Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LIPIDS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed2005

Reduced whole-body lipid oxidation is associated with insulin resistance, but not with intramyocellular lipid content in offspring of type 2 diabetic patients.

AIMS/HYPOTHESIS: Intramyocellular lipid accumulation and insulin resistance are thought to be due to reduced lipid oxidation in a human model of high risk of developing type 2 diabetes. METHODS: We studied 32 offspring of type 2 diabetic parents and 32 control individuals by means of DXA, indirect calorimetry, insulin clamp and 1H MRS of the calf muscles, and differences between and within study groups were analysed before and after segregation by quartiles of fasting lipid oxidation. RESULTS: In comparison with control subjects, the offspring showed impaired insulin sensitivity, which was associated with higher fasting intramyocellular lipid content (Spearman's rho -0.35; p=0.04), but fasting lipid oxidation did not differ between groups (1.21+/-0.46 vs. 1.25+/-0.37 mg.kg(-1) lean body mass per min; p=0.70). Nevertheless, offspring in the lowest quartile of lipid oxidation had the most severe impairment of insulin sensitivity and a strong association was shown between lipid oxidation and insulin sensitivity within quartiles (Spearman's rho 0.47; p=0.01); this was not observed within the control group (Spearman's rho 0.13; p=0.47). Intramyocellular lipid content was not significantly different within quartiles of lipid oxidation in either of the groups. CONCLUSIONS/INTERPRETATION: Insulin sensitivity improved across increasing quartiles of fasting lipid oxidation in the offspring group, but remained constant in the control group, supporting the hypothesis that impaired fat oxidation is a primary pathogenic factor of insulin resistance in people with a genetic background for type 2 diabetes. Despite their association with impaired insulin sensitivity, soleus and tibialis anterior intramyocellular lipid content remained constant across increasing quartiles of fasting lipid oxidation within both groups.

Adiponectin↗
PubMed1986

Lipid peroxidation in newborn rabbits: effects of oxygen, lipid emulsion, and vitamin E.

The extent of in vivo lipid peroxidation and the in vivo antioxidant effects of alpha-tocopherol and alpha-tocopheryl acetate were studied in newborn rabbits exposed to one of two oxidant stresses: hyperoxia (FIO2 greater than 0.9) or parenteral lipid emulsion infusion. Lipid peroxidation was monitored by measurement of expired ethane and pentane, tissue thiobarbituric acid (TBA) reactants, and tissue lipid peroxides. Seventy-two h of hyperoxia did not increase any of the parameters of lipid peroxidation although mortality was higher in oxygen exposed animals. alpha-Tocopherol (100 mg/kg, intravenous) lowered expired hydrocarbons and tissue TBA reactants, but raised liver lipid peroxides in both air and hyperoxia exposed pups. Infusion of soybean oil emulsion increased production of ethane and pentane, liver TBA reactants, and lung lipid peroxides. Both alpha-tocopherol and alpha-tocopheryl acetate prevented the soybean oil emulsion induced increase in volatile hydrocarbons. alpha-Tocopherol (100 mg/kg, intravenous) administration also prevented the increase in liver TBA reactants and lung lipid peroxides. In identically treated animals, alpha-tocopheryl acetate administration decreased liver TBA reactants but had no effect on lung lipid peroxides. We conclude that alpha-tocopherol reduces lipid peroxidation in newborn rabbits including animals exposed to hyperoxia or infused with lipid emulsions. alpha-Tocopheryl acetate results in lower tissue alpha-tocopherol concentrations and is less effective as an antioxidant in lipid emulsion infused rabbits.

Animals↗
PubMed1994

Appearance of homogeneous smectic multilamellar microenvironments in biomembranes undergoing superoxide-initiated lipid peroxidation: lipid-dienyl radical accumulation and fluidity management in lipid bilayers.

Erythrocyte ghosts were exposed to various levels of oxyradical shock in order to identify the extent of accumulation of peroxidative intermediates. Malondialdehyde reacting end products were the same in all different models. But, the accumulation of dienyl radical species increased with higher intensity of oxyradical shock. These dienyl radicals may rearrange to create a homogeneous smectic multilamellar microenvironment which may be more fluid in terms of the molecular dynamics.

Erythrocyte Membrane↗
PubMed1977

Lipids of cultured hepatoma cells: VIII. Utilization of D-[1-14C] glucose for lipid biosynthesis.

Minimal deviation hepatoma 7288C cells (HTC) were incubated in serum-supplemented and serum-free Swim's 77 medium in the presence of D-[1-14C] glucose for 1, 2, 4, 8, 12 and 24 hr. Glucose oxidation to CO2, incorporation into total cell mass, and incorporation into cell and medium lipids were determined. The percentage distribution of total cell lipid radioactivity in individual neutral and polar lipid classes was followed as a function of time. Degradation studies of individual lipid classes were performed to ascertain the percentage of radioactivity in acyl and glycerol moieties. The percentage of D-[1-14C] glucose oxidized to 14CO2, incorporated into cell matter and cell lipids was elevated in cells incubated in serum-free medium as opposed to serum-supplemented medium. The percentage distribution of total cell lipid radioactivity into individual neutral lipid classes from both serum-free and serum-supplemented cultures was as follows: sterols greater than triglycerides greater than free fatty acids greater than sterol esters. The percentage distribution of total cell lipid radioactivity into individual polar lipid classes of serum-supplemented cultures was as follows: phosphatidylcholine greater than phosphatidylinositol greater than sphingomyelin greater than phosphatidylethanolamine greater than phosphatidylserine. The distribution of glucose radiolabel into individual polar lipid classes of serum-free HTC cells was different from their serum-supplemented counterparts: sphingomyelin greater than phosphatidylcholine greater than phosphatidylinositol greater than phosphatidylethanolamine greater than phosphatidylserine. Glycerol from glyceride classes contained a higher percentage of radioactivity than the acyl moieties, with this percentage significantly elevated in serum-free cultures. The data indicate that, although glucose is a substrate for HTC cell lipids, other precursors present in the culture system also contribute to the lipid constituency of this hepatoma cell line.

Blood↗
PubMed1983

The effect of dietary lipids on the thermotropic behaviour of rat liver and heart mitochondrial membrane lipids.

Diets supplemented with relatively high levels of either saturated fatty acids derived from sheep kidney fat (sheep kidney fat diet) or unsaturated fatty acids derived from sunflower seed oil (sunflower seed oil diet) were fed to rats for a period of 16 weeks and changes in the thermotropic behaviour of liver and heart mitochondrial lipids were determined by differential scanning calorimetry (DSC). The diets induced similar changes in the fatty acid composition in both liver and heart mitochondrial lipids, the major change being the omega 6 to omega 3 unsaturated fatty acid ratio, which was elevated in mitochondria from animals on the sunflower seed oil diet and lowered with the mitochondria from the sheep kidney fat dietary animals. When examined by DSC, aqueous buffer dispersions of liver and heart mitochondrial lipids exhibited two independent, reversible phase transitions and in some instances a third highly unstable transition. The dietary lipid treatments had their major effect of the temperature at which the lower phase transition occurred, there being an inverse relationship between the transition temperature and the omega 6 to omega 3 unsaturated fatty acid ratio. No significant effect was observed for the temperature of the higher phase transition. These results indicate that certain domains of mitochondrial lipids, probably containing some relatively higher melting-point lipids, independently undergo formation of the solidus or gel phase and this phenomenon is not greatly influenced by the lipid composition of the mitochondrial membranes. Conversely, other domains, representing the bulk of the membrane lipids and which probably contain the relatively lower melting point lipids, undergo solidus phase formation at temperatures which reflect changes in the membrane lipid composition which are in turn, a reflection of the nature of the dietary lipid intake. These lipid phase transitions do not appear to correlate directly with those events considered responsible for the altered Arrhenius kinetics of various mitochondrial membrane-associated enzymes.

Animals↗
PubMed2004

Orientation and lipid-peptide interactions of gramicidin A in lipid membranes: polarized attenuated total reflection infrared spectroscopy and spin-label electron spin resonance.

Gramicidin A was incorporated at a peptide/lipid ratio of 1:10 mol/mol in aligned bilayers of dimyristoyl phosphatidylcholine (DMPC), phosphatidylserine (DMPS), phosphatidylglycerol (DMPG), and phosphatidylethanolamine (DMPE), from trifluoroethanol. Orientations of the peptide and lipid chains were determined by polarized attenuated total reflection infrared spectroscopy. Lipid-peptide interactions with gramicidin A in DMPC bilayers were studied with different spin-labeled lipid species by using electron spin resonance spectroscopy. In DMPC membranes, the orientation of the lipid chains is comparable to that in the absence of peptide, in both gel and fluid phases. In gel-phase DMPC, the effective tilt of the peptide exceeds that of the lipid chains, but in the fluid phase both are similar. For gramicidin A in DMPS, DMPG, and DMPE, the degree of orientation of the peptide and lipid chains is less than in DMPC. In the fluid phase of DMPS, DMPG, and DMPE, gramicidin A is also less well oriented than are the lipid chains. In DMPE especially, gramicidin A is largely disordered. In DMPC membranes, three to four lipids per monomer experience direct motional restriction on interaction with gramicidin A. This is approximately half the number of lipids expected to contact the intramembranous perimeter of the gramicidin A monomer. A selectivity for certain negatively charged lipids is found in the interaction with gramicidin A in DMPC. These results are discussed in terms of the integration of gramicidin A channels in lipid bilayers, and of the interactions of lipids with integral membrane proteins.

Electron Spin Resonance Spectroscopy↗
PubMed1997

Effect of co-lipids in enhancing cationic lipid-mediated gene transfer in vitro and in vivo.

Complexes of DNA and cationic lipids are promising vectors for gene transfer. Most cationic lipid formulations contain both a cationic component and a neutral co-lipid. We found that the co-lipid could influence DNA uptake in COS-1 cells, but processes subsequent to uptake were even more important in determining gene expression. We compared dioleoylphosphatidylethanolamine (DOPE) and structural analogs of DOPE combined with cationic lipids and found that DNA uptake and transgene expression did not always correlate. Transgene expression was dependent on DNA uptake into the cell, on entry of DNA into the cytoplasm, and on release of DNA from the lipid complex. We found that some co-lipids had a greater effect on DNA uptake, whereas others had a greater effect on steps subsequent to entry. Based on those results, we tested the hypothesis that co-lipids conferring different properties could be combined to enhance gene transfer. The results showed that a combination of co-lipids had a synergistic effect on expression. We also found that structural analogs of DOPE were more effective than DOPE in enhancing gene transfer to mature human airway epithelia studied in vitro and to mouse lung studied in vivo. These data provide insight into the mechanism by which co-lipids influence cationic lipid-mediated gene transfer and show that optimization of the effects of co-lipids can enhance gene transfer both in vitro and in vivo.

Animals↗
PubMed1978

The role of lipid components of the diet in the regulation of the fatty acid composition of the rat liver endoplasmic reticulum and lipid peroxidation.

The fatty acid compositions of the lipids and the lipid peroxide concentrations and rates of lipid peroxidation were determined in suspensions of liver endoplasmic reticulum isolated from rats fed on synthetic diets in which the fatty acid composition had been varied but the remaining constituents (protein, carbohydrate, vitamins and minerals) kept constant. Stock diet and synthetic diets containing no fat, 10% corn oil, herring oil, coconut oil or lard were used. The fatty acid composition of the liver endoplasmic reticulum lipid was markedly dependent on the fatty acid composition of the dietary lipid. Feeding a herring-oil diet caused incorporation of 8.7% eicosapentaenoic acid (C(20:5)) and 17% docosahexaenoic acid (C(22:6)), but only 5.1% linoleic acid (C(18:2)) and 6.4% arachidonic acid (C(20:4)), feeding a corn-oil diet caused incorporation of 25.1% C(18:2), 17.8% C(20:4) and 2.5% C(22:6) fatty acids, and feeding a lard diet caused incorporation of 10.3% C(18:2), 13.5% C(20:4) and 4.3% C(22:6) fatty acids into the liver endoplasmic-reticulum lipids. Phenobarbitone injection (100mg/kg) decreased the incorporation of C(20:4) and C(22:6) fatty acids into the liver endoplasmic reticulum of rats fed on a lard, corn-oil or herring-oil diet. Microsomal lipid peroxide concentrations and rates of peroxidation in the presence of ascorbate depended on the nature and quantity of the polyunsaturated fatty acids in the diet. The lipid peroxide content was 1.82+/-0.30nmol of malonaldehyde/mg of protein and the rate of peroxidation was 0.60+/-0.08nmol of malonaldehyde/min per mg of protein after feeding a fat-free diet, and the values were increased to 20.80nmol of malonaldehyde/mg of protein and 3.73nmol of malonaldehyde/min per mg of protein after feeding a 10% herring-oil diet in which polyunsaturated fatty acids formed 24% of the total fatty acids. Addition of alpha-tocopherol to the diets (120mg/kg of diet) caused a very large decrease in the lipid peroxide concentration and rate of lipid peroxidation in the endoplasmic reticulum, but addition of the synthetic anti-oxidant 2,6-di-t-butyl-4-methylphenol to the diet (100mg/kg of diet) was ineffective. Treatment of the animals with phenobarbitone (1mg/ml of drinking water) caused a sharp fall in the rate of lipid peroxidation. It is concluded that the polyunsaturated fatty acid composition of the diet regulates the fatty acid composition of the liver endoplasmic reticulum, and this in turn is an important factor controlling the rate and extent of lipid peroxidation in vitro and possibly in vivo.

Animals↗
PubMedDate not supplied

Lipid entrapment and cellular changes in the rat myocard, lung and liver after long-term parenteral nutrition with lipid emulsion. A light microscopic and ultrastructural study.

We have demonstrated organ damage after long-term administration of lipid-based parenteral nutrition, possibly initiated by intravascular pooling of lipid and phagocytes, in both rats and pigs. To evaluate whether accumulation of lipid could simply be caused by mechanical filtration, a comparative study of three separate capillary beds was performed. Rats were given lipid emulsion (n = 5) or isotonic saline (n = 4) through central venous catheters for 3 weeks. Using both light and electron microscopy, lipid accumulation and structural changes in the rat myocard were compared to those in the lung and liver. The study provides evidence that within myocardial capillaries both peripheral blood monocytes and endothelial cells performed phagocytosis of lipid droplets following administration of lipid emulsion, but no large-scale intravascular pooling of lipid resulted. Morphometry of the myocard detected no lipid increase in the myocytes from the rats given lipid emulsion compared with controls and in neither were there any stigmata of vasculitis or myocardial damage, in contrast to the lung and liver, where intravascular pooling of lipid and phagocytes was seen. This indicates that phagocytosis was an important mechanism involved in entrapment and elimination of lipid.

Animals↗
PubMed1976

Lipid metabolism in Achlya: changes in lipid composition during development.

Fractionation of total lipid extracted from Achlya sp. at various stages of its developmental cycle revealed that in spores total lipid was composed of 62% neutral lipid, 13% phospholipid, and 25% glycolipid. After germination, the proportion of neutral lipid rose slightly after 2 h then fell sharply to 10% after 8 h, whereupon it rose to 55% of total lipid after 30 h of growth, when sporulation was completed. Conversely, phospholipid rose to 77% of total lipid after 8 h, then declined to 40% after 30 h. Glycolipid was maintained at 10-20% of total lipid throughout the life cycle after spore germination. Quantitative determination of neutral lipid components by photo-reflectometry showed that triglycerides accounted for 20% of neutral lipid in spores, and free fatty acids made up 50%. During growth, the absolute levels of both components fell precipitously on germination, remained at low levels throughout vegetative growth, and rose at the time of sporulation. The fatty acid composition of total lipid, phospholipid, neutral lipid, and free fatty acid fractions extracted from vegetative and sporulating Achlya cells was determined. The principal fatty acids present in all fractions of both stages of the life cycle were hexadecanoic and octadecanoic acids. Hydroxyhexadecanoic acid, eicosatetraenoic acid, and an unidentified long-chain acid were completely absent from the phospholipids of vegetative cells, although they were found in significant quantities in lipid fractions from other stages of growth.

Fatty Acids, Nonesterified↗