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Results for “Lipid Mobilization”

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PubMed2002

Human alpha 2A-adrenergic receptor gene expressed in transgenic mouse adipose tissue under the control of its regulatory elements.

Catecholamines regulate white adipose tissue function and development by acting through beta- and alpha2-adrenergic receptors (ARs). Human adipocytes express mainly alpha 2A- but few or no beta 3-ARs while the reverse is true for rodent adipocytes. Our aim was to generate a mouse model with a human-like alpha2/beta-adrenergic balance in adipose tissue by creating transgenic mice harbouring the human alpha 2A-AR gene under the control of its own regulatory elements in a combined mouse beta 3-AR-/- and human beta 3-AR+/+ background. Transgenic mice exhibit functional human alpha 2A-ARs only in white fat cells. Interestingly, as in humans, subcutaneous adipocytes expressed higher levels of alpha2-AR than perigonadal fat cells, which are associated with a better antilipolytic response to epinephrine. High-fat-diet-induced obesity was observed in transgenic mice in the absence of fat cell size modifications. In addition, analysis of gene expression related to lipid metabolism in isolated adipocytes suggested reduced lipid mobilization and no changes in lipid storage capacity of transgenic mice fed a high-fat diet. Finally, the development of adipose tissue in these mice was not associated with significant modifications of glucose and insulin blood levels. Thus, these transgenic mice constitute an original model of diet-induced obesity for in vivo physiological and pharmacological studies with respect to the alpha2/beta-AR balance in adipose tissue.

Adipocytes↗
PubMed1998

Effect of intracerebroventricular injection of atropine on metabolic responses during exercise in untrained rats.

To investigate the role of the central cholinergic system in the regulation of metabolism during exercise, we injected atropine (5 x 10(-7) mol) into the lateral cerebral ventricle of normal and adrenodemedullated (ADM) untrained rats submitted to exercise on a treadmill (15 m min(-1), 5% grade) until exhaustion. Concentrations of blood glucose, plasma free fatty acids (FFA), and lactate were measured before and every 10 min after the start of exercise for a period of 60 min. Adrenomedullectomy had no effect on the maximal capacity of exercise (MCE), but atropine administered intracerebroventricularly (i.c.v.) reduced the maximal capacity of exercise of both normal and ADM rats. In normal rats, blood concentrations of glucose and plasma free fatty acids remained essentially unchanged compared to the levels at rest, whereas in ADM rats a rapid increase in plasma glucose and plasma free fatty acids levels occurred during exercise. These data indicate that adrenomedullectomy disrupted the accuracy of the feedback mechanism that regulates the mobilization of extramuscular fuels during exercise in normal rats. In addition, ADM rats showed an increased lipid mobilization as a source of energy during exercise, which might explain the increased plasma glucose by an inhibition of muscle glucose uptake. These results suggest that central cholinergic neurons might be involved in the control of energy substrate adjustment during exercise, thereby reducing the maximal capacity of exercise. In addition, the results of this study suggest that the adrenal glands are important for an accurate feedback mechanism during exercise.

Adrenal Medulla↗
PubMed2003

Fatty acid mobilization from adipose tissue during exercise.

By far the largest energy reserve in the human body is adipose tissue triglycerides, and these reserves are an important source of fuel during prolonged endurance exercise. To use this rich source of potential energy during exercise, adipose tissue triglycerides must first be hydrolyzed and the resultant fatty acids delivered to the working muscles. The aims of this review are to describe how exercise alters lipid mobilization from adipose tissue, to identify alternative sources of lipids and to discuss some of the key factors regulating fatty acid mobilization, uptake and oxidation during exercise. The impact of understanding factors involved in the coordinated regulation of lipid mobilization and oxidation during exercise goes far beyond its relevance for endurance exercise performance. A better understanding of the regulation of these processes will facilitate the development of more effective treatment modalities for obesity-related metabolic disorders.

Adipose Tissue↗
PubMed2006

[Fatty acid mobilization and their use in adipose tissue].

An excess of fat mass excess predisposes to multiple complications such as type 2 diabetes, cardiovascular diseases or cancer. A dysregulation of lipid metabolism contributes to the development of obesity and the metabolic syndrome. Recent data on lipid mobilization in adipose tissue have revealed a complex pathway involving a human specific hormonal control of lipolysis via the natriuretic peptides and a new triglyceride lipase, ATGL. Activation of fatty acid reesterification and oxidation can lead to an increase in fatty acid utilization. Targeting these key steps of lipid metabolism (adipose tissue lipolysis and fatty acid oxidation) constitutes a potential strategy for the treatment of obesity and associated metabolic disorders.

Adipose Tissue↗
PubMedDate not supplied

Hyperthermia effect on lipolytic processes in rat blood and adipose tissue.

Rats anaesthetized with Brevinarcon were placed in a high-temperature chamber (air temperature 50 degrees C, relative humidity 50%) for induction of hyperthermia (rectal temperature 41.0 +/- +/- 0.5 degrees C). The control group comprised rats anaesthetized in the same way but kept at room temperature. In the serum in both groups glucose, free fatty acids, immunoreactive insulin, lipolytic activity and ability to mobilize lipids in vitro were determined. It was shown that the glucose and free fatty acid levels and the activity mobilizing serum lipids in vitro in the rats subjected to hyperthermia were lower than in the control group by 12%, 23% and 150% respectively. The lipolytic activity of the serum of rats subjected to hyperthermia was 42% higher, and the level of immunoreactive insulin rose by about 224% in relation to the control group. These results point to inhibition of lipolysis in the adipose tissue with simultaneous activation of intravascular lipolysis during hyperthermia in rats.

Adipose Tissue↗
PubMed1981

The mobilization of plasma lipids by histamine in dogs.

The aim of the present work was to study the mechanism of the mobilization of plasma lipids produced by histamine in the dog, in vivo. The increase of plasma lipids by histamine in vivo was suppressed by cimetidine, but not by diphenhydramine. Although, histamine increased the level of plasma adrenaline, adrenaline does not appear to contribute to the lipolysis stimulated by histamine, because propranolol and alprenolol, beta-adrenergic blocking agents, did not affect the lipolysis stimulated by histamine. From these data it is concluded that the increase of plasma lipids in vivo is not attributable to the release of adrenaline from adrenal glands by histamine, but is produced by the stimulation through H2-receptors in fat cells.

Adrenergic beta-Antagonists↗
PubMed1976

Metabolic and hormonal effects of exercise in mild streptozotocin diabetes.

Metabolic and hormonal changes produced by muscular exercise were studied in rats with mild streptozotocin diabetes. In both diabetic and control animals the mean blood glucose increased and liver glycogen decreased during exercise. The postexercise blood glucose level correlated with the liver glycogen content in diabetic rats. A decrease of blood glucose occurred in some diabetic animals, and these also showed a decrease of liver glycogen to very low levels during exercise. During exercise the rise of plasma glycerol was higher in diabetic than in control animals, but changes in circulating free fatty acids, acetone bodies, insulin, corticosterone, lactate, and acid-base equilibrium were similar in the two groups. The results indicate that the only abnormal metabolic response to exercise in rats with mild diabetes is a slight increase of lipid mobilization.

Animals↗
PubMed2004

Triacylglycerol hydrolase is localized to the endoplasmic reticulum by an unusual retrieval sequence where it participates in VLDL assembly without utilizing VLDL lipids as substrates.

The majority of hepatic intracellular triacylglycerol (TG) is mobilized by lipolysis followed by reesterification to reassemble TG before incorporation into a very-low-density lipoprotein (VLDL) particle. Triacylglycerol hydrolase (TGH) is a lipase that hydrolyzes TG within hepatocytes. Immunogold electron microscopy in transfected cells revealed a disparate distribution of this enzyme within the endoplasmic reticulum (ER), with particularly intense localization in regions surrounding mitochondria. TGH is localized to the lumen of the ER by the C-terminal tetrapeptide sequence HIEL functioning as an ER retention signal. Deletion of HIEL resulted in secretion of catalytically active TGH. Mutation of HIEL to KDEL, which is the consensus ER retrieval sequence in animal cells, also resulted in ER retention and conservation of lipolytic activity. However, KDEL-TGH was not as efficient at mobilizing lipids for VLDL secretion and exhibited an altered distribution within the ER. TGH is a glycoprotein, but glycosylation is not required for catalytic activity. TGH does not hydrolyze apolipoprotein B-associated lipids. This suggests a mechanism for vectored movement of TGs onto developing VLDL in the ER as TGH may mobilize TG for VLDL assembly, but will not access this lipid once it is associated with VLDL.

Animals↗
PubMed1996

Proton detection of choline and lactate in EMT6 tumors by spin-echo-enhanced selective multiple-quantum-coherence transfer.

An extension of the Sel-MQC pulse sequence--SEE-SelMQC (spin-echo-enhanced selective multiple-quantum coherence transfer)--that completely suppresses lipid and water in tissues containing mobile lipid in a single scan and detects 1H resonances of multiple metabolites is described. As in the Sel-MQC lactate-editing experiments [Q. He et al., J Magn. Reson. B 106,203 (1995)], SEE-SelMQC acquires lactate from its ZQ --> DQ coherence-transfer pathway; in addition, the method recovers signal from other metabolites by selective generation of additional spin echoes using extra frequency-selective pulses and gradients. This method introduces no loss of lactate signal intensity beyond the 50% that is lost through the multiple-quantum coherence-transfer process. The spatial distributions of choline and lactate with a phantom and in vivo, in subcutaneously implanted murine EMT6 tumors, have been simultaneously mapped.

Animals↗
PubMed1997

Mechanisms of formation and function of eosinophil lipid bodies: inducible intracellular sites involved in arachidonic acid metabolism.

Lipid bodies, inducible lipid-rich cytoplasmic inclusions, are characteristically abundant in cells associated with inflammation, including eosinophils. Here we reviewed the formation and function of lipid bodies in human eosinophils. We now have evidence that the formation of lipid bodies is not attributable to adverse mechanisms, but is centrally mediated by specific signal transduction pathways. Arachidonic acid and other cis fatty acids by an NSAID-inhibitable process, diglycerides, and PAF by a 5-lipoxygenase dependent pathway are potent stimulators of lipid body induction. Lipid body formation develops rapidly by processes that involve PKC, PLC, and de novo mRNA and protein synthesis. These structures clearly serve as repositories of arachidonyl-phospholipids and are more than inert depots. Specific enzymes, including cytosolic phospholipase A2, MAP kinases, lipoxygenases and cyclooxygenases, associate with lipid bodies. Lipid bodies appear to be dynamic, organelle-like structures involved in intracellular pathways of lipid mobilization and metabolism. Indeed, increases in lipid body numbers correlated with enhanced production of both lipoxygenase- and cyclooxygenase-derived eicosanoids. We hypothesize that lipid bodies are distinct inducible sites for generating eicosanoids as paracrine mediators with varied activities in inflammation. The capacity of lipid body formation to be specifically and rapidly induced in leukocytes enhances eicosanoid mediator formation, and conversely pharmacologic inhibition of lipid body induction represents a potential novel and specific target for anti-inflammatory therapy.

Arachidonic Acid↗
PubMed2002

Nuclear magnetic resonance-visible lipids induced by cationic lipophilic chemotherapeutic agents are accompanied by increased lipid droplet formation and damaged mitochondria.

Proton nuclear magnetic resonance (NMR) spectroscopy, histological lipid staining, and electron microscopy were used to assess the biochemical and structural changes induced by treating the cultured human breast cell line HBL-100 with the cationic lipophilic phosphonium salts p-(triphenylphosphoniummethyl) benzaldehyde chloride (drug A) and [4-(hydrazinocarboxy)-1-butyl] tris-(4-dimethylaminophenyl) phosphonium chloride (drug B). The major biochemical change detected by (1)H NMR in drug-treated cells was a significant time- and concentration-dependent increase in lipid acyl chain resonances arising from mobile lipids. The amount of NMR-visible lipid strongly correlated with morphometric measurements of oil red O-staining lipid detected in the cytoplasm by light microscopy. Ultrastructural investigations revealed substantial damage to mitochondria and the progressive development of lipid droplets accompanied by end-stage autophagic vacuoles, in the form of densely staining myelinoid bodies, after treatment of HBL-100 cells with drug B at the IC(50). No apparent increase in acid phosphatase activity was observed using electron microscopy, indicating that the accumulation of phospholipids in myelinoid bodies may result from substrate inundation of the lysosome, rather than increased lysosomal activity. These results indicate a potential role for lysosomal lipid catabolism in the formation of NMR-visible lipids in models of cytotoxic insult.

Antineoplastic Agents↗
PubMed2000

Post-exercise adipose tissue and skeletal muscle lipid metabolism in humans: the effects of exercise intensity.

One purpose of the present experiments was to examine whether the relative workload or the absolute work performed is the major determinant of the lipid mobilization from adipose tissue during exercise. A second purpose was to determine the co-ordination of skeletal muscle and adipose tissue lipid metabolism during a 3 h post-exercise period. Six subjects were studied twice. In one experiment, they exercised for 90 min at 40% of maximal O2 consumption (VO2,max) and in the other experiment they exercised at 60% VO2,max for 60 min. For both experiments, catheters were inserted in an artery, a subcutaneous abdominal vein and a femoral vein. Adipose tissue metabolism and skeletal muscle (leg) metabolism were measured using Fick's principle. The results show that the lipolytic rate in adipose tissue during exercise was the same in each experiment. Post-exercise, there was a very fast decrease in lipolysis, but it began to increase about 1 h post-exercise and remained elevated for the following 2 h. The increase in post-exercise non-esterified fatty acid (NEFA) mobilization was greater after 60% exercise than after 40 % exercise. It is concluded that the lipolytic rate in abdominal subcutaneous adipose tissue during exercise is the same whether the relative workload is 40% or 60% of maximum. Post-exercise, there is a substantial lipid mobilization from adipose tissue and only a small fraction of this is taken up in the lower extremities. This leaves a substantial amount of NEFAs for either NEFA/TAG (triacylglycerol) recirculation post-exercise or immediate oxidation.

Adipose Tissue↗
PubMed1997

In vivo resistance of lipolysis to epinephrine. A new feature of childhood onset obesity.

A decreased mobilization of triglycerides may contribute to fat accumulation in adipocytes, leading to obesity. However, this hypothesis remains to be proven. In this study, epinephrine-induced lipid mobilization was investigated in vivo in nine markedly obese children (160+/-5% ideal body weight) aged 12.1+/-0.1 yr during the dynamic phase of fat deposition, compared with six age-matched nonobese children. As an in vivo index of lipolysis, we measured glycerol flux using a nonradioactive tracer dilution approach, and plasma free fatty acid concentrations. In the basal state, the obese children had a 30% lower rate of glycerol release per unit fat mass than the lean children. To study the regulation of lipolysis, epinephrine was infused stepwise at fixed doses of 0.75 and then 1. 50 microg/min in both groups. In lean children, glycerol flux and plasma free fatty acid increased to an average of 249-246% of basal values, respectively, in response to a mean plasma epinephrine of 396+/-41 pg/ml. The corresponding increase was only 55-72% in the obese children, although their mean plasma epinephrine reached 606+/-68 pg/ml. All obese and nonobese children, except an Arg64Trp heterozygote, were homozygotes for Trp at position 64 of their beta3-adrenoreceptor. The resistance of lipolysis to epinephrine showed no relationship with the Arg64 polymorphism of the beta3-adrenoreceptor gene. In summary, in vivo lipolysis, which mostly reflects the mobilization of lipid stores from subcutaneous adipose tissue, shows a decreased sensitivity to epinephrine in childhood onset obesity. Since our study was carried out in obese children during the dynamic phase of fat accumulation, the observed resistance to catecholamines might possibly be causative rather than the result of obesity.

Adolescent↗
PubMed1977

[Change in the concentration of total lipids, phospholipids and neutral lipids in rat liver mitochondria and microsomes during chemical carcinogenesis].

Sharp increase in the content of total lipids and, especially, neutral lipids, and considerable decrease in the content of phospholipids were observed in liver microsomes and mitochondrias from liver of tumour-bearing rats in the process of the growth of sarcoma, induced by a single injection of 3,4-benzpyrene. The injection of anthracene, a non-cancerogenous hydrocarbon, practically did not affect the lipid composition of rat liver subcellular particles. Thus, the disturbances in normal functioning of subcellular particles under cancerogenesis are due to considerable change in the chemical composition of biomembranes. The data obtained confirm our hypothesis on lipid mobilization under tumour growth.

Animals↗
PubMedDate not supplied

Effect of ethanol administration on plasma glycerol levels in the rat.

Many mechanisms have been postulated as being responsible for the fatty liver resulting from ethanol ingestion. Lipid mobilization has been strongly implicated in both acute and chronic ethanol administration--the difference between the two lying in the source of the fat. In the acute situation, the lipid is mobilized from depot fat, whereas in the chronic situation, it apparently comes from the diet. One possibility not explored is the mobilization of glycerol. This substance is the backbone of triglyceride. Hence, an influx of glycerol to the liver coupled with increased amounts of fatty acids could help explain, in part, the fatty liver resulting from alcohol administration. The purpose of the following study was to determine if such an effect does occur.

Animals↗
PubMed2002

Mobilization of seed storage lipid by Arabidopsis seedlings is retarded in the presence of exogenous sugars.

BACKGROUND: Soluble sugar levels must be closely regulated in germinating seeds to ensure an adequate supply of energy and building materials for the developing seedling. Studies on germinating cereal seeds indicate that production of sugars from starch is inhibited by increasing sugar levels. Although numerous studies have focused on the regulation of starch metabolism, very few studies have addressed the control of storage lipid metabolism by germinating oilseeds. RESULTS: Mobilization of storage lipid by germinating seeds of the model oilseed plant Arabidopsis thaliana (L.) Heynh. occurs at a greatly reduced rate in the presence of exogenous glucose or mannose, but not in the presence of equi-molar 3-O-methylglucose or sorbitol. The sugar-insensitive5-1/abscisic acid-insensitive4-101 (sis5-1/abi4-101) mutant is resistant to glucose inhibition of seed storage lipid mobilization. Wild-type seedlings become insensitive to glucose inhibition of storage lipid breakdown within 3 days of the start of imbibition. CONCLUSIONS: Growth in the presence of exogenous glucose significantly retards mobilization of seed storage lipid in germinating seeds from wild-type Arabidopsis. This effect is not solely due to the osmotic potential of the media, as substantially higher concentrations of sorbitol than of glucose are required to exert significant effects on lipid breakdown. The inhibitory effect of glucose on lipid breakdown is limited to a narrow developmental window, suggesting that completion of some critical metabolic transition results in loss of sensitivity to the inhibitory effect of glucose on lipid breakdown.

3-O-Methylglucose↗