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PubMed1995

Interaction of alpha-lactalbumin with phosphatidylglycerol. Influence of protein binding on the lipid phase transition and lipid acyl chain mobility.

The mobility of spin-labeled lipids has been studied in dioleoyl and dimyristoyl phosphatidylglycerol bilayers and in their complexes with alpha-lactalbumin at pH 4.0, by using electron spin resonance (ESR) spectroscopy. The ESR spectra of phosphatidylglycerol spin-labeled at position 5 of the sn-2 chain indicate that association of alpha-lactalbumin with dimyristoyl phosphatidylglycerol bilayers increases the chain mobility at temperatures in the lipid gel phase, restricts the chain mobility at temperatures corresponding to the lipid fluid phase, and abolishes the cooperative lipid chain-melting transition. The ESR spectra of phosphatidylglycerols spin-labeled at eight different positions in the sn-2 chain show that binding of alpha-lactalbumin to dioleoyl phosphatidylglycerol bilayers at pH 4.0 causes a motional restriction throughout the full length of the lipid acyl chain. For phosphatidylglycerols spin-labeled at the terminal methyl end of the chains, a population of motionally restricted lipids that directly contacts membrane penetrant portions of the protein is detected. This population corresponds to 6.3 +/- 0.7 lipids/alpha-lactalbumin at saturation binding, and the high degree of motional restriction (maximum hyperfine splitting approximately 60 G) suggests that the protein may traverse the lipid bilayer. A small selectivity of phosphatidylglycerol over zwitterionic phospholipids for interaction with alpha-lactalbumin is found at subsaturating levels of binding at pH 4.0. Binding of alpha-lactalbumin also strongly restricts the motion of lipids spin-labeled in the polar head group region. These results are of direct relevance to the insertion and translocation of a protein in the molten globule state across lipid membranes.

Electron Spin Resonance Spectroscopy↗

PubMed1997

Spin-label studies on the anchoring and lipid-protein interactions of avidin with N-biotinylphosphatidylethanolamines in lipid bilayer membranes.

The specific binding of hen egg white avidin to phosphatidylcholine lipid membranes containing spin-labeled N-biotinylphosphatidylethanolamines (biotin-PESLs) was investigated by using ESR spectroscopy. Spin-labeled biotin-PEs were prepared with the nitroxide group at position C-5, C-8, C-10, C-12, or C-14 of the sn-2 chain and were incorporated at 1 mol % in lipid bilayer membranes of dimyristoylphosphatidylcholine. Binding of avidin produced a strong and selective restriction of the biotin-PE lipid mobility at all positions of chain labeling, as shown by the ESR spectra recorded in the fluid lipid phase. The spectral components of the fraction of the biotin-PESLs that were not complexed by avidin indicated that the mobility of the bulk membrane lipids was unperturbed by binding avidin, as demonstrated by difference spectroscopy. Comparison of the positional profiles and temperature dependences of the outer hyperfine splittings from the biotin-PESLs suggests that the C-12 and C-14 positions of the avidin-bound biotin-PEs are in register with the C-5 and C-7/C-6 positions, respectively, of the chains of the bulk membrane lipids. This indicates that the biotin-PEs are partially withdrawn from the membrane, with a vertical displacement of ca. 7-8 A, on complexation with avidin. In addition, the specific lipid-protein interaction with avidin results in a selective reduction in the rates of lipid chain motion, as shown by the increased ESR line widths. These data define the way in which avidin is anchored to lipid membranes containing biotin-PEs.

Avidin↗

PubMed1992

Molecular motions and thermotropic phase behavior of triacylglycerols and cholesteryl esters in herpesvirus-infected arterial smooth muscle cells: a deuterium nuclear magnetic resonance study.

The physical state of lipids in arterial smooth muscle cells (SMC) may contribute to lipid accumulation following injury. We have previously demonstrated that herpes simplex virus (HSV) infection alters the physical state of the neutral lipid accumulating in arterial SMC, as determined by differential scanning calorimetry (Biochem. J. 268 (1990) 693-697). To more precisely determine the molecular packing of neutral lipids in HSV-infected cells, the influence of HSV-infection on the thermotropic and phase-behavior of the lipids in intact arterial smooth muscle cells and in cell-free lipid extracts was evaluated using [2H]-NMR, employing U-[2H]-oleic acid incorporated into cells. Inspection of the [2H]-line-widths indicate that the lipid of HSV-infected cells exhibited more restricted motion or a greater chemical shift dispersity than lipids from uninfected cells, as evidenced by significant broadening of the -CD = CD- signals at 25 degrees C and 45 degrees C. Fatty acid compositional analysis of the neutral lipids of control and HSV-infected cells following C18:1 supplementation (an amount added similar to the NMR experiments) reveals that: (1) there is approximately 55-fold more triacylglycerols (TG) than cholesteryl esters (CE) in control cells and 40-fold more TG than CE in the HSV-infected cells; (2) HSV infection significantly increases the C18:1 content of CE, and C18:3 and C20:4 in TG; and (3) HSV-infection does not alter the ratio of TG to CE. These data support the hypothesis that the greater restriction of the neutral lipids in HSV-infected cells may be due to the rigidifying effects of C18:1 on lipid mobility. Thus, alterations in the physical state of neutral lipids in HSV-infected cells may lead to reduced CE hydrolysis which, in turn, may contribute to or exacerbate lipid accumulation.

Cells, Cultured↗

PubMed2005

Skeletal muscle and nuclear hormone receptors: implications for cardiovascular and metabolic disease.

Skeletal muscle is a major mass peripheral tissue that accounts for approximately 40% of the total body mass and a major player in energy balance. It accounts for >30% of energy expenditure, is the primary tissue of insulin stimulated glucose uptake, disposal, and storage. Furthermore, it influences metabolism via modulation of circulating and stored lipid (and cholesterol) flux. Lipid catabolism supplies up to 70% of the energy requirements for resting muscle. However, initial aerobic exercise utilizes stored muscle glycogen but as exercise continues, glucose and stored muscle triglycerides become important energy substrates. Endurance exercise increasingly depends on fatty acid oxidation (and lipid mobilization from other tissues). This underscores the importance of lipid and glucose utilization as an energy source in muscle. Consequently skeletal muscle has a significant role in insulin sensitivity, the blood lipid profile, and obesity. Moreover, caloric excess, obesity and physical inactivity lead to skeletal muscle insulin resistance, a risk factor for the development of type II diabetes. In this context skeletal muscle is an important therapeutic target in the battle against cardiovascular disease, the worlds most serious public health threat. Major risk factors for cardiovascular disease include dyslipidemia, hypertension, obesity, sedentary lifestyle, and diabetes. These risk factors are directly influenced by diet, metabolism and physical activity. Metabolism is largely regulated by nuclear hormone receptors which function as hormone regulated transcription factors that bind DNA and mediate the patho-physiological regulation of gene expression. Metabolism and activity, which directly influence cardiovascular disease risk factors, are primarily driven by skeletal muscle. Recently, many nuclear receptors expressed in skeletal muscle have been shown to improve glucose tolerance, insulin resistance, and dyslipidemia. Skeletal muscle and nuclear receptors are rapidly emerging as critical targets in the battle against cardiovascular disease risk factors. Understanding the function of nuclear receptors in skeletal muscle has enormous pharmacological utility for the treatment of cardiovascular disease. This review focuses on the molecular regulation of metabolism by nuclear receptors in skeletal muscle in the context of dyslipidemia and cardiovascular disease.

Cardiovascular Diseases↗

PubMed2005

Aluminum ions stimulate the oxidizability of low density lipoprotein by Fe2+: implication in hemodialysis mediated atherogenic LDL modification.

OBJECTIVE: Al(3+) stimulates Fe(2+) induced lipid oxidation in liposomal and cellular systems. Low-density lipoprotein (LDL) oxidation may render the particle atherogenic. As elevated levels of Al(3+) and increased lipid oxidation of LDL are found in sera of hemodialysis patients, we investigated the influence of Al(3+) on LDL oxidation. MATERIALS AND METHODS: Using different LDL modifying systems (Fe(2+), Cu(2+), free radical generating compounds, human endothelial cells, hemin/H(2)O(2) and HOCl), the influence of Al(3+) on LDL lipid and apoprotein alteration was investigated by altered electrophoretic mobility, lipid hydroperoxide-, conjugated diene- and TBARS formation. RESULTS: Al(3+) could stimulate the oxidizability of LDL by Fe(2+), but not in the other systems tested. Al(3+) and Fe(2+) were found to bind to LDL and Al(3+)could compete with Fe(2+) binding to the lipoprotein. Fluorescence polarization data indicated that Al(3+) does not affect the phospholipid compartment of LDL. CONCLUSIONS: The results indicate that increased LDL oxidation by Fe(2+) in presence of Al(3+) might be due to blockage of Fe(2+) binding sites on LDL making more free Fe(2+) available for lipid oxidation.

Aluminum↗

PubMed1982

Effects of prazosin on human fat-cell lipolysis and adenylate cyclase activity in vitro.

The effects of prazosin on adrenergic-stimulated fat-cell lipolysis and adenylate cyclase activity were investigated. The results revealed that the antilipolytic alpha-adrenergic catecholamine effects on human fat-cell metabolism are mediated via alpha 2-receptor sites displaying extremely low affinity to prazosin, which is alpha 1-site selective. The data provide an explantation for the lack of effect of prazosin on lipid mobilization in vivo. The molecular sites mediating the lipid-lowering action of the drug, however, remain to be elucidated.

Adenylyl Cyclase Inhibitors↗

PubMed1976

Hypoglycemia in small-for-dates newborn infants.

In 24% (18 out of 76) small-for-dates a "significant" though asymptomatic hypoglycemia was demonstrated during the first six hours of life. The cord blood glucose concentration was lower in the hypoglycemic compared to that of the small-for-date normoglycemic group. In the hypoglycemic infants, the disappearance rate of glucose was significantly elevated and the lipid mobilization disturbed. It is suggested that a lack of lipids for energy metabolism increases the glucose expenditure and hence increases the risk for hypoglycemia.

Birth Weight↗

PubMed1988

Lipid dynamics in fish: aspects of absorption, transportation, deposition and mobilization.

1. Aspects of lipid metabolism, including absorption and depositional processes, appear quite different in fish as compared to homeothermic vertebrates. 2. Dietary lipids in fish are absorbed as fatty acids and as triacylglycerols aggregated into chylomicra particles. 3. Interorgan transport of lipids, like that of mammals, consists of an exogenous (dietary) loop and an endogenous loop. 4. Fish store lipids among several depot organs, including mesenteric membranes, liver and muscle. 5. Several fast-acting and slow-acting agents modulate depot lipid mobilization. 6. Mobilized lipids may be transported in the serum as free fatty acids bound to specific carrier proteins.

Absorption↗

PubMed1985

A relay model of lipid peroxidation in biological membranes.

It is believed that in lipid peroxidation in membranes an important role is played by unoxygenated hydrocarbon radicals whose movement within the hydrocarbon moiety of the membrane is through intra-and intermolecular relay rearrangements (H-shift). in membranes containing a high concentration of polyunsaturated lipids, mobility may be higher than the lateral diffusion of the lipids allowed by the microviscosity of the membrane. The action mechanism of antioxidants having a side hydrocarbon tail (e.g., tocopherols) rests upon the relay radical reaction, as a multistep process. The initial step is the relay transfer of unoxygenated free radical to the side hydrocarbon chain of antioxidant. In subsequent steps the aroxyl radical is formed by the intramolecular rearrangement of radical in an antioxidant molecule. Hence, the inhibitor interrupts the propagation chain in the membrane by the scavenge of unoxygenated hydrocarbon radical.

Antioxidants↗

PubMedDate not supplied

[Changes in blood lipids in humans during long-term ski crossing in the Extreme North].

Serum lipids were measured in the men who made two ski crosses in the Far North during polar night. The first trip, which was to train the athletes, took 17 days and the second took 38 days. In both studies, lipid mobilization and utilization increased, which led to changes in the lipid spectrum: decrease of the concentration of LDL and, in the second trip, of VLDL and HDL3, and increase of the concentration of HDL2 and cholesterol HDL. In the second trip, lipids were most intensively utilized: lipolysis enhanced and free fatty acids declined. This was also indicated by an increase of the capillary-venous difference in terms of the total fraction of LDL and VLDL as well as free fatty acids. At the end of the second trip, the positive capillary-venous difference in terms of LDL and VLDL and, accordingly, the negative capillary-venous difference in terms of HDL2 and HDL3 increased. At the end of both trips the synthesis of transport lipids grew; in the most strenuous second trip, their active utilization in the working organs was stronger.

Adult↗

PubMed1984

Blood and milk lipid responses induced by growth hormone administration in lactating cows.

Nine multiparous Holstein cows (average 5.8 yr, 63 to 132 days postpartum) were in a 28-day single reversal experiment in the Beltsville open circuit respiration chambers with two 14-day injection periods (placebo versus bovine growth hormone, 51.5 IU/day). With growth hormone treatment, milk fat percentage increased 25 to 29%, milk fat yield increased 41%, and cows averaged -13.7 Mcal/day energy balance. There were small increases of triglycerides and 1,2-diglycerides, core lipids, and small decreases of cholesterol and phospholipids, the membrane lipids. Fat from growth hormone treatment had 6% less short (6:0, 8:0, 10:0) and medium (12:0, 14:0, 14:1, 15:0, 16:0) chain fatty acids and 6% more long chain 18:1 fatty acids. Plasma of cows treated with growth hormone had an increase of concentrations of free fatty acids, but no shifts were apparent among other lipid classes. Analysis of total plasma fatty acids did not show any net changes, but within individual plasma lipid classes, 18:1 increased and 18:2 decreased. Overall changes of blood and milk lipids are consistent with the concept that adipose tissue reserves were mobilized in response to hormone treatment and that these mobilized lipids were the major carbon source for the 41% increase of milk fat secretion. Increases of de novo synthesis of short and medium chain fatty acids also occurred but much less. Cows treated with growth hormone were in negative energy balance, and the mechanism may differ when cows are in positive energy balance.

Animals↗

PubMed1992

Cell and membrane lipid analysis by proton magnetic resonance spectroscopy in five breast cancer cell lines.

The lipid composition of five human breast cancer cell lines (MCF-7, T47D, ZR-75-1, SKBR3 and MDA-MB231) was assessed by proton magnetic resonance spectroscopy (MRS) in whole cells and membrane-enriched fractions. The proportions of the three main lipid resonances in 1D spectra were different for each cell line. These resonances included mobile methyl and methylene functions from fatty acids of triglycerides and phospholipids and N-trimethyl from choline of phospholipids. T47D and ZR-75-1 cells presented a high methylene/methyl ratio (6.02 +/- 0.35 and 6.28 +/- 0.90). This ratio was significantly lower for SKBR3, MCF-7 and MDA-MB231 cells (2.76 +/- 0.22, 2.27 +/- 0.57 and 1.39 +/- 0.39). The N-trimethyl/methyl ratio was high for MDA-MB231 and SKBR3 cells (1.38 +/- 0.54 and 0.86 +/- 0.32), but lower for MCF-7, T47D and ZR-75-1 cells (0.49 +/- 0.11, 0.16 +/- 0.07 and 0.07 +/- 0.03). 2D COSY spectra confirmed these different proportions in mobile lipids. From 1D spectra obtained on membrane preparations, T47D and ZR-75-1 were the only cell lines to retain a signal from mobile methylene functions. These differences might be related to the heterogeneity found for several parameters of these cells (tumorigenicity, growth rate, hormone receptors); an extended number of cases from fresh samples might enable clinical correlations.

Breast Neoplasms↗

PubMed1996

Lipobeads: a hydrogel anchored lipid vesicle system.

A new vesicle system is described that combines complementary properties of liposomes and polymeric beads. 'Lipobeads' consist of a lipid bilayer shell anchored on the surface of a hydrogel polymer cores which acts like a cytoskeleton. Anchoring is provided by fatty acids covalently attached to the surface of the hydrogel. These hydrophobic chains drive spontaneous assembly of a lipid bilayer shell around the modified hydrogel bead when exposed to a suspension of liposomes. The bilayer is stable and acts as a permeability barrier to compound loaded by prior absorption into the polymer core. Lipid mobility in the shell is similar to that found in other unanchored lipid bilayers. The system has potential application in drug delivery and for functional reconstitution of membrane proteins.

Acylation↗

PubMed1984

Synthesis of shrimp red pigment-concentrating hormone analogs and their biological activity in locusts.

Two analogs of the red pigment-concentrating hormone (RPCH) have been synthesized by the solid-phase method: [Thr6]-RPCH (I) and [Tyr4, Thr6]-RCPH (II). Analog I has the same amino acid composition as the second adipokinetic hormone (AKH-II) isolated from locust corpora cardiaca. Bioassay for lipid-mobilizing activity in adult male locusts gave the following increases in hemolymph lipid content: AKH-I, 3.5; I, 2.4; II, 2.9. The biological response shown by I lends support to the conclusion that its sequence is that of the presumptive AKH-II. Replacement of Phe in position 4 by Tyr does not reduce the adipokinetic response.

Animals↗

PubMed1999

Calcium and cAMP are second messengers in the adipokinetic hormone-induced lipolysis of triacylglycerols in Manduca sexta fat body.

We have previously shown that stereospecific hydrolysis of stored triacylglycerol by a phosphorylatable triacylglycerol-lipase is the pathway for the adipokinetic hormone-stimulated synthesis of sn -1, 2-diacylglycerol in insect fat body. The current series of experiments were designed to determine whether cAMP and/or calcium are involved in the signal transduction pathway for adipokinetic hormone in the fat body. After adipokinetic hormone treatment, cAMP-dependent protein kinase activity in the fat body rapidly increased and reached a maximum after 20 min, suggesting that adipokinetic hormone causes an increase in cAMP. Forskolin (0.1 micrometer), an adenylate cyclase activator, induced up to a 97% increase in the secretion of diacylglycerol from the fat body. 8Br-cAMP (a membrane-permeable analog of cAMP) produced a 40% increase in the hemolymph diacylglycerol content. Treatment with cholera toxin, which also stimulates adenylate cyclase, induced up to a 145% increase in diacylglycerol production. Chelation of extracellular calcium produced up to 70% inhibition of the adipokinetic hormone-dependent mobilization of lipids. Calcium-mobilizing agents, ionomycin and thapsigargin, greatly stimulated DG production by up to 130%. Finally, adipokinetic hormone caused a rapid increase of calcium uptake into the fat body. Our findings indicate that the action of adipokinetic hormone in mobilizing lipids from the insect fat body involves both cAMP and calcium as intracellular messengers.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1990

Reduced suppression of plasma saturated fatty acid mobilization and oxidation by feeding in lymphoma-bearing mice.

Lymphoma-bearing mice have a circulating lipid-mobilizing factor, but increased plasma free fatty acid (FFA) turnover has not been demonstrable in earlier studies using postabsorptive tumor-bearing mice. We hypothesized that FFA mobilization in lymphoma-bearing mice is only elevated in fed mice and may best be observed at night (dark, reversed light cycle). AKR mice with early and advanced tumors (10(6) SL-3 lymphoma cells, i.p.) and controls were fed ad libitum (reversed light cycle, dark) or fasted 4 h (daylight, regular cycle), given injections of [14C]bicarbonate of [1-14C]palmitate-mouse serum albumin, i.v., and plasma [14C]FFA disappearance and/or breath 14CO2 were monitored. Plasma FFA mobilization, estimated by multicompartmental analysis (SAAM) of the oxidation rate was lower in fasted mice with advanced tumors [tumor, 9.5 +/- 6.0% (%SE); controls, 14 +/- 4.4% micrograms-atoms fatty acid-carbon/min/30 g body weight, n = 3 to 6 mice/time point/group]. Feeding reduced these rates 90% in control mice and 53% in mice with early tumors, but only 14% in mice with advanced tumors. Plasma FFA fractional catabolic rates were 2.5 times faster in fed mice with advanced tumors than in controls. Diminished suppression of fatty acid mobilization in fed tumor-bearing mice (at night) probably accounts partially for the body fat loss.

Adipose Tissue↗

PubMed1991

Fatty acid metabolism by the porcine placenta.

Two experiments were performed to determine whether esterification is a major pathway of fatty acid utilization within porcine placenta and to determine what metabolic parameters may limit fatty acid transfer to the fetal pig. Maternal (endometrium) and fetal (chorioallantois) placenta were obtained by Caesarean section at d 110 of gestation in both experiments. Eight gilts were used in the first experiment. Tissue sections were incubated with palmitate at concentrations ranging from .25 to 2.0 mM. Maternal placenta metabolized palmitate at a higher rate than fetal placenta, although fetal placenta was more efficient in esterifying palmitate. Esterification composed the majority of palmitate utilization within fetal and maternal placenta. The second experiment evaluated the effect of dietary lipid on placental fatty acid metabolism and evaluated the ability of placenta to mobilize lipids. Fourteen gilts were divided into two groups of seven and fed a diet containing 15% tallow diet or a diet not supplemented with tallow (control) from d 90 to 110 of gestation. Dietary lipid had no detectable effects on lipoprotein lipase activity, [14C]palmitate metabolism, or lipolysis by the maternal or fetal placenta. Lipolytic activity of placental tissues was minimally affected by incubation with various proposed lipolytic activity of placental tissues was minimally affected by incubation with various proposed lipolytic agents. The data indicate that supply of fatty acids to the fetal pig may be limited by transfer of plasma fatty acids into the cytoplasm of placental cells or by regulatory enzymes for intermediate esterification; both types of limitations have been proposed to be influenced by fatty-acid binding proteins.

Animals↗

PubMed2000

Steroid hormone-induced effects on membrane fluidity and their potential roles in non-genomic mechanisms.

Steroid hormones are lipophilic suggesting they intercalate into the bilayer of target cell plasma membranes, potentially altering the fluidity and function of the membrane. The present study measured the effects of steroidal exposure on both phospholipid fluidity and integral protein mobility. Studies were performed on the effects of a variety of steroids on phosphatidylcholine liposomes, synaptosomal plasma membranes and sarcoplasmic reticulum membranes. Progesterone decreased the lipid fluidity, whereas testosterone had no effect on lipid movement. The estrogen, 17 beta-estradiol, an aromatised metabolite of testosterone, increased lipid mobility. In each case, the steroid action was concentration-dependent. The steroids all increased the activity of the Ca2+ ATPase of SR membrane, in keeping with their effects on this enzyme's aggregation state. The results suggest that, although lipid fluidity is a factor influencing protein activity, their mobility within the bilayer is the primary determinant of enzyme activity in the membrane for most proteins.

Animals↗