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H Bar-On

Publications and source records attributed to H Bar-On.

At least 55 records · Page 3Linked to original sources
PubMed1985

Hepatotoxicity of hornet's venom sac extract in isolated perfused rat liver.

The changes in the activity of some enzymes in parenchymal liver cells were measured in the perfusate of rat isolated liver after a single envenomation with two different doses of Hornet's (Vespa orientalis) venom sac extract (VSE). The maximal observed enzymatic changes were significant: twenty four fold rise of alkaline phosphatase E.C.3.1.3.1(ALP), six fold rise of alanine aminotransferase E.C.2.6.1.2. (ALT) and nine fold rise of aspartate aminotransferase E.C.2.6.1.1. (AST) activity. There were moderate changes (four fold) in lactic dehydrogenase activity E.C.1.1.1.2.7. (LDH) and a non-significant change in gamma-glutamyl-transferase E.C.2.3.2.1. (GGT) activity. These changes varied with the venom's dose. Also a decrease in the rate of effluent draining out via the hepatic vein was noted as an additional sign of liver damage. In light of the biochemical evidence presented here, as well as in previous work, it seems that no further biochemical proof is needed to establish the hepatotoxicity of VSE in rats, cats and probably humans too. It seems that VSE is a predictable hepatotoxin causing a pattern of enzyme changes of the cholangiocellular type.

Alanine Transaminase↗
PubMed1984

Comparative pharmacokinetic analysis of a novel sustained-release dosage form of theophylline in humans.

The pharmacokinetics and relative bioavailability of theophylline from a new sustained-release formulation ( Theotard ) and from a standard sustained-release formulation (Theo-Dur) were compared in 6 healthy, adult, male volunteers. After a single oral dose of 300 mg Theotard , a mean maximal plasma concentration ( Cbmax of 3.49 +/- 1.05 mg/l was obtained after 8 h (tmax). After an identical dose of Theo-Dur, a peak plasma concentration of 4.68 +/- 1.33 mg/l was obtained after 6.33 h. The mean relative bioavailability of theophylline from Theotard was 1.02 +/- 0.16 relative to that of Theo-Dur. In 5 of the volunteers the Theotard formulation exhibited a more prolonged and uniform absorption rate and yielded more sustained plasma levels.

Adult↗
PubMed1983

Bile salts facilitate the absorption of heparin from the intestine.

Heparin was absorbed through the rectal mucosa of rodents and primates only when administered in solutions containing sodium cholate or sodium deoxycholate (DOC). The absorption of heparin was monitored by following the increase in plasma radioactivity after administration of [35S]heparin, and by measurement of its biological effects: plasma lipase activity and prolongation of partial thromboplastin time (PTT). Following administration of the same concn of heparin in solutions lacking bile salts, there was almost no radioactivity in the blood, no prolongation of PTT and no release of plasma lipase activity. The PTT effect was found to be a less sensitive test of heparin absorption than the plasma lipase activity.

Animals↗
PubMed1982

Association of blood pressure with ethnic origin in 17-year-olds: the Jerusalem Lipid Research Clinic Prevalence Study.

Blood pressure and pulse rate were measured in a random sample of 1,200 17-yr-old Jewish boys and girls examined in 1976-79 during Visit 2 of the Lipid Research Clinic Prevalence Study. Mean systolic pressures were 110.1 and 106.1 mm Hg in boys and girls, respectively, diastolic pressures 69.9 and 70.4, pulse pressure 40.2 and 35.7, pulse rates 73.3 and 77.3 beats/min, and double products 8,082 and 8,228 mm Hg x beat x min-1. Multiple regression analysis showed that there were significant differences in systolic pressures between boys and girls whose fathers had immigrated from different countries, pressures being highest in those of European origin and lowest in those of North African origin. These differences were of the order of 3 to 4 mm Hg and were not explained by the distribution of height, Quetelet index, skinfold thickness, smoking, drinking, social class or education of subject. Pulse pressures followed a similar pattern, but the differences between origin groups were significant only for boys. Diastolic pressures and pulse rates did not vary with origin.

Adolescent↗
PubMed1981

Origin and pattern of glucocorticoid-induced hyperlipidemia in rats. Dose-dependent bimodal changes in serum lipids and lipoproteins in relation to hepatic lipogenesis and tissue lipoprotein lipase activity.

Rats maintained for five days on a low dose of triamcinolone (0.5 mg/kg) showed a 2-fold increase in serum triacylglycerol concentration, paralleled by a rise in all very low density lipoprotein (VLDL) components but no significant change in serum cholesterol or high density lipoproteins (HDL). In contrast, a high dose of triamcinolone (12.5 mg/kg) produced a fall in triacylglycerol and VLDL to the range of control levels coincident with doubling in serum cholesterol and HDL. The rise in VLDL was attributed in a large part to enhanced hepatic fatty acid synthesis as evident from the marked rises in activity of rate-limiting enzymes of lipogenesis and in 3H incorporation into liver and serum fatty acids from in vivo administered 3H2O. The induction of fatty acid synthesis was linked to pronounced hyperinsulinemia, elicited by the triamcinolone treatment, to which the liver remained selectively responsive, contrary to the general insulin antagonism in peripheral tissues. Triamcinolone treatment also resulted in small rises in serum glucagon but these changes did not appear to be of importance for the observed bimodal serum lipoprotein perturbations. Dexamethasone, prednisolone and cortisol, administered in doses equipotent to 0.5 mg/kg triamcinolone, produced similar changes in the levels of serum triacylglycerol and insulin and activities of hepatic enzymes of lipogenesis.

Acetyl-CoA Carboxylase↗
PubMed1981

Lipoprotein secretion by isolated perfused livers from streptozotocin-diabetic rats.

In liver perfusion from sucrose-fed, streptozotocin-diabetic rats there was in comparison with normal animals, a decrease in very low density lipoprotein concentration in the perfusion medium (38.6 +/- 6.3 versus 64.4 +/- 8.4 microgram . g liver -1 3 h-1, p less than 0.05) and an increase in high density lipoprotein concentration (33.5 +/- 6.5 versus 14.0 +/- 1.9 microgram . g liver-1 3 h-1, p less than 0.005), which was paralleled by enhanced secretion of apoprotein A-I. The triglyceride: protein ratio was lower in very low density lipoprotein from diabetic animals (8.8 versus 13.4). Analysis of the apoprotein composition showed that diabetic very low density lipoprotein lacked arginine-rich protein (apo-E) and apo-C peptides; diabetic high density lipoprotein also lacked arginine-rich protein but contained more A-IV and apo-C-peptides. This may indicate net transfer of C peptides to high density lipoprotein from the degradation of very low density lipoprotein particles. The ratio of 3H-leucine: 14C-glucosamine incorporation was decreased in all diabetic lipoprotein classes suggesting increased glycosylation of apoproteins. These changes in particle composition may influence lipoprotein metabolism in diabetes through their effects on lipoprotein lipase and lecithin cholesterol acyl transferase activity, plasma half-life and tissue binding.

Animals↗
PubMed1981

Role of the liver in the degradation of very low density lipoproteins: a study of lipolysis by heparin releasable liver lipase and uptake during isolated rat liver perfusion.

The role of the liver and of a heparin-releasable liver lipase in the metabolism of very low density lipoprotein (VLDL) was investigated in vitro and during recycling rat liver perfusion. Rat plasma VLDL and nascent hepatic VLDL were labelled biosynthetically in their lipid moieties. Incubation in vitro of VLDL with the lipase caused hydrolysis of VLDL-triglycerides (greater than 80%) and VLDL-phosphatidylcholine (greater than 30%). Nascent VLDL was a better substrate for the enzyme. The hydrolytic activities were inhibited by 70--90% when rat plasma (10--30 vol%) was added to the incubation mixture. VLDL-triglycerides and cholesterol esters were taken up by the liver during 180 min recycling perfusion. The rate of disappearance of nascent VLDL was faster than that of plasma VLDL (half-life times of 56.2 +/- 13.9 and 125.0 +/- 24.8 min respectively). Injection of heparin into the perfusion medium caused accelerated uptake of the hydrolysed VLDL-triglyceride by the liver. Addition of plasma (d greater than 1.006 g/ml) to the perfusion at a concentration of 10 vol% delayed the rate of disappearance of VLDL from the perfusate by about 50--75%. These studies have established the capacity of the hepatic lipase to hydrolyse VLDL-lipids and the ability of the liver to degrade nascent and plasma VLDL particles. These two activities, however, are depressed by plasma and therefore previous studies of VLDL metabolism may have to be re-examined when based on incubations or perfusions in the absence of plasma.

Animals↗
PubMed1981

Enteral administration of insulin in the rat.

1 The effect of the surfactant, Cetomacrogol 1000, on the absorption of insulin across the rectal mucosa has been studied. 2 Rectal administration of microenemata containing Cetomacrogal 1000 and insulin causes a rise in the plasma concentration of insulin and a consequent fall in the blood glucose concentration in diabetic and non-diabetic rats. 3 The hypoglycaemic response is dependent on both the concentration of surfactant and the dose of insulin administered. 4 The results suggest that the transport of insulin across the rectal mucosa is facilitated by Cetomacrogal 1000.

Animals↗
PubMed1981

Evidence for a new cause of defective plasma removal of very low density lipoproteins in insulin-deficient rats.

These studies were initiated to see if factors other than reduced lipoprotein lipase activity might contribute to the defect in plasma removal of very low density lipoprotein (VLDL) that is observed in insulin-deficient rats. VLDL-triglyceride (TG) was labeled in vivo with 3H-glycerol in control and diabetic rats, and aliquots of plasma containing 3H-VLDL were injected into normal recipient rats. The half-time (t 1/2) of removal was almost twice as long when plasma from diabetic rats was injected, and this was true when the diabetic rats were fed either sucrose or regular chow. A comparable increase in t 1/2 was observed when 3H-VLDL isolated from normal rats was recombined with VLDL-free plasma from control and diabetic rats and injected into normal recipients. As before, the changes observed were not dependent upon antecedent diet. However, no significant difference in t 1/2 was observed when 3H-VLDL was isolated from control and diabetic rats and injected into normal recipients. Thus, there appears to be a factor present in VLDL-free plasma obtained from diabetic rats that interferes with removal of VLDL from the vascular compartment. Whether this factor is found in diabetic plasma in vivo, or is transferred from diabetic VLDL to diabetic plasma in the isolation procedure, remains to be clarified. In either event, there appears to be a factor, other than reduced LPL activity, that may play a role in the defect of VLDL-TG removal seen in insulin deficiency.

Animals↗
PubMed1981

Patterns of glucose intolerance and free fatty acid behavior in viral hepatitis.

Twenty-one viral hepatitis patients underwent i.v. glucose tolerance tests during the acute phase of the illness. The results, expressed as the constant of glucose disappearance (Kg), were compared with those of 10 healthy control subjects. When the patients were grouped according to Kg-less than 0.9 or greater than 1.2 min-1-it was found that eight showed a delayed glucose disappearance together with a moderate hypoinsulinemic response (pattern 1). Another eight showed a normal glucose disappearance together with a hyperinsulinemic response (pattern 2). Five patients had intermediate Kg values. High levels of plasma free fatty acids (FFA) were a consistent finding in all patients, indicating that unrestrained lipolysis is an important feature of hepatitis. The extent of decrease in plasma FFA in response to the glucose load was markedly lower in all hepatitis patients than in the control subjects; the rate of decrease was most delayed in the pattern 1 patients. This suggested that the increased FFA availability is an expression of adipose tissue insulin resistance, which, in contrast to glucose disappearance, remains uncompensated by the relative hyperinsulinemia. It may contribute to the diminished peripheral glucose utilization, particularly in pattern 1 patients. We conclude that the different patterns of response in hepatitis may be discerned in one patient group by extending the diagnostic criteria of the glucose tolerance test. In addition to the differences in the magnitude of the peripheral insulin resistance, the main distinction between the two patterns lies in the capacity of the pancreas to adjust insulin secretion in order to maintain normal glucose homeostasis.

Adolescent↗
PubMed1981

Lipoprotein profiles in a heterogeneous group of patients with nephrotic syndrome.

Lipoprotein composition was determined by ultracentrifugation in 13 unselected hospitalized patients with nephrotic syndrome (proteinuria 6.2 +/- 0.5 g/24 h) and compared with that of 13 healthy subjects. Plasma levels of cholesterol and triglycerides (TG) were 407 +/- 45 (mean +/- SE) and 285 +/- 35 mg/dl in the patients vs. 195 +/- 11 and 108 +/- 12 mg/dl in the control group. Type IIb was the only hyperlipoproteinemia pattern in 10 patients (77%). The protein component of very low density lipoproteins (VLDL) was the only slightly elevated, but cholesterol and TG were markedly increased in relation to protein. Low density lipoproteins (LDL) were considerably elevated, and their cholesterol and TG components rose in relation to protein. Of interest was a small but distinct rise in high density lipoproteins (HDL), which was not observed by other investigators studying patients mostly with higher proteinuria and VLDL elevations. The mean HDL/LDL cholesterol ratio, and apparent atherogenic index, was not significantly reduced. Both plasma cholesterol and TG were inversely related to plasma albumin. Plasma cholesterol and even HDL cholesterol were positively related to proteinuria. The finding that in nephrosis with moderate proteinuria all lipoproteins are elevated and enriched in their lipid content, and that HDL rise along with VLDL--contrary to their reciprocal behavior in other lipoproteinemias--indicates that the elevation was due to a universal increase in lipoprotein synthesis. With regard to atherogenicity of nephrosis, no salient, general lipoprotein-related change was discerned. An individual appraisal of lipoprotein composition, including the extent of urinary HDL loss, is suggested.

Adolescent↗
PubMed1980

Protein and glycoprotein synthesis and secretion by the diabetic liver.

Protein and glycoprotein synthesis and secretion by isolated perfused livers and isolated hepatocytes from control and streptozotocin diabetic rats have been investigated. (3)H-Leucine and (14)C-glucosamine incorporation were used as markers for protein and glycoprotein synthesis and secretion. Total protein secretion was reduced by 50% in the perfusate (p < 0.001) and by 36% in hepatocytes (p < 0.05), but glycoprotein secretion was unchanged in both preparations from diabetic animals. These differences were not due to changes in the available pool sizes of the different labels. On liver fractionation, all membrane components from the liver of diabetic animals had lowered (3)H-leucine: (14)Cd-glucosamine ratios in relation to the control animals. This was caused by enhanced glucosamine incorporation in relation to that of leucine. It is suggested that whereas protein synthesis is decreased in acutely diabetic rats, the production of glycoproteins is normal and occurs by the same pathway as in control animals.

Animals↗