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Results for “Lipid Mobilization”

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At least 433 records · Page 24Linked to original sources
PubMed1990

Effect of temperature on the assembly of tight junctions and on the mobility of lipids in membranes of HT29 cells.

In the human colon adenocarcinoma cell line HT29, tight junctions can be induced by treatment with appropriate proteases or salt solutions. The temperature dependence of induced tight junction formation is characterized by a marked sigmoidal behavior. The different methods of induction used in this study were characterized by threshold temperatures ranging from 15 to 32 degrees C. Fluorescence photobleaching recovery measurements of the lateral diffusion of a fluorescent phospholipid probe in the cellular plasma membrane gave no evidence for a phase transition or for alteration in the organization of membrane lipids in lateral domains in the temperature range between 0 and 37 degrees C. Moreover, dynamic parameters of the probe in the plasma membrane did not change substantially on mild treatment with trypsin. Thus, the temperature dependence of tight junction formation is not dictated by the bulk properties of the cytoplasmic membrane lipids. The observed temperature dependence suggests that the assembly of tight junctions is a cooperative process, which may involve conformational rearrangement in a protein precursor subsequent to its proteolytic activation.

Freeze Fracturing↗
PubMed1998

Effects of food restriction on the responses of the mammary gland and adipose tissue to prolactin and growth hormone in the lactating rat.

Exogenous GH is used extensively in the USA to stimulate milk production in dairy cattle but its effectiveness is reduced in undernourished animals. It has been proposed that GH increases milk yield by stimulating IGF-I secretion and that this IGF-I-response is nutritionally sensitive and thus acts as a 'sensor' of energy balance. To investigate this possibility, we placed lactating rats on three planes of nutrition, ad libitum, 50% or 25% of ad libitum for 48 h. Subgroups of these animals were treated for 48 h with bromocriptine, to suppress prolactin secretion, and anti-rat GH, to neutralize GH action. From 24 to 48 h some of the treated animals were assessed for their milk yield response to prolactin or GH. Food restriction reduced milk yield in control rats by approximately 50% and was accompanied by a catabolic state, as judged by lipid mobilization from adipose tissue and by low concentrations of serum insulin, IGF-I, triiodothyronine and thyroxine, and increased serum nonesterified fatty acid concentrations. In animals fed ad libitum, anti-rat GH plus bromocriptine treatment produced an 80% decrease in milk yield and a dramatic fall in the activity of acetyl-CoA carboxylase in mammary tissue. GH was able to stimulate milk yield when given from 24 to 48 h; however, its effectiveness decreased progressively as food intake was reduced. The milk yield response to GH was accompanied by an increase in serum IGF-I concentrations and this response also decreased progressively with reduction of food intake, consistent with the hypothesis that IGF-I determines the milk yield response to GH and thus regulates GH action on the mammary gland in a nutritionally dependent fashion. However, the milk yield response to prolactin and the milk yield of control rats decreased in line with food intake without any changes in serum IGF-I concentrations. This clearly indicates that factors other than IGF-I are responsible for restricting milk yield. In order to assess other possible candidates for this role, we monitored serum glucose, non-esterified fatty acids, insulin triiodothyronine and thyroxine concentrations, but found no evidence for any simple relationship between these parameters and the milk yield response to prolactin and GH. Surprisingly we found that the ability of GH or prolactin to prevent epithelial cell loss in in the mammary gland was completely insensitive to nutrient intake, despite the fact that IGF-I is considered to be an important survival factor for mammary epithelial cells. Finally, we also demonstrated that, at least during short-term food restriction, the lactating rat is capable of mobilizing significant amounts of lipid from adipose tissue, such that it could provide the total output of triglyceride in milk, which is much greater than has previously been proposed.

Acetyl-CoA Hydrolase↗
PubMed2002

Cell structure and mobilization of lipids and proteins from cotyledon under microgravity influence.

The structural-functional organization of cotyledon parenchyma cells of 6-day soybean (Glycine max L.) seedlings that were grown on board the space Shuttle Columbia (STS-87) have been studied. The purafil (KMnO4) was used in the experiment for the removing of some part of ethylene that secretes out from seedlings. There were four variants of the experiment: ground control (+purafil), ground control (-purafil), microgravity (+purafil) and microgravity (-purafil). The electron microscopy, srereological, and pyroantimonate cytochemical methods have been used. It is established the some indices of changes of storage substances in cotyledon parenchyma cells under influence of microgravity. It is displayed in the change of cell ultrastructure, the decrease of relative volume of storage cytoplasmic lipid bodies, a disappearance of storage protein body into vacuole and the redistribution of ionized calcium in cell. It was supposed that microgravity is influenced on the acceleration of storage substances catabolism.

NASA Discipline Plant Biology↗
PubMed1994

Effects of scalaradial, a type II phospholipase A2 inhibitor, on human neutrophil arachidonic acid mobilization and lipid mediator formation.

The role of scalaradial (SLD) (or its 12-epi analog), a marine natural product purified from sponge (Cacospongia mollior) in human neutrophil (polymorphonuclear leukocyte, PMN) arachidonic acid metabolism was studied. SLD potently inhibited human recombinant (rh) type II-14 kDa-phospholipase A2 (PLA2) (IC50 = 0.07 microM) but displayed weak inhibition of U937 cell, 85 kDa-PLA2 (IC50 = 20 microM). Sn-2 acylhydrolytic activity expressed in human PMN acid extract, that was completely neutralized by anti-rh type II-14 kDa-PLA2 monoclonal antibody, was inhibited by SLD in a concentration-dependent manner (IC50 = 35 microM). Exposure of human PMN to SLD resulted in a concentration-dependent inhibition of calcium ionophore (A23187)-induced leukotriene B4 release (IC50 = 0.1-0.6 microM). In contrast to the action of selective 5-lipoxygenase inhibitors (WY 50295 or zileuton), SLD decreased A23187-induced PMN liberation of arachidonic acid mass and platelet-activating factor biosynthesis (IC50 = 1-2 microM). PMN acetyltransferase activity was not significantly affected by SLD suggesting that platelet-activating factor inhibition was due, predominantly, to inactivation of PLA2 activity. In vivo, topical application of SLD on mouse ear treated with phorbol ester, not only inhibited edema formation but also the increase in myeloperoxidase activity (an index of cellular infiltration). SLD had little or no effect on arachidonic acid-induced ear edema or myeloperoxidase which is consistent with an action on PLA2. Take together these data suggest that the predominant mechanism of SLD is via inhibition of 14 kDa-like-PLA2 and suggests that this enzyme may participate in PMN arachidonic acid liberation and lipid mediator formation.

Animals↗
PubMed1998

[The dependence of thrombocyte aggregation on temperature].

The effect of temperature (range of 4-44 degrees C) upon induced aggregation of platelets from normal subjects was studied. It was shown that temperature dependences of aggregation degree and rate have maxima. A relationship between aggregation agonist kind and some features of the temperature dependence curve of the aggregation parameters is established. It was shown that the limitation of platelet membrane lipids mobility by means of lipids peroxidation leads to the shift of maxima of the temperature dependence curve of platelet aggregation degree and rate. It was concluded that character of aggregation temperature dependence was governed by phase transition in platelet membrane lipids at room temperature.

Adenosine Diphosphate↗
PubMed1975

Factors regulating blood levels of free fatty acids during alimentary lipemia.

Transient lowering of blood levels of free fatty acids (FFA) in man and experimental animals after ingestion of fat has been noted by many investigators and has been attributed to inhibition of mobilization of fatty acids from adipose tissue. Studies on lipid mobilizing activity in in vitro systems containing glucagon, insulin and anti-insulin anti-bodies as factors modifying lipolysis indicate that insulin is the basic inhibitor of lipolysis in the blood in the period immediately following feeding of animals. This observation has been confirmed by direct determinations of insulin levels by the radioimmunologic method. Experiments in which substances influencing activity of the autonomic nervous system were used show that ingestion of fats stimulates insulin secretion as a result of cholinergic stimulation. Studies on lipolytic activity of blood serum confirmed an essential role of lipoprotein lipase in the mechanism of deposition of triglycerides in adipose tissue during alimentary lipemia. The role of prostaglandins and intestinal hormones (enteroinsular axis) in the mechanism of regulation of FFA levels during alimentary lipemia is also discussed.

Adipose Tissue↗
PubMed1985

Enhanced metabolic response to caffeine in exercise-trained human subjects.

The effect of caffeine on resting metabolic rate (RMR) was investigated in eight trained and eight nontrained young male subjects. The ingestion of 4 mg/kg caffeine produced a greater increase of RMR in trained subjects. This effect was associated with a greater increase in plasma free fatty acids and a larger fall in respiratory quotient, indicating an enhanced lipid oxidation following caffeine in exercise-trained subjects. An initial fall in plasma glucose was observed but only in trained subjects, and caffeine did not change plasma insulin in either group studied. Caffeine caused a significant fall in plasma norepinephrine and an increase in plasma epinephrine in both groups of subjects, but this action was significantly greater in trained subjects. It is suggested that the greater increase in RMR observed in trained subjects following caffeine ingestion is related to an enhanced lipid mobilization, possibly produced by a greater epinephrine secretion and by subsequent increased lipid oxidation.

Adipose Tissue↗
PubMed2005

Formation and mobilization of neutral lipids in the yeast Saccharomyces cerevisiae.

Since energy storage is a basic metabolic process, the synthesis of neutral lipids occurs in all kingdoms of life. The yeast Saccharomyces cerevisiae, widely accepted as a model eukaryotic cell, contains two classes of neutral lipids, namely STEs (steryl esters) and TAGs (triacylglycerols). TAGs are synthesized through two pathways governed by the acyl-CoA diacylglycerol acyltransferase Dga1p and the phospholipid diacylglycerol acyltransferase Lro1p. STEs are formed by two STE synthases Are1p and Are2p, two enzymes with overlapping function, which also catalyse TAG formation, although to a minor extent. Neutral lipids are stored in the so-called lipid particles and can be utilized for membrane formation under conditions of lipid depletion. For this purpose, storage lipids have to be mobilized by TAG lipases and STE hydrolases. A TAG lipase named Tgl3p was identified as a major yeast TAG hydrolytic enzyme in lipid particles. Recently, a new family of hydrolases was detected which is required for STE mobilization in S. cerevisiae. These enzymes, named Yeh1p, Yeh2p and Tgl1p, are paralogues of the mammalian acid lipase family. The role of these proteins in biosynthesis and mobilization of TAG and STE, and the regulation of these processes will be discussed in this minireview.

Acyltransferases↗
PubMed1992

Effect of chronic ACTH treatment on the physical state of lipid droplets in rat adrenocortical cells.

A histophysical method has been adapted to determine the thermotropic phase transitions of adrenocortical lipid droplets using a polarizing microscope equipped with a cold/hot stage. Cryosections of freshly-removed, unfixed adrenals, derived from control (untreated), and 14 days ACTH-treated rats were examined. The lipid droplets in the zona fasciculata and zona reticularis of the untreated rats were birefringent at room temperature (22 degrees C). The birefringence of zona glomerulosa lipids selectively increased in the temperature range from -10 to -15 degrees C. In cryosections prepared from ACTH-treated rats, thermotropic phase transitions of the lipid droplets appeared at a temperature range between -30 and -40 degrees C in each cortical zone. The chemical analysis of the isolated lipids revealed that the relative amount of triglycerides in the zona fasciculata lipids increased, while that of free and esterified cholesterol decreased after chronic ACTH treatment. Present data suggest that the increased fluidity of lipid droplets promotes lipid mobilization in response to the enhanced demand of the chronically stimulated adrenocortical cells. Viscosity-dependent mobilization of free cholesterol from lipid droplets is not a rate-limiting process in adrenal steroidogenesis, but rather may represent an important control of the availability of precursor from lipid stores.

Adrenal Cortex↗