Biomedical subjects

B Landin

Publications and source records attributed to B Landin.

28 records · Page 2Linked to original sources

PubMed1988

Plasma apolipoprotein A-I levels and bile lipid secretion during thoracic duct drainage in the rat.

A large part of the circulating apolipoprotein A-I (apoA-I) is produced by the intestine. Yet the plasma levels of apoA-I are retained or even increased in rats with thoracic duct drainage (Johansson, B. and Nilsson, A, (1981) FEBS Lett. 130, 305-308 and Franzén, J. et al. (1987) Biochim. Biophys. Acta 918, 11-15). In this study we examined the effects of biliary drainage and of combined biliary and lymphatic drainage on the plasma apoA-I levels, and also the effects of lymphatic drainage on the output of biliary lipids in the rat. 63 h of biliary drainage caused a 40% decrease of the serum apoA-I concentration. In contrast the concentration in rats with combined thoracic duct and biliary drainage was 153% of that in control rats. The biliary secretion of bile acids, phosphatidylcholine and cholesterol declined to a lower level in rats with combined thoracic duct and biliary drainage, but increased at the later time intervals to the same levels as in rats with bile fistulas only. Intravenous chyle infusion 3-36 h after commencing the biliary drainage did not prevent the decrease in biliary lipid output. The study thus provided no evidence that the reduced hepatic inflow of apoB-containing lipoproteins during biliary drainage is of importance for the reduced biliary lipid output. The loss of all the chyle lipoproteins leads, however, to an even more pronounced decrease in the biliary lipid secretion. The drainage of all the chyle constituents also leads to an increased apoA-I synthesis that more than compensates for the apoA-I loss in chyle, whereas biliary drainage only lowers the plasma apoA-I levels.

Animals↗

PubMed1988

Metabolism of chylomicron arachidonic and linoleic acid in the rat.

Chyle and chylomicrons, obtained after feeding thoracic duct cannulated rats [3H]arachidonic (20:4) and [14C]linoleic acid (18:2) in cream, were injected i.v. into recipient animals. 7.5-15 min after injection, the 14C/3H ratio of the triacylglycerols remaining in plasma was about half of that in the injected chylomicrons, indicating that the chylomicron remnants formed retained relatively more [3H]20:4 than [14C]18:2. The 14C/3H ratio of plasma diacylglycerols was about 6-fold lower than that of plasma free fatty acids. The proportion of [3H]20:4 found in plasma cholesteryl esters was several-fold higher than that of [14C]18:2. Inhibition of hepatic lipase by a specific antiserum did not significantly influence the clearance of triacylglycerols, but increased the amount of 3H in plasma diacylglycerols. It also prevented the rapid clearance of phosphatidylethanolamine from plasma. The liver uptake of [3H]20:4 exceeded that of [14C]18:2. Antiserum against hepatic lipase diminished the difference. In contrast, the 14C/3H ratio of adipose tissue was higher than that of the injected chyle lipoproteins.

Adipose Tissue↗

PubMed1987

Absorption and lymphatic transport of exogenous and endogenous arachidonic and linoleic acid in the rat.

[3H]Arachidonic (20:4) and [14C]linoleic acid (18:2) were fed to thoracic duct-cannulated rats in test meals of either tracers alone, cream, Intralipid, pure arachidonic acid, or pure linoleic acid. Less [3H]20:4 than [14C]18:2 was recovered in chyle during the first 5 h. After cream feeding, the proportion of radioactivity found in phospholipids was high and increased during the first 3 h. After the meal (3-5 h) 61 +/- 6% of the 3H and 57 +/- 10% of the 14C was in phosphatidylcholine, and 11 +/- 3% of the 3H and 3.0 +/- 4% of the 14C was in phosphatidylethanolamine. Changing the fat vehicle to Intralipid or pure 18:2 decreased the proportion of label in the phospholipids and increased the 3H and 14C radioactivity in the triacylglycerol fraction, the distribution of 14C being influenced more than that of 3H. After feeding the tracers in 200 microliters of pure 20:4, greater than 90% of both isotopes was in triacylglycerol. During fasting, triacylglycerol transported 56% (0.7 mumol/h), phosphatidylcholine transported 34% (0.4 mumol/h), and phosphatidylethanolamine transported 10% (0.1 mumol/h) of the 20:4 mass. After cream or Intralipid feeding, the output of 20:4-containing phosphatidylcholine and phosphatidylethanolamine increased 2.1- to 2.8-fold, whereas the transport of 20:4 with triacylglycerol remained constant. Phospholipids thus became the predominant transport form for 20:4. After feeding 200 microliters of 20:4, the intestine produced, however, 20:4-rich triacylglycerols that transported 89% of the chyle 20:4.

Animals↗

PubMed1987

Factors affecting the impaired hepatic uptake of chylomicron remnants in the cholestatic rat.

We have previously shown that bile duct ligation inhibits the hepatic uptake of chylomicron remnants in rats. In the present study we have investigated different possible causes of this inhibition. Intravenous infusion of bile or sodium taurocholate reduced the hepatic chylomicron remnant uptake. Perfused livers from bile duct-ligated rats metabolized chylomicron remnants at a reduced rate. Rat hepatocyte monolayer cultures metabolized remnants formed in cholestatic rats and those formed in hepatectomized animals equally well, but serum from cholestatic rats inhibited remnant uptake more strongly than control serum. Bile duct ligation did not influence the clearance from plasma of human low-density lipoprotein, and the inhibition of hepatic remnant uptake was not affected by treatment of cholestatic rats with ethinylestradiol. The clearance of 125I-labeled asialofetuin was only slightly impaired by cholestasis, indicating that no strong inhibition of all endocytic processes of the hepatocytes occurred. The reduced hepatic uptake of chylomicron remnants in the cholestatic rat is thus not due to formation of abnormal remnant particles. An increased plasma bile acid concentration rapidly reduced the hepatic remnant uptake without causing any significant hyperlipidemia. However, the pathological lipoproteins accumulating in the cholestatic rat aggravated the hepatic uptake defect even further.

Animals↗

PubMed1987

Hydrolysis of chylomicron arachidonate and linoleate ester bonds by lipoprotein lipase and hepatic lipase.

Chylomicrons labeled with [3H]arachidonic and [14C]linoleic acid were incubated with bovine milk lipoprotein lipase or rat postheparin plasma, containing both lipoprotein lipase and hepatic lipase. During incubation with bovine lipoprotein lipase, [3H]arachidonic acid was released from chylomicron triacylglycerols at a slower rate than [14C]linoleic acid. Only small amounts of [14C]linoleic acid were found as 1,2(2,3)-diacylglycerols, whereas a transient accumulation as [14C]monoacylglycerols was observed. In contrast, significantly more [3H]arachidonic acid was found as 1,2(2,3)-diacylglycerols than as monoacylglycerols at all time intervals investigated. The initial pattern of triacylglycerol hydrolysis by postheparin plasma was similar to that of bovine lipoprotein lipase. However, in contrast to the results obtained with bovine lipoprotein lipase, little [3H]1,2(2,3)-diacylglycerol accumulated. The addition of antiserum to hepatic lipase increased the amount of 3H found in 1,2(2,3)-diacylglycerols and inhibited the formation of free [3H]arachidonic acid. The antiserum also caused a significant inhibition of the hydrolysis of [3H]-but not of [14C]triacylglycerol. With regard to chylomicron phospholipids, the rate of hydrolysis of [14C]linoleoyl phosphatidylcholine with milk lipoprotein lipase was twofold higher than that of the [3H]arachidonyl phosphatidylcholine. However, the hepatic lipase of postheparin plasma had similar activity towards the two phosphatidylcholine species. Postheparin plasma rapidly hydrolyzed chylomicron 3H-labeled and 14C-labeled phosphatidylethanolamine to the same degree, and lipoprotein lipase similarly hydrolyzed 3H-labeled and 14C-labeled phosphatidylethanolamine at approximately equal rates. Antiserum to hepatic lipase inhibited the postheparin plasma hydrolysis of phosphatidylethanolamine and 3H-labeled phosphatidylcholine by about 60%, but the 14C-labeled phosphatidylcholine by only 27%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Rat alpha 1-microglobulin. Purification from urine and synthesis by hepatocyte monolayers.

Rat alpha 1-microglobulin was isolated from the urine of rats treated with sodium chromate, and was purified by the use of gel chromatography, affinity chromatography on concanavalin-A-Sepharose and ion-exchange chromatography. The protein was heterogeneous in charge, had a tendency to form dimers, and was associated with a brown-coloured chromophore. The size of the protein (25 kDa) was similar to guinea pig alpha 1-microglobulin but smaller than the human protein, when measured with sodium dodecyl sulfate/polyacrylamide gel electrophoresis. Immunological cross-reaction with human and guinea pig alpha 1-microglobulin was demonstrated. The concentration of alpha 1-microglobulin in rat serum was 16.4 mg/l (SD = 8.5 mg/l, n = 13) and rat serum alpha 1-microglobulin was eluted from a gel chromatography column at two different positions corresponding to monomeric alpha 1-microglobulin and IgA. The latter alpha 1-microglobulin activity could be absorbed by anti-IgA serum. Rat alpha 1-microglobulin and albumin were continuously released into the medium of rat hepatocyte monolayers, and alpha 1-microglobulin was isolated from the medium by the use of immunoprecipitation with anti-(alpha 1-microglobulin). Tritiated leucine, added to the medium, was incorporated into the protein, suggesting a de novo synthesis of alpha 1-microglobulin by the hepatocytes. The size of hepatic alpha 1-microglobulin was similar to that of purified urinary rat alpha 1-microglobulin, when determined with sodium dodecyl sulfate/polyacrylamide gel electrophoresis.

Animals↗

PubMed1985

Efficient hepatic uptake of chylomicron remnant cholesterol in rats with a portacaval anastomosis.

Portacaval-shunted and sham-operated male rats, fed ad libitum and of similar weight, were studied 2-3 weeks after surgery. At this time serum cholesterol levels did not differ significantly between the two groups, whereas serum triacylglycerols and phospholipids were lower in the shunted group. These animals also showed an increased serum bile acid level and an increased serum estradiol to testosterone ratio. The metabolism of native chyle labeled with [3H]cholesterol and [14C]linoleic acid or of preformed chylomicron remnants with the same labeling was studied in the groups of rats. Ten minutes after intravenous injection of chylomicron remnants 10.6 +/- 0.5% (means +/- SEM, n = 8) of the injected [3H]cholesterol and 7.6 +/- 0.4% of the [14C]linoleic acid were found per 1 g liver in the portacaval-shunted rats; the corresponding figures in the sham-operated group (n = 8) were 6.4 +/- 0.4 and 4.9 +/- 0.3, respectively (p less than 0.001 for both 3H and 14C). Thus, despite a greater than 40% reduction of liver weight induced by the shunting procedure, the total liver uptake of chylomicron remnants was not significantly decreased. The uptake of chylomicron lipids per unit liver weight was normal in the atrophic livers of portacaval-shunted rats also when very large loads of chyle were administered.

Animals↗

PubMed1984

Metabolism of chylomicron phosphatidylethanolamine in the rat.

10 min after intravenous injection of 32P-labelled chylomicrons 69% of the [32P]phosphatidylethanolamine, but only 34% of the [32P]phosphatidylcholine, was cleared from plasma. Over this time period the plasma phosphatidylethanolamine concentration that was increased after the chylomicron injection returned to normal, indicating that the rapid clearance of [32P]phosphatidylethanolamine was primarily due to metabolism and not due to exchange with tissue phospholipids. Also after chylomicron [32P]phospholipids had been transferred to high-density lipoproteins in vitro a greater fraction of [32P]phosphatidylethanolamine than of [32P]phosphatidylcholine was eliminated both in the intact rat and in the perfused rat liver. In the latter system the uptake of [32P]phosphatidylethanolamine was reduced by preperfusion with heparin to remove heparin-releasable hepatic lipase. Experiments with hepatocytes and non-parenchymal liver cells, which both contain only minor amounts of surface-bound hepatic lipase, did not demonstrate any rapid uptake of [32P]phosphatidylethanolamine by exchange with cellular phospholipids. This study shows that there is a mechanism for rapid clearance of chylomicron phosphatidylethanolamine, which maintains a low plasma phosphatidylethanolamine level (30-40 micrograms/ml) despite a significant transport of phosphatidylethanolamine with the intestinal lipoproteins. A major part of the rapid phosphatidylethanolamine metabolism occurs in the liver, where the activity of the hepatic lipase is likely to be of crucial importance.

Animals↗

PubMed1984

A role for hepatic lipase in chylomicron and high density lipoprotein phospholipid metabolism.

The rate of removal of phosphatidylethanolamine and phosphatidylcholine from the plasma of rats treated with antiserum to hepatic lipase was measured. The hepatic lipase antiserum was injected intravenously into animals prior to injection of 32P-labeled chylomicrons or 32P-labeled high density lipoproteins. In experiments in which 32P-labeled chylomicrons were injected, antiserum treatment inhibited removal of [32P]phosphatidylethanolamine from chylomicrons, and the unlabeled serum phosphatidylethanolamine levels increased 2-2.5-fold in 30 min. In contrast, hepatic lipase antiserum had no significant effect on the clearance of chylomicron [32P]phosphatidylcholine or on unlabeled phosphatidylcholine concentrations in serum after injection of chylomicrons. In experiments in which 32P-labeled high density lipoproteins were injected, the inhibitory effect of the antiserum on the rapid removal of [32P]phosphatidylethanolamine from the circulation was even more marked than its effect on the removal from chylomicrons. The removal of high density lipoprotein phosphatidylcholine on the other hand was unaffected by the antiserum, although a moderate increase in serum phosphatidylcholine concentration was seen. In antiserum-treated rats injected with 32P-labeled chylomicrons or high density lipoproteins, hepatic [32P]phosphatidylethanolamine radioactivity was decreased. Significantly more [32P]phosphatidylethanolamine was recovered from blood plus liver in the antiserum-treated rats, indicating that the antiserum inhibited the overall degradation of injected [32P]phosphatidylethanolamine. The data suggest that phosphatidylethanolamine is a preferred substrate for hepatic lipase in the metabolism of chylomicron and high density lipoprotein phospholipid.

Animals↗

PubMedDate not supplied

Follow-up of plasma semicarbazide-sensitive amine oxidase activity and retinopathy in Type 2 diabetes mellitus.

Plasma activity of the enzyme semicarbazide-sensitive amine oxidase (SSAO) is high in diabetes. Production of angiotoxic substances (an aldehyde, hydrogen peroxide, and ammonia) in vessel walls is catalysed by SSAO, suggesting a role for SSAO in the development of complications of diabetes. The objective of the present study was to follow up plasma SSAO activity (measured radiometrically), HbA(1c) (using ion exchange chromatography), and retinopathy (by fundus photography) after 2.8 years, in 34 patients with Type 2 diabetes. We also measured urinary levels of an SSAO substrate, methylamine, by fluorometric high-performance liquid chromatography (HPLC). As at baseline, plasma SSAO activity was now higher in subjects with retinopathy (mean 19.5) than in subjects without retinopathy (mean 16.0), 95% confidence interval (CI) for difference 0.6-6.3 nmol benzylamine ml(-1) plasma h(-1). SSAO activity had not changed significantly since baseline, mean difference -1.65 and 95% CI for difference -3.76 to 0.46 nmol benzylamine ml(-1) plasma h(-1). Mean HbA(1c) level remained higher for patients with retinopathy (now 7.9%) compared to those without retinopathy (6.1%), 95% CI for difference 0.6-3.0%. Comparing baseline and the present study, retinopathy was nonproliferative; level had worsened for five and improved for two patients. Urinary methylamine/creatinine ratio was lower in the group of patients with retinopathy (mean 0.99) than in those without retinopathy (mean 1.78), 95% CI for difference 0.1-1.5 microg mg(-1). The results of the present study are compatible with a role for SSAO in the development of diabetic retinopathy.

Aged↗