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Biomedical subjects

Y Stein

Publications and source records attributed to Y Stein.

At least 271 records · Page 15Linked to original sources
PubMed1967

Lipid synthesis, intracellular transport, storage, and secretion. I. Electron microscopic radioautographic study of liver after injection of tritiated palmitate or glycerol in fasted and ethanol-treated rats.

A time sequence study of intracellular movement of labeled lipid in the liver was carried out on fasted and ethanol-treated rats injected with either palmitate-(3)H or glycerol-(3)H by electron microscopic radioautography. The elimination of water-soluble lipid precursors during specimen preparation was checked and found to be complete. The labeled lipid product in the tissue was identified as mostly triglyceride. A dehydration procedure was adapted to minimize the loss of lipid during specimen preparation. At 2 min after injection, the earliest time interval studied, both precursors were found to have penetrated the liver cells, and the label was found over both rough and smooth elements of the endoplasmic reticulum, which is the site of glyceride esterification. From 5 min on, in fasted and especially in ethanol-treated rats, the label was seen also over lipid droplets 0.5-2.0 micro in diameter, which represent "storage lipid" (slowly turning over compartment). Mitochondria became labeled mostly at later time intervals after injection. From 10 min on, concentration of label was seen over the Golgi apparatus, containing small osmiophilic particles. Association of label with groups of particles in smooth-surfaced vesicles and vacuoles in and near the Golgi apparatus and in the vicinity of the sinusoidal border was seen, both after palmitate-(3)H and glycerol-(3)H. It is proposed that these particles represent lipoproteins which are formed in the endoplasmic reticulum, "processed" in the Golgi apparatus, and transported in vacuoles to the sinusoid surface to be discharged into the circulation.

Adipose Tissue↗
PubMed1967

Lipid synthesis, intracellular transport, and secretion. II. Electron microscopic radioautographic study of the mouse lactating mammary gland.

In the mammary glands of lactating albino mice injected intravenously with 9, 10-oleic acid-(3)H or 9, 10-palmitic acid-(3)H, it has been shown that the labeled fatty acids are incorporated into mammary gland glycerides. The labeled lipid in the mammary gland 1 min after injection was in esterified form (> 95%), and the radioautographic reaction was seen over the rough endoplasmic reticulum and over lipid droplets, both intracellular and intraluminal. At 10-60 min after injection, the silver grains were concentrated predominantly over lipid droplets. There was no concentration of radioactivity over the granules in the Golgi apparatus, at any time interval studied. These findings were interpreted to indicate that after esterification of the fatty acid into glycerides in the rough endoplasmic reticulum an in situ aggregation of lipid occurs, with acquisition of droplet form. The release of the lipid into the lumen proceeds directly and not through the Golgi apparatus, in contradistinction to the mode of secretion of casein in the mammary gland or of lipoprotein in the liver. The presence of strands of endoplasmic reticulum attached to intraluminal lipid droplets provides a structural counterpart to the milk microsomes described in ruminant milk.

Animals↗
PubMedDate not supplied

Effects of smoking and physical activity on serum uric acid in a Jerusalem population sample.

In 932 adult males and 531 adult females, we found large independent correlations of serum uric acid (SUA) with body mass and serum creatinine. In males, but not in females, SUA was lower in smokers than in non-smokers and in men who reported themselves to be physically active, compared to non-active men. After controlling for confounding variables by multiple regression analysis, we found that smoking remained a significant predictor of SUA in males (P = 0.003) but the effects of reported physical activity dropped to borderline significance (P = 0.056). In females, no significant relationship of SUA with reported physical activity was seen. These results, the first from an unselected free-living Israeli population, are generally in agreement with previously reported studies.

Adult↗
PubMedDate not supplied

Expression of lipoprotein lipase mRNA in rat heart is localized mainly to mesenchymal cells as studied by in situ hybridization.

The expression of lipoprotein lipase mRNA (LPL mRNA) was studied in rat hearts by use of a sulfur-35-labeled antisense mRNA probe. Rats were studied under three conditions: fed, fasted, and injected with cholera toxin (an irreversible agonist of adenylate cyclase) and then fasted. The highest LPL activity was found in the hearts of cholera toxin-injected, fasted rats. After injection of cholera toxin, LPL mRNA levels were 3.5-fold higher than those from fed rats. Using in situ hybridization, we studied the site of expression of LPL mRNA under the same three experimental conditions. In sections of hearts from cholera toxin-injected, fasted rats, concentrations of autoradiographic grains, representing the site of LPL mRNA, were seen over interstitial elements, which comprise capillary and perivascular cells. A more diffuse and sparse reaction was seen over cardiac myocytes and was not always distinguishable from background. A similar but much less definitive localization was seen in sections of hearts from fasted rats. The present results indicate that in the rat heart, the main site of LPL synthesis and processing, especially after stimulation with an irreversible agonist of adenylate cyclase, is localized to interstitial elements rather than to adult cardiac myocytes.

Adenylyl Cyclase Inhibitors↗
PubMedDate not supplied

Use of 3H-cholesteryl linoleyl ether for the quantitation of plasma cholesteryl ester influx into the aortic wall in hypercholesterolemic rabbits.

In this study use was made of 3H-cholesteryl linoleyl ether CLE), a nondegradable analogue of cholesteryl ester (CE) to measure plasma lipoprotein CE influx into rabbit aorta. Autologous serum labeled with 3H-CLE was injected into seven hypercholesterolemic rabbits, and more than 90% of the label was recovered in the plasma compartment 10 minutes after injection. Between 4 hours and 3 days the label was cleared from the circulation with a t1/2 of about 24 hours. Between 4 and 24 hours the lipoproteins isolated at d less than 1.006, d less than 1.019, and d less than 1.063 approached similar specific activity, assuming that 3H-CLE had mixed with the lipoprotein CE pool. The rabbits were killed 7 to 14 days after injection when plasma radioactivity decreased to less than 0.03% of injected dose/ml. Total recovery of the CLE ranged from 70% to 95% and 48% to 72% were found in the liver. The minimum influx of plasma CE into the aortic intima was determined by dividing the label found in the artery by the mean specific activity of the labeled compound in the plasma. The minimum influx into regions with atheromatous involvement ranged from 0.8 to 3.4 micrograms CE/cm2/hr. The rate of influx was highly correlated with the amount of CE mass in the intima and media indicating that the bulk of aortic CE is derived from plasma lipoprotein CE. The method described might be useful in distinguishing between possible effects of "antiatherogenic" drugs on plasma CE influx into the aortic wall from an effect on intracellular CE hydrolysis and subsequent efflux of free cholesterol from the artery.

Animals↗
PubMedDate not supplied

Effect of weight loss in moderate obesity on plasma lipoprotein and apolipoprotein levels and on high density lipoprotein composition.

Plasma lipids, lipoprotein and apolipoprotein levels were determined in seven women and seven men with moderate obesity before, during 7 weeks of continuous weight loss (10.4% to 9.6% of body weight, 1000 kCal/day diet), and after 3 months at a stable, reduced weight. Plasma triglyceride levels decreased by 30.4% in men and by 39.4% in women (p less than 0.0001) after 1 week of caloric restriction and remained at this level throughout the study period. The plasma cholesterol decreased by 19.0% in men (p less than 0.001) and by 10.9% in women (p less than 0.01) in the period of active weight loss, but returned to prediet values after stabilization at a leaner body mass. Similar changes were observed in LDL cholesterol levels. No change in high density lipoprotein (HDL) cholesterol levels occurred during active weight reduction, but after 3 months at a reduced weight, a significant increase in HDL cholesterol was evident, and the ratio of HDL cholesterol to plasma cholesterol increased over prediet values (p less than 0.001), women). Separation of HDL subpopulations by zonal ultracentrifugation before and after weight reduction revealed that HDL2 increased slightly in men and decreased slightly in women. In both genders, HDL3 tended to decrease after weight reduction. Plasma levels of apolipoprotein A-I decreased during active weight loss, but this was significant only in women (p less than 0.05). After 3 months of reduced weight, plasma apo A-I increased to prediet levels. No significant changes in plasma apo A-II or apo E were noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

In vitro metabolism of LDL labeled with a nondegradable cholesteryl ester analogue.

Low density lipoprotein (LDL) metabolism by human skin fibroblasts was studied using LDL labeled in the neutral lipid fraction with a nonhydrolysable cholesteryl ester analogue 3H-cholesteryl linoleyl ether (3H-CLE-LDL). LDL uptake could be quantitated accurately using 3H-CLE-LDL, since the label accumulated intracellularly due to its resistance to hydrolysis. 3H-CLE-LDL was taken up via apo B,E receptor-mediated endocytosis in a manner similar to 125I-labeled LDL. This was demonstrated by similar rates of uptake of the two differently labeled LDL preparations, saturation kinetics of uptake with respect to 3H-CLE-LDL concentration, regulation of 3H-CLE-LDL uptake by procedures that up-regulate or down-regulate the number of apo B,E receptors, and negligible uptake of 3H-CLE-LDL by receptor-negative cell strains. The major difference between the handling of 125I-LDL and 3H-CLE-LDL was the finding that, while the amount of trypsin-releasable (surface) 3H-CLE increased progressively over a 24-hour experimental period, trypsin-releasable 125I-LDL reached a maximum within 30 minutes. After 24 hours of incubation, the 3H radioactivity released by brief trypsinization was three to four times higher than could be accounted for by 125I radioactivity released by a similar treatment. Possible reasons for this behavior are discussed.

Cholesterol↗
PubMedDate not supplied

Verapamil enhances receptor-mediated endocytosis of low density lipoproteins by aortic cells in culture.

Bovine aortic endothelial and smooth muscle cells (SMC) and human skin fibroblasts (HSF) were used to study the effect of verapamil on cellular interactions with human low density lipoprotein (LDL). Verapamil, 10 to 50 microM, increased 125I-LDL uptake and degradation by 70% to 200% in the various cells after 24 to 48 hours of incubation. The increase in the total amount of LDL endocytosed, labeled with 3H-cholesteryl linoleate (3H-CL), was comparable to that determined with 125I-LDL. In HSF and SMC, a delay in 125I-LDL degradation and hydrolysis of 3H-CL was seen in cells treated for 3 to 24 hours with verapamil. Pretreatment of HSF with 50 microM verapamil for 24 hours and incubation with 2 to 50 micrograms 125I-LDL protein/ml for 1 hour resulted in a 50% to 200% increase in heparin releasable and in a 40% to 130% increase in cellular 125I-LDL. Thus, the increase in 125I-LDL binding and uptake in verapamil-treated cells was apparently due to an increase in receptor number, rather than in receptor affinity. The effect of verapamil on LDL uptake and degradation was also seen in cells that were pretreated for 24 hours and incubated with 125I-LDL in the absence of verapamil. The effect of verapamil was not apparent in LDL receptor-negative cells. Cycloheximide blocked the verapamil effect. The Na+ channel blocker, tetrodotoxin x 10(-6) M, caused a 30% to 50% increase in the total amount of LDL endocytosed, but no delay in LDL degradation; amiloride 2 x 10(-3) M was not effective. If the presently described effect of verapamil also occurs in vivo, this might contribute to the reported beneficial effects of Ca++ channel blockers in experimental atherosclerosis by promoting transfer of LDL cholesteryl ester from the aortic interstitium to a catabolic compartment.

Animals↗