonstrates that injury-induced mobile lipids may make appreciable contributions to regions of brain tissue spectra that have recently been assigned to lactate or polypeptides alone.

Animals↗
PubMed2001

Effect of a tumour-produced lipid-mobilizing factor on protein synthesis and degradation.

Treatment of murine myoblasts, myotubes and tumour cells with a tumour-produced lipid mobilizing factor (LMF), caused a concentration-dependent stimulation of protein synthesis, within a 24 h period. There was no effect on cell number or [(3)H] thymidine incorporation, but a similar concentration-dependent stimulation of 2-deoxyglucose uptake. LMF produced an increase in intracellular cyclic AMP levels, which was linearly (r(2)= 0.973) related to the increase in protein synthesis. The effect of LMF was attenuated by the adenylate cyclase inhibitor MDL(12330A), and was additive with the stimulation produced by forskolin. Both propranolol (10 microM) and the specific beta(3)-adrenergic receptor antagonist SR 59230A (10(-5)M), significantly reduced the stimulation of protein synthesis induced by LMF. Protein synthesis was also increased by 69% (P = 0.006) in soleus muscles of mice administered LMF, while there was a 26% decrease in protein degradation (P = 0.03). While LMF had no effect on the lysosomal enzymes, cathepsins B and L, there was a decrease in proteasome activity, as determined both by the 'chymotrypsin-like' enzyme activity, as well as expression of proteasome alpha-type subunits, determined by Western blotting. These results show that in addition to its lipid-mobilizing activity LMF also increases protein accumulation in skeletal muscle both by an increase in protein synthesis and a decrease in protein catabolism.

Animals↗
PubMed1998

Mechanism of inhibition of a tumor lipid-mobilizing factor by eicosapentaenoic acid.

Stimulation of lipolysis or adenylate cyclase activity by either isoprenaline or a tumor-derived lipid-mobilizing factor was effectively attenuated in isolated white adipocytes or in adipocyte plasma membranes pretreated with eicosapentaenoic acid (EPA) dissolved in ethanol or from mice dosed p.o. with EPA (1.25 g/kg). A similar effect was observed with docosahexanoic acid (DHA) that may be partly due to retroconversion to EPA. Stimulation of adenylate cyclase activity by forskolin, which acts directly on the enzyme without the involvement of a receptor, was also decreased in membranes of mice treated with EPA, suggesting a direct interaction between EPA and adenylate cyclase. Pertussis toxin eliminated the inhibition of lipolysis and the stimulation of adenylate cyclase by isoprenaline and lipid-mobilizing factor in the presence of EPA, but not DHA. This suggests that the attenuation of hormonal stimulation of adenylate cyclase by EPA was due, at least in part, to an inhibitory guanine nucleotide-binding protein-mediated inhibition of adenylate cyclase activity. The effect of DHA may be due to a direct inhibition of the cyclase catalytic component. The ability of EPA to preserve fat stores during the process of cachexia seems to arise from the attenuation of the stimulation of adenylate cyclase.

Adenylyl Cyclase Inhibitors↗
PubMed2006

[Physiological and pathophysiological features of the control of lipolysis and lipid mobilization by natriuretic peptides].

We have demonstrated a potent and specific lipolytic effect of natriuretic peptides (NP) in human and primates' fat cells. The lipolytic effect of NP is mediated through intracellular production of cGMP and activation of the cGMP-dependent kinase 1alpha. Local infusion of atrial-NP (ANP), directly within the subcutaneous adipose tissue through a microdialysis catheter, increases lipolysis and stimulates blood flow through its vasodilating effect in lean healthy men. This effect is blunted in overweight men and can be recovered by endurance training. Intravenous infusion of physiological doses of ANP induces lipid mobilization. Higher concentrations of ANP that are encountered during heart failure also stimulate lipid oxidation. ANP activates lipolysis and free fatty acids release from adipose tissue during endurance exercise. This effect is paradoxically amplified when exercise is performed under beta-blockade treatment, because of an enhanced cardiac release of ANP. No gender differences in ANP-induced lipid mobilization during exercise have been found. Heart failure is associated with high circulating levels of NP that could participate to the progression toward cachexia. On contrary, a negative correlation between NP levels and body mass index is found in obese persons. The molecular basis of this inverse correlation is not yet demonstrated from a functional standpoint. Further studies are needed to clearly define the pathophysiological role of NP in obesity and heart failure.

Adipose Tissue↗
PubMed1995

Lipoxygenase-catalyzed oxygenation of storage lipids is implicated in lipid mobilization during germination.

The etiolated germination process of oilseed plants is characterized by the mobilization of storage lipids, which serve as a major carbon source for the seedling. We found that during early stages of germination in cucumber, a lipoxygenase (linoleate: oxygen oxidoreductase, EC 1.13.11.12) form is induced that is capable of oxygenating the esterified fatty acids located in the lipid-storage organelles, the so-called lipid bodies. Large amounts of esterified (13S)-hydroxy-(9Z,11E)-octadecadienoic acid were detected in the lipid bodies, whereas only traces of other oxygenated fatty acid isomers were found. This specific product pattern confirms the in vivo action of this lipoxygenase form during germination. Lipid fractionation studies of lipid bodies indicated the presence of lipoxygenase products both in the storage triacylglycerols and, to a higher extent, in the phospholipids surrounding the lipid stores as a monolayer. The degree of oxygenation of the storage lipids increased drastically during the time course of germination. We show that oxygenated fatty acids are preferentially cleaved from the lipid bodies and are subsequently released into the cytoplasm. We suggest that they may serve as substrate for beta-oxidation. These data suggest that during the etiolated germination, a lipoxygenase initiates the mobilization of storage lipids. The possible mechanisms of this implication are discussed.

Journal Article↗
PubMed1986

Both somatostatin and the caudal neuropeptide, urotensin II, stimulate lipid mobilization from coho salmon liver incubated in vitro.

The direct effects of somatostatin-14 (SRIF; synthetic ovine) and the fish caudal neuropeptide, urotensin II (UII; synthetic Gillichthys), on fatty acid (FA) release and on lipolytic enzyme (triacylglycerol lipase) activity were determined on coho salmon liver slices incubated in vitro. FA release was continuously measured by pH-stat titration. Additionally, gas chromatographic analysis of the incubation medium was performed to determine the type and relative composition of medium fatty acid constituents. SRIF and UII both stimulated FA release in a dose-dependent manner; the two peptides appeared to stimulate FA release in an equimolar manner. Maximal response was obtained at 1 X 10(-5) M; ED50 was approximately 2 X 10(-7) M. SRIF-stimulated FA release did not result in differential secretion of any particular FA type. Tissue triacylglycerol lipase activity was significantly enhanced by addition of UII or SRIF (2 X 10(-6) M). Dibutyryl cAMP and IBMX both stimulated FA release and lipase activity; dbcAMP stimulated FA release in dose-dependent manner. These results indicate that SRIF and UII directly enhance lipid mobilization from salmon liver slices and suggest that SRIF- and UII-stimulated lipid mobilization from salmon liver slices is mediated through cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Purification and characterization of a tumor lipid-mobilizing factor.

Cancer patients with weight loss showed urinary excretion of a lipid-mobilizing factor (LMF), determined by the ability to stimulate lipolysis in isolated murine epididymal adipocytes. Such bioactivity was not detectable in the urine of cancer patients without weight loss or in normal subjects. The LMF was purified using a combination of ion exchange, exclusion, and hydrophobic interaction chromatographies to give a single component of apparent Mr 43,000, which showed homology in amino acid sequence with human plasma Zn-alpha2-glycoprotein. Both substances showed the same mobility on denaturing and nondenaturing gels and the same chymotrypsin digestion pattern, both stained heavily for carbohydrate, and they showed similar immunoreactivity. Polyclonal antisera to human plasma Zn-alpha2-glycoprotein was also capable of neutralization of the bioactivity of human LMF in vitro. Using competitive PCR to quantify expression of Zn-alpha2-glycoprotein, we found that only those tumors that were capable of producing a decrease in carcass lipid expressed mRNA for Zn-alpha2-glycoprotein. These results provide strong evidence to suggest that tumor production of Zn-alpha2-glycoprotein is responsible for the lipid catabolism seen in cancer patients.

Adipocytes↗
PubMed1984

Acute in vivo stimulatory effects of human pituitary lipid-mobilizing factor on plasma levels of glucagon and insulin in rabbits.

The lipid-mobilizing factor LMF is prepared from deep-frozen human pituitary glands by alkaline extraction, followed by acetone precipitation at pH 4.8, Sephadex gel filtration and DEAE-cellulose chromatography. In addition to its adipokinetic effect in rabbits, LMF also increased the plasma levels of glucagon and insulin in rabbits in doses of 15 to 100 micrograms. The LMF-induced increases in the plasma levels of glucagon were most pronounced in fasted rabbits, whereas the increases in the plasma levels of insulin were most pronounced in fed rabbits. Glucose infusions decreased the LMF-induced hyperglucagonaemia and increased the LMF-induced hyperinsulinaemia. Somatostatin did not inhibit the LMF-induced hyperglucagonaemia with statistical significance, but inhibited the LMF-induced hyperinsulinaemia. The plasma levels of glucose were slightly decreased by 20 and 40 micrograms LMF in fasted rabbits and were unchanged in fed rabbits. In fasted rabbits, LMF had a toxic effect and 100 micrograms LMF killed one rabbits. Human growth hormone (hGH), prepared from the pituitary glands after removal of LMF, also increased the plasma levels of glucagon and insulin in rabbits. It is possible that the observed effects of LMF and hGH were due to the presence of some biologically active substances from the pituitary gland. These postulated substances could be involved in the pituitary control of the endocrine pancreas, and work is in progress to isolate them from the LMF preparation.

Animals↗
PubMed1968

Toxic effects of glucagon-induced acute lipid mobilization in geese.

The toxic effects associated with rapid lipid mobilization and a high plasma free fatty acid (FFA) concentration produced by glucagon were evaluated. Glucagon (0.5 mg/kg of body wt) was injected intravenously into nonfasting geese. The geese developed rapid respirations and high plasma FFA levels within 15 min after the glucagon injection; three of eleven died. Control geese, injected with saline, did not exhibit toxic signs. Peak FFA concentrations developed 15 min after glucagon and high levels persisted for over 90 min. Geese injected with glucagon frequently developed electrocardiographic abnormalities that included supraventricular tachycardia, premature ventricular contractions, and signs of myocardial ischemia. Light and electron microscopy revealed acute myocardial degeneration and fatty infiltration of the liver. The increase in plasma FFA concentrations and toxic effects were not prevented by pretreatment with nicotinic acid or propranolol.

Animals↗
PubMed1999

Modifications induced by dietary lipid source in adipose tissue phospholipid fatty acids and their consequences in lipid mobilization.

The aim of the present work was to assess the influence of dietary lipid source on fatty acid phospholipid profiles and on lipid mobilization. Forty male Wistar rats were divided into four groups and fed on high-fat diets which provided olive oil, sunflower oil, palm oil or beef tallow. All rats received the same amount of energy to avoid hyperphagia and differences in energy intake among groups. Phospholipid fatty acids were determined by GC. Lipolysis was stimulated in subcutaneous and perirenal isolated adipocytes by several lipolytic agents, and assessed by the determination of released glycerol. After 4 weeks of feeding, differences in body and adipose tissue weights were not observed. Dietary regimens caused great changes in adipose tissue phospholipid composition: rats fed on palm oil and beef tallow had higher concentrations of saturated fatty acids and animals fed on olive oil or sunflower oil had greater amounts of oleic and linoleic acids, respectively. These modifications did not lead to important changes in adipocyte lipolysis. Significant differences were only observed between palm-oil- and beef-tallow-fed groups when lipolysis was stimulated by isoproterenol in subcutaneous adipocytes. The fact that our feeding protocol did not induce differences in fat accumulation among groups avoids misinterpretations due to adiposity changes. The differences observed between both saturated-fat-fed groups, therefore, should only be attributable to dietary lipids. Despite this effect, the data from this work indicate that some diet-induced changes in adipose tissue fatty acid composition may have little effect on overall function.

Adipocytes↗
PubMed2004

2D J-resolved spiral spectroscopic imaging at 7 T: application to mobile lipid mapping in a rat glioma.

Lactate (Lac) and mobile lipids (Lip), which are present in rat gliomas, are difficult to map because their 1H resonances overlap in the 1.3 ppm region. 2D J-resolved spectroscopy enables proper separation of the two resonance lines. To obtain high-spatial-resolution mapping of Lac and Lip resonances within a reasonable experiment time, we coupled 2D J-resolved spectroscopy with a fast spectroscopic imaging (SI) method, based on an out-and-in spiral k-space description. The method was applied to a rat glioma at 7 T, and Lac and Lip maps were reconstructed. The duration of SI (2D spatial, 2D spectral) was 64 min for a theoretical in-plane resolution of 1 x 1 mm, and a slice thickness of 2 mm (voxel size 8.2 microl, taking into account the point-spread function (PSF)).

Animals↗
PubMed2005

Training enhances ANP lipid-mobilizing action in adipose tissue of overweight men.

PURPOSE: This study was designed to evaluate whether a 4-month endurance training program could improve ANP- as well as isoproterenol-mediated (beta-adrenergic receptor agonist) in situ lipolysis and adipose tissue blood flow (ATBF) in the subcutaneous adipose tissue (SCAT) of untrained overweight subjects. METHODS: Ten overweight men aged 26.0 +/- 1.4 yr with a mean body mass index of 27.6 +/- 0.2 kg.m(-2), performed aerobic exercise 5 d.wk(-1) for 4 months. Before and after the training period, SCAT responsiveness was investigated in situ during a 60-min infusion of 1 micromol.L(-1) isoproterenol and 10 micromol.L(-1) ANP through microdialysis probes. Plasma metabolic parameters and physical fitness variables were measured as well. RESULTS: Endurance training significantly increased fat-free mass and VO2max, while reducing plasma insulin, glucose, NEFA, low density lipoprotein (LDL)-C and the respiratory exchange ratio at rest. Training significantly lowered resting dialysate glycerol levels in SCAT. The lipid-mobilizing effect of ANP was markedly enhanced (by 191%, P < 0.05) after training as was that of isoproterenol (by 145%, P < 0.05). Resting adipose tissue blood flow as well as ANP- and isoproterenol-mediated rise in ATBF was increased after training. CONCLUSION: The present study shows that endurance training improves ANP- as well as beta-adrenergic-receptor-mediated lipid mobilization and ATBF in the SCAT of overweight subjects. The recovery of a higher lipolytic efficiency in adipose tissue is an important benefit of a training program in overweight subjects.

Adipose Tissue↗