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PubMed1975

Lipid mobilizing hormones of the hypothalamus and pituitary.

Lipid mobilizing substances (LMS) are present in the hypothalamus and pituitary of mammals and probably are involved in the central neural control of obesity. Most of these have direct lipolytic effects, like lipid mobilizing factor (LMF) and LH-RH from the hypothalamus as well as lipotropin (LPH), melanocyte-stimulating hormone (MSH), corticotropin (ACTH), and growth hormone (GH) from the pituitary gland. Some of the substances, like GH-release inhibiting hormone (GH-RIH), affect lipolysis by secondary actions on pancreatic hormones such as insulin and glucagon. Other hypothalamic hormones, like GH-releasing hormone (GH-RH) may influence lipolysis secondarily through the pituitary hormones (e.g. GH) whose release they control. Regardless of how lipid mobilization is affected, investigations into the problem of obesity should take these LMS into consideration.

Adipose Tissue↗
PubMed2005

Lipid mobility and molecular binding in fluid lipid membranes.

The lateral mobility of dilute concentrations of fluorescently labeled lipids doped into supported membranes is found to change upon receptor ligand binding at the membrane surface, even when the lipid is not directly involved in the binding event. Experiments using membrane microarrays are performed that illustrate the use of lipid mobility measurements as an effectively label-free strategy of detecting binding on membrane surfaces.

Animals↗
PubMed2002

Adipokinin, a proopiomelanocortin-derived lipid-mobilizing anterior pituitary hormone.

Hormonal control of lipid metabolism during prolonged fasting is unclear. The involvement of the classical, lipid-mobilizing hormone from the anterior pituitary, i.e., beta-lipotropin (beta-LPH), is suspect. It and adrenocorticotropin (ACTH) are formed concurrently in the pituitary during the processing of the prohormone, proopiomelanocortin (POMC), and are secreted together. During prolonged fasting the control of metabolism requires minimal participation by ACTH and maximal lipid-mobilizing activity which is inconsistent with the present concept of ACTH and beta-LPH secretion. Hypothetically, the needed control can be satisfied by the alteration of the accepted processing of POMC so as to form beta-LPH and a new lipid-mobilizing hormone which also has modest ACTH-like activity. It is proposed that this hormone be named 'adipokinin'. An analog of this proposed hormone appears to have been isolated previously from porcine pituitaries.

Adrenocorticotropic Hormone↗
PubMed2005

Proton NMR visible mobile lipid signals in sensitive and multidrug-resistant K562 cells are modulated by rafts.

BACKGROUND: Most cancer cells are characterized by mobile lipids visible on proton NMR (1H-NMR), these being comprised mainly of methyl and methylene signals from lipid acyl chains. Erythroleukemia K562 cells show narrow signals at 1.3 and 0.9 ppm, corresponding to mobile lipids (methylene and methyl, respectively), which are reduced when K562 cells are multidrug resistant (MDR). While the significance of the mobile lipids is unknown, their subcellular localization is still a matter of debate and may lie in the membrane or the cytoplasm. In this study, we investigate the role of cholesterol in the generation of mobile lipid signals. RESULTS: The proportion of esterified cholesterol was found to be higher in K562-sensitive cells than in resistant cells, while the total cholesterol content was identical in both cell lines. Cholesterol extraction in the K562 wild type (K562wt) cell line and its MDR counterpart (K562adr), using methyl-beta-cyclodextrin, was accompanied by a rise of mobile lipids in K562wt cells only. The absence of caveolae was checked by searching for the caveolin-1 protein in K562wt and K562adr cells. However, cholesterol was enriched in another membrane microdomain designated as "detergent-insoluble glycosphingomyelin complexes" or rafts. These microdomains were studied after extraction with triton X-100, a mild non-ionic detergent, revealing mobile lipid signals preserved only in the K562wt spectra. Moreover, following perturbation/disruption of these microdomains using sphingomyelinase, mobile lipids increased only in K562wt cells. CONCLUSION: These results suggest that cholesterol and sphingomyelin are involved in mobile lipid generation via microdomains of detergent-insoluble glycosphingomyelin complexes such as rafts. Increasing our knowledge of membrane microdomains in sensitive and resistant cell lines may open up new possibilities in resistance reversion.

Journal Article↗
PubMed1987

Morphine and dynorphins in lipid mobilization in rats in vitro.

In vitro lipid-mobilizing activities of morphine (MO) and dynorphin-(1-10) amide (DYA) were compared using adipocytes of young adult rats (body weight 170-200 g, age 50-60 days, diameter of adipocytes 54 +/- 1.12 microns) and of 20-month-old rats (body weight 500-690 g, diameter of adipocytes 99.5 +/- 3.0 microns). The adipokinetic activities of adenosine deaminase (ADA) and dynorphin-(1-13) (DY) were also tested. In the experiments 0.16 units of ADA did not influence basal or stimulated lipolysis, whereas DY exerted a slight but statistically significant adipokinetic effect. In three experimental series the EC50 of MO ranged between 0.89 and 14.60 mumol l-1, the EC50 of DYA in young rats was estimated as 0.8 mumol l-1 and in old animals, 1.3 mumol l-1. Statistically significant differences in the lipid-mobilizing potency between DYA and MO could be observed only in one experimental series in young rats. Expressed in percent of maximum lipolysis induced by isoprenaline, the maximum lipolytic response to DYA in young animals was significantly lower (Emax 26.1 +/- 1.9) when compared to the maximum effect of MO (Emax 76.3 +/- 8.5 and 68.9 +/- 3.5, respectively). Adipocytes of old rats seemed to be more sensitive not only against MO but also against DYA. When studying lipolysis no signs of competitive dualism could be observed in the interaction between MO and DYA. The possibility of two or more independent lipid-mobilizing mechanisms in the effect of the two opioids compared cannot be excluded.

Adenosine Deaminase↗
PubMed1997

The generation of 1H-NMR-detectable mobile lipid in stimulated lymphocytes: relationship to cellular activation, the cell cycle, and phosphatidylcholine-specific phospholipase C.

Mobile lipids detected using 1H-NMR in stimulated lymphocytes were correlated with cell cycle phase, expression of the interleukin-2 receptor alpha and proliferation to assess the activation status of the lymphocytes. Mobile lipid levels, IL-2R alpha expression and proliferation increased after treatment with PMA and ionomycin. PMA or ionomycin stimulation alone induced increased IL-2R alpha expression but not proliferation. PMA- but not ionomycin-stimulation generated mobile lipid. Treatment with anti-CD3 antibody did not increase IL-2R alpha expression or proliferation but did generate increased amounts of mobile lipid. The cell cycle status of thymocytes treated with anti-CD3, PMA or ionomycin alone indicated an accumulation of the cells in the G1 phase of the cell cycle. The generation of mobile lipid was abrogated in anti-CD3 antibody-stimulated thymic lymphocytes but not in splenic lymphocytes, using a phosphatidylcholine-specific phospholipase C (PC-PLC) inhibitor which blocked cells in the G1/S phase of the cell cycle. This suggests that the 1H-NMR-detectable mobile lipid may be generated in anti-CD3 antibody-stimulated thymic lymphocytes by the action of PC-PLC activity via the catabolism of PC, in the absence of classical signs of activation.

Animals↗
PubMed2005

An unsuspected metabolic role for atrial natriuretic peptides: the control of lipolysis, lipid mobilization, and systemic nonesterified fatty acids levels in humans.

In normal and obese humans, lipid mobilization and systemic nonesterified fatty acid levels are thought to be acutely controlled by catecholamines (ie, epinephrine and norepinephrine) and insulin. Natriuretic peptides (NPs) are known to play a key role in the regulation of salt and water balance and blood pressure homeostasis. They are involved in the pathophysiology of hypertension and heart failure. NPs have recently been found to exert potent lipolytic effects (ie, activating the breakdown of stored triacylglycerols) in isolated human fat cells and to promote lipid mobilization in vivo. Atrial natriuretic peptide increases the intracellular 3', 5'-cyclic guanosine monophosphate (cGMP) concentration which activates cGMP-dependent protein kinase leading to perilipin and hormone-sensitive lipase phosphorylation and lipolysis. NPs promote lipid mobilization when administered intravenously. NPs are also responsible for the residual lipid-mobilizing action observed under oral beta-blockade in subjects performing physical exercise. NPs are therefore novel factors which may open promising research pathways to explain the control of lipid mobilization in physiological and pathological conditions. The metabolic impact of altered production and circulation of NPs remains to be established. The potential influence of NPs on the development of lipid disorders, obesity-related cardiovascular events, and cardiac cachexia will be discussed in this review.

Atrial Natriuretic Factor↗
PubMed2000

Interactions between leptin and NPY affecting lipid mobilization in adipose tissue.

Lipid turnover and deposition is under the control of developmental, nutritional, metabolic and neuroendocrine influences. The aim of the current investigations was focused on the study of the involvement of leptin and neuropeptide Y in lipid mobilization. The lipolytic rate was assessed through glycerol release after incubation with leptin and NPY at concentrations ranging from 10(-6) to 10(-12) M in isolated adipocytes obtained from female rats. The presence of leptin at concentrations of 10(-12) to 10(-7) M in the incubation medium of isolated fat cells significantly increased (p < 0.0001) glycerol release, except at the concentration of 10(-11) M, where the increase was (p < 0.01) as compared to the basal lipolytic activity. On the other hand, isolated fat cells of Wistar rats bathed in 10(-10) to 10(-6) M concentrations of NPY demonstrated a statistically significant decrease (p < 0.0001) in glycerol release. At equimolar concentrations of leptin and NPY (10(-12) to 10(-6) M) the observed lipolytic activity is comparable to the basal lipolytic activity, except at a concentration of 10(-9) M where upon a significant increase in lipolysis is observed. A further increase in the equimolar concentrations, beyond 10(-9) M results in a return to the basal lipolytic activity. Summing up, new evidence suggests that NPY and leptin may interact in a homeostatic loop to regulate body-fat mass and energy balance not only at the central nervous system level, but also directly at the adipocyte level.

Adipocytes↗
PubMed1976

Lipid mobilizing activity in the blood of obese patients during prolonged fasting.

Lipid mobilizing activity is lowered in the serum of obese patients. During short-term fasting, this activity increases in non-obese subjects. The present study was concerned with the changes in lipid mobilizing activity in the blood of obese patients during prolonged fasting, and with the behavior of esterified and free fatty acids. Serum levels of free fatty acids in the control subjects were significantly lower than in the obese women. During a 14-day period of complete fasting, levels of free fatty acids increased in all cases. In non-obese subjects this was accompanied by a significant rise in lipid mobilizing acitivity, but in obese subjects no significant change took place in this activity. The findings indicate that high levels of free fatty acids in obese persons during fasting are caused by inhibition of their esterification.

Adult↗
PubMed2000

Arabidopsis thaliana mutants disrupted in lipid mobilization.

To isolate mutants in the process of lipid mobilization during post-germinative growth we employed a screen using the pro-herbicide 2,4-dichlorophenoxybutyric acid (2,4-DB). The phenotypes of a number of 2,4-DB-resistant mutants are compared with previously characterized mutants disrupted in beta-oxidation or the glyoxylate cycle. We conclude that the strength of 2,4-DB resistance and the ability of the seedlings to grow in the absence of exogenous sugar are inversely correlated. Sugar dependence of 2,4-DB-resistant seedlings is a consequence of impaired storage-lipid mobilization.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2002

Role of beta3-adrenergic receptors in the action of a tumour lipid mobilizing factor.

Induction of lipolysis in murine white adipocytes, and stimulation of adenylate cyclase in adipocyte plasma membranes, by a tumour-produced lipid mobilizing factor, was attenuated by low concentrations (10(-7)--10(-5)M) of the specific beta3-adrenoceptor antagonist SR59230A. Lipid mobilizing factor (250 nM) produced comparable increases in intracellular cyclic AMP in CHOK1 cells transfected with the human beta3-adrenoceptor to that obtained with isoprenaline (1 nM). In both cases cyclic AMP production was attenuated by SR59230A confirming that the effect is mediated through a beta3-adrenoceptor. A non-linear regression analysis of binding of lipid mobilizing factor to the beta3-adrenoceptor showed a high affinity binding site with a Kd value 78 +/- 45 nM and a B(max) value (282 +/- 1 fmole mg protein(-1)) comparable with that of other beta3-adrenoceptor agonists. These results suggest that lipid mobilizing factor induces lipolysis through binding to a beta3-adrenoceptor.

Adenylyl Cyclases↗
PubMed1982

Lipid mobilization and metabolism after thermal trauma.

Lipid mobilization following thermal injury was studied in 25 patients with burns of between 35 and 95% TBSA for 30 to 50 days postinjury. The concentration of free fatty acids and glycerol in the plasma was elevated. The concentration of plasma triglycerides was elevated, while the concentration of ketone bodies remained normal. Thus it is suggested that the free fatty acids are primarily being re-esterified to triglycerides rather than being utilized for ketone body production. During the first 10 days postinjury, the plasma carnitine level was slightly decreased, while the concentration of carnitine in liver and muscle was elevated. The level of carnitine in burn wound fluid was similar to that in plasma. Therefore, the early decrease in plasma carnitine appeared to result from wound losses, as well as the sustained increased uptake by liver and muscle throughout the burn course.

Burns↗
PubMed1998

Biological evaluation of a lipid-mobilizing factor isolated from the urine of cancer patients.

We have previously shown human lipid-mobilizing factor (LMF) to be homologous with the plasma protein Zn-alpha2-glycoprotein in amino acid sequence, electrophoretic mobility, and immunoreactivity. In this study, both LMF and Zn-alpha2-glycoprotein have been shown to stimulate glycerol release from isolated murine epididymal adipocytes with a comparable dose-response profile. Both LMF and Zn-alpha2-glycoprotein caused a stimulation of adenylate cyclase in murine adipocyte plasma membranes in a GTP-dependent process, with maximum stimulation at 0.1 microM GTP and with saturation at protein concentrations of >5 microg/assay. Administration of LMF to exbreeder male mice over a 89-h period produced a decrease in body weight without a change in food and water intake. Body composition analysis showed a 42% reduction in carcass lipid when compared with controls. Treatment of ob/ob mice with human LMF over a 160-h period also produced a decrease in body weight, with a 19% reduction in carcass fat, without a change in body water or nonfat mass. Serum levels of glycerol and 3-hydroxybutyrate were significantly increased, as was oxygen uptake by interscapular brown adipose tissue, providing evidence of increased lipid mobilization and utilization. Human white adipocytes responded to both LMF and isoprenaline to the same extent, although the maximal response was lower than that for murine white adipocytes. These results suggest that LMF not only has the capacity to induce lipid mobilization and catabolism in mice, but it also has the potential to exert similar effects in cachectic cancer patients.

Adenylyl Cyclases↗
PubMedDate not supplied

The use of decapitated insects to study lipid mobilization in adult Manduca sexta: effects of adipokinetic hormone and trehalose on fat body lipase activity.

In order to perform studies on lipid mobilization in adult M. sexta, it is necessary to overcome the effects of starvation and handling, which both provoke an increase in hemolymph lipid concentration. When trehalose was injected into intact insects, a 35% decrease in the content of the diacylglycerol (DG)-rich hemolymph lipoprotein, low density lipophorin (LDLp) was observed within 30 min, but the level of LDLp returned to control values after 1 h. Decapitated insects exhibited 60% reduction in LDLp concentration and the levels remained low for at least 24 h. In contrast to intact insects, injection of trehalose into decapitated animals did not alter the LDLp concentration. After decapitation, the response to adipokinetic hormone (AKH) and the ability of the fat body to release DG into the hemolymph was maintained for at least 24 h. In decapitated insects, 6 pmol of AKH-stimulated measurable lipid mobilization and a near maximum response was obtained with 100 pmol of the hormone. The action of trehalose and AKH on the fat body triacylglycerol (TG)-lipase activity in decapitated animals was studied. Fat body homogenates from trehalose-treated insects exhibited a TG-lipase activity 40% lower than the control insects. Activation of fat body triacylglycerol-lipase was observed after injection of AKH, with the extent of activation ranging between 97 and 380% ten min after AKH injection. A time course study showed that the activation of the fat body triacylglycerol lipase preceded the increase in hemolymph LDLp concentration, suggesting that activation of the lipase initiates lipid mobilization. It is concluded that decapitated insects injected with trehalose is a very useful system for investigating the hormonal regulation of lipid mobilization in adult M. sexta.

Animals↗
PubMed1998

Metabolic bypass of the tricarboxylic acid cycle during lipid mobilization in germinating oilseeds. Regulation Of nad+-dependent isocitrate dehydrogenase versus fumarase

Biosynthesis of sucrose from triacylglycerol requires the bypass of the CO2-evolving reactions of the tricarboxylic acid (TCA) cycle. The regulation of the TCA cycle bypass during lipid mobilization was examined. Lipid mobilization in Brassica napus was initiated shortly after imbibition of the seed and proceeded until 2 d postimbibition, as measured by in vivo [1-14C]acetate feeding to whole seedlings. The activity of NAD+-isocitrate dehydrogenase (a decarboxylative enzyme) was not detected until 2 d postimbibition. RNA-blot analysis of B. napus seedlings demonstrated that the mRNA for NAD+-isocitrate dehydrogenase was present in dry seeds and that its level increased through the 4 d of the experiment. This suggested that NAD+-isocitrate dehydrogenase activity was regulated by posttranscriptional mechanisms during early seedling development but was controlled by mRNA level after the 2nd or 3rd d. The activity of fumarase (a component of the nonbypassed section of the TCA cycle) was low but detectable in B. napus seedlings at 12 h postimbibition, coincident with germination, and increased for the next 4 d. RNA-blot analysis suggested that fumarase activity was regulated primarily by the level of its mRNA during germination and early seedling development. It is concluded that posttranscriptional regulation of NAD+-isocitrate dehydrogenase activity is one mechanism of restricting carbon flux through the decarboxylative section of the TCA cycle during lipid mobilization in germinating oilseeds.

Journal Article↗
PubMed1985

Glucocorticoid effects on membrane lipid mobility during differentiation of murine B lymphocytes.

The lateral motion of membrane lipids on lipopolysaccharide-stimulated murine B lymphocytes was measured using photobleaching recovery techniques. The mobility of the phospholipid analog 3,3'-dioctadecylindocarbocyanine iodide (DiI) was measured at 37 degrees C on B lymphocytes 48 h after stimulation by various concentrations of lipopolysaccharide. DiI mobility on lymphoblasts from cultures stimulated with 10 micrograms/ml lipopolysaccharide was reduced 50% compared with unstimulated, small B cells. However, both lower and higher lipopolysaccharide concentrations caused some decrease in lipid mobility. Lipid mobility was measured on B cells stimulated with 10 micrograms/ml lipopolysaccharide at zero time, on lymphoblasts at 18, 24, 48 and 72 h, and on immunoglobulin (Ig) -secreting lymphocytes at 96 h. The diffusion coefficient of DiI on both control and lipopolysaccharide-treated cells at zero time is 6.3 X 10(-9) cm2 X s-1. This value remains unchanged for unstimulated cells over 72 h. Lipid mobility of lipopolysaccharide-activated lymphoblasts decreased during incubation with lipopolysaccharide to 5.0, 3.4, 2.8 and 2.4 X 10(-9) cm2 X s-1 after 18, 24, 48 and 72 h, respectively. DiI mobility on immunoglobulin (Ig) -secreting lymphocytes identified at the foci of Protein A-coated sheep red blood cells plaques is 8.6 X 10(-9) cm2 X s-1, a value similar to that of unstimulated B cells. The effect of introducing various concentrations of a synthetic glucocorticoid, triamcinolone acetonide (TA), to 48 h lipopolysaccharide-stimulated cells for 6 h was examined. Maximal TA effect was observed at a concentration of 10(-7) M, which caused an increase in lipid mobility to 7.5 X 10(-9) cm2 X s-1. Exposing resting B cells (t = 0) or lymphoblasts (t = 24, 48 or 72 h) to TA for 3 h had no effect on lipid mobility. Treatment for 6 h with 10(-7) MTA increased DiI diffusion to 12.6, 9.9, 7.5 and 6.8 X 10(-9) cm2 X s-1 on control cells and on 24, 48 and 72 h lipopolysaccharide-activated lymphoblasts, respectively. A longer incubation of 12 h with 10(-7) MTA caused no further change in lipid lateral diffusion. The response was glucocorticoid-specific. In lymphoblasts (48 h) incubated an additional 6 h with 10(-7) MTA and a 100-fold excess of cortexolone or progesterone, the increase in lipid mobility was substantively blocked; estradiol and testosterone had no effect on lipid lateral diffusion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Purification and characterization of a lipid-mobilizing factor associated with cachexia-inducing tumors in mice and humans.

A scheme is described for the purification of a lipid-mobilizing factor from a cachexia-inducing murine tumor (MAC16) using a combination of ion exchange (Mono Q), exclusion (Superose), and hydrophobic (C8) chromatography. This process yields an active material with an apparent molecular weight of 24,000 with an overall purification of 3,500 from the tumor homogenate and representing 0.005% of the total protein present. The material tends to aggregate to high molecular mass, is acidic (pI < 4), and displays heterogeneity of charge as evidenced by a broad elution profile on ion exchange and exclusion chromatography and multiple peaks on hydrophobic columns. The purified material was heat and alkali (pH 10.4) labile and activity could be completely inhibited by sulfatase, suggesting that the negative charge could arise from sulfate residues. There was no evidence that the material possessed triglyceride lipase activity. Animals transplanted with the MAC16 tumor and with a delayed weight loss contained in their serum antibodies that recognized a M(r) 24,000 band on Western blots. This material copurified with the lipid-mobilizing factor. Such antibodies were not present in the serum of mice transplanted with the MAC13 tumor, which does not induce cachexia, suggesting that the antibodies were directed to the induction of cachexia rather than the tumor itself. Urine from patients with cancer cachexia also contained a lipid-mobilizing factor which adhered to DEAE-cellulose and gave an apparent M(r) of 24,000 by exclusion chromatography. Western blotting using serum from MAC16 tumor-bearing animals showed the presence of a band of M(r) 24,000 in such fractions, which was not detected using serum from mice bearing the MAC13 tumor. This band was not present in Western blots of urine from normal subjects. The fact that serum from mice bearing the MAC16 tumor can detect the human lipid-mobilizing activity suggests a high degree of structural similarity between the two and raises the possibility that cachexia in humans may be caused by the same species as in the mouse.

Animals↗
PubMed2005

Lipid mobilization with physiological atrial natriuretic peptide concentrations in humans.

CONTEXT: Atrial natriuretic peptide (ANP) in pharmacological concentrations stimulates lipid mobilization in humans. OBJECTIVE: The objective was to determine the hemodynamic and metabolic response to physiologically relevant ANP concentrations. DESIGN: The design was a human physiological study, conducted in 2004. SETTING: The study was conducted at an academic research institute. PARTICIPANTS: Fourteen healthy normal-weight men (30 +/- 1.2 yr) participated in the study. INTERVENTION: Intravenous infusion of human ANP (h-ANP) was administered at rates of 6.25, 12.5, and 25 ng/kg.min. MAIN OUTCOME MEASURES: We studied local changes in blood flow and glucose and lipid metabolism of abdominal sc adipose tissue and femoral skeletal muscle by microdialysis. Overall changes in energy expenditure and substrate oxidation rates were monitored by indirect calorimetry. RESULTS: The increase in serum nonesterified fatty acids and glycerol concentrations were correlated with ANP plasma concentrations (r(2) = 0.86 and r(2) = 0.76, respectively). In adipose tissue, glycerol increased from 53 +/- 6 micromol/liter to 87+/-13 micromol/liter (P < 0.001). In femoral skeletal muscle, glycerol concentrations did not change, whereas lactate-to-pyruvate ratio decreased from 91 +/- 23 to 32 +/- 4 (P < 0.001). Indirect calorimetry indicated an increase in lipid oxidation (P < 0.05) concomitantly with a decrease in carbohydrate oxidation (P < 0.01), without changes in overall energy expenditure. CONCLUSIONS: ANP briskly stimulates lipid mobilization and oxidation at plasma concentrations that are encountered in conditions such as heart failure. Natriuretic-peptide induced lipid mobilization might contribute to cardiac cachexia. Drugs that interfere with the natriuretic peptide system should be evaluated for potential metabolic side effects.

Adipose Tissue↗