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During the last few years a growing amount of data has accumulated showing phospholipid par tic i pa tion in nu clear sig nal transduction. Very re cent data strongly sup port the hy poth e sis that sig nal transduction in the nu cleus is au to nomic. Lo cal pro duc tion of inositol polyphosphates, be gin ning with the ac ti va tion of phospholipase C is required for their specific function in the nucleus. Enzymes which modify poly- phosphoinositols may control gene expression. Much less information is available about the role of other lipids in nuclear signal transduction. The aim of this minireview is to stress what is cur rently known about nu clear lipids with re spect to nu clear sig nal transduction.
 Wax synthases are membrane-associated enzymes catalysing the esterification reaction between fatty acyl-CoA and a long chain fatty alcohol. In living organisms, wax esters function as storage materials or provide protection against harmful environmental influences. In industry, they are used as ingredients for the production of lubricants, pharmaceuticals, and cosmetics. Currently the biological sources of wax esters are limited to jojoba oil. In order to establish a large-scale production of desired wax esters in transgenic high-yielding oilseed plants, enzymes involved in wax esters synthesis from different biological resources should be characterized in detail taking into consideration their substrate specificity. Therefore, this study aims at determining the substrate specificity of one of such enzymes - the mouse wax synthase. The gene encoding this enzyme was expressed heterologously in Saccharomyces cerevisiae. In the in vitro assays (using microsomal fraction from transgenic yeast), we evaluated the preferences of mouse wax synthase towards a set of combinations of 11 acyl-CoAs with 17 fatty alcohols. The highest activity was observed for 14:0-CoA, 12:0-CoA, and 16:0-CoA in combination with medium chain alcohols (up to 5.2, 3.4, and 3.3 nmol wax esters/min/mg microsomal protein, respectively). Unsaturated alcohols longer than 18°C were better utilized by the enzyme in comparison to the saturated ones. Combinations of all tested alcohols with 20:0-CoA, 22:1-CoA, or Ric-CoA were poorly utilized by the enzyme, and conjugated acyl-CoAs were not utilized at all. Apart from the wax synthase activity, mouse wax synthase also exhibited a very low acyl-CoA:diacylglycerol acyltransferase activity. However, it displayed neither acyl-CoA:monoacylglycerol acyltransferase, nor acyl-CoA:sterol acyltransferase activity.
Background & Aims: Green tea is known worldwide for its high content of polyphenolic compounds and multifactorial beneficial effects on human health. The role of green tea as an inhibitor of lipid hydrolysis is widely discussed. The aim of the study was to assess the influence of green tea extract on lipid digestion and absorption. Methods: The study comprised 32 healthy volunteers aged 23 to 30 years with normal exocrine pancreatic function. In all subjects 13C-labelled mixed triglyceride breath test was performed twice with and without green tea extract ingestion. Cumulative percentage dose recovery was considered to reflect digestion and absorption of lipids. Values are expressed as medians and 1st-3rd quartile distribution. Results: In all subjects, cumulative percentage dose recovery values were normal in a placebo test (36.8% <30.1-43.3%>). These results were significantly higher (p=0.021) than those obtained in green tea extract test (28.8% <23.1-37.2%>). Results of six tests with GTE were abnormal. Conclusions: Single dose of green tea extract taken with a test meal decreases lipid digestion and absorption in humans.
IL-6 is a biologically active substance and is thought to contribute to the development of obesity. Recent findings suggest that susceptibility to intracellular lipid accumulation is to a large extent determined by changes in the expression of fatty acid transporters such as FAT/CD36, FABPpm and FATP-1. The aim of the present study was to determine the effect of IL-6 deficiency on the expression of fatty acid transporters, as well as, assess the concomitant changes in intracellular lipids. We found that Il-6 deficiency upregulated the myocardial expression of FAT/CD36 (+40%) and did not significantly affect the content of FABPpm and FATP-1 (+15% and +5% respectively). Although no change in the intramyocardial total lipid content was noted, there was a significant increase in the intracellular content of both free fatty acid (FFA), diacylglicerol (DG) and ceramide fractions (+45%, +37% and +48%, respectively) in hearts from IL-6 -/- mice. A trend for IL-6 deficiency to increase in saturated FA species in these fractions was also observed (+8%, +12% and +10%, respectively). In contrast, IL-6 deficiency has no effect on the content of monounsaturated fatty acid (MUFA) and polyunsaturated fatty acid (PUFA) species in each intramyocardial lipid fractions examinated. These findings suggest that IL-6 deficiency results in 1) upregulation of myocardial content of FAT/CD36, 2) the increase in the content of biologically active lipid pools (FFA, DG and ceramide). This lipid accumulation with concomitant trend for increase in the saturation status of these lipid fractions may, at least in part, provide a factor related to the development of intramyocardial lipotoxicity, observed in obese individuals.
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