Liquid chromatographic assay of cerfuroxime in serum.

We describe a procedure for determining cefuroxime concentrations in serum by using high-performance liquid chromatography. The drug is extracted from serum with dimethylformamide and separated from other substances in the extract by reversed-phase chromatography. The ultraviolet (280-nm) absorption of the effluent was monitored and quantitated based on the height of the cefuroxime peak.

Lipoproteins in plasma from patients with low LCAT activity due to biliary obstruction.

A high density lipoprotein (HDL) fraction, designated cholestatic HDL1, has been isolated by zonal ultracentrifugation from patients with long-standing biliary obstruction. This lipoprotein fraction consists exclusively of disc-shaped particles rich in phospholipid and unesterified cholesterol. The fatty acid composition of the minor cholesteryl ester fraction was characterized by a low content of linoleic acid.

Alterations of lipid metabolism in healthy volunteers during long-term ethanol intake.

Nine young, healthy male volunteers were given ethanol (75 g/day) for 5 weeks. The ethanol was divided into five daily doses and taken so that blood ethanol levels never exceeded 0.04% (w/v).

A stable, radioactive substrate emulsion for assay of lipoprotein lipase.

A method is described for the assay of lipoprotein lipase, using a stable, radioactive substrate emulsion. Fatty acid-labeled trioleoylglycerol was emulsified by homogenization in glycerol with lecithin as detergent. This anhydrous emulsion was stable for at least six weeks.

Hydrolysis of tri- and monoacylglycerol by lipoprotein lipase: evidence for a common active site.

The relationship between triacylglycerol and monoacylglycerol hydrolyzing activities of purified rat heart lipoprotein lipase was studied using emulsified trioleoylglycerol and micellar or albumin-bound monooleoylglycerol as substrates. The maximal reaction rates obtained with the two substrates were similar (650 and 550 nmol of fatty acid released per min per mg of protein, respectively). Addition of apolipoprotein C-II or serum increased the maximal reaction rate for the trioleolyglycerol hydrolyzing activity about four-fold, but had no effect on the monooleolyglycerol hydrolyzing activity.

Intra- and extracellular forms of lipoprotein lipase in adipose tissue.

The location of lipoprotein lipase activity in rat adipose tissue was studied using intact epididymal fat pads, isolated adipocytes, and lipoprotein lipase activity secreted from adipocytes as enzyme sources. The enzyme activities of these preparations were characterized by gel filtration. The method used for isolation of adipocytes had been modified to minimize activation of lipoprotein lipase during the procedures.

Regulation of lipoprotein lipase. Induction by insulin.

Lipoprotein lipase activity in intact epididymal adipose tissue of fasted rats increased rapidly after treatment with insulin in vivo. In contrast, lipoprotein lipase activity in adipocytes isolated from the contralateral fat pads remained essentially unchanged. When adipocytes were incubated for 30 min at ambient temperature in vitro, about 2 times more lipoprotein lipase activity was found in the medium of cells from insulin-treated rats than in medium from cells of control animals.

Effects of apolipoproteins on lipoprotein lipase activity of human adipose tissue.

The effect of apolipoproteins isolated from HDL and VLDL on the activity of lipoprotein lipase (LPL) of adipose tissue was studied. The CII apoprotein was found to activate LPL. This activation was strongly inhibited by CI, AI (apo-Lp-Gln I), and the arginine-rich apoprotein, whereas AII and CIII exhibited a considerably lower inhibitor effect.

Rapid effect on lipoprotein lipase activity in adipose tissue of humans after carbohydrate and lipid intake.

Glucose or corn oil was given perorally to fasting, young healthy volunteers, and the time course of acute effects on lipoprotein lipase activity (LLA) in adipose tissue, plasma glycerol, triglyceride, insulin, and blood glucose levels was followed. After glucose intake, adipose tissue LLA increased rapidly, reaching a maximum of 80 per cent above initial level after 2 h. Plasma glycerol, reflecting the rate of lipolysis of depot lipids, decreased rapidly, temporally well correlated to the LLA changes.