Retinyl ester secretion by intestinal cells: a specific and regulated process dependent on assembly and secretion of chylomicrons.
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Retinyl esters (RE) have been used extensively as markers to study chylomicron (CM) catabolism because they are secreted in the postprandial state with CM and do not exchange with other lipoproteins in the plasma. To understand the mechanism of secretion of RE by the intestine under the fasting and postprandial states, differentiated Caco-2 cells were supplemented with radiolabeled retinol under conditions that support or do not support CM secretion. We observed that these cells assimilate vitamin A by a rapid uptake mechanism. After uptake, cells store retinol in both esterified and unesterified forms. Under fasting conditions, cells do not secrete RE but secrete free retinol unassociated with lipoproteins. Under postprandial conditions, cells secrete significant amounts of RE only with CM. The secretion of RE with CM was independent of the rate of uptake of retinol and intracellular free and esterified retinol levels, and was absolutely dependent on the assembly and secretion of CM. The secretion of RE was correlated with the secretion of CM and not with the secretion of total apolipoprotein B. Inhibition of CM secretion by Pluronic L81 decreased the secretion of RE and did not result in their increased secretion with smaller lipoproteins. These data strongly suggest that RE secretion by the intestinal cells is a specific and regulated process that occurs in the postprandial state and is dependent on the assembly and secretion of CM. We propose that RE are added to CM during final stages of lipoprotein assembly and may serve as signposts for these steps. (+info)
Influence of a high ambient temperature on lipid metabolism in the growing pig.
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Because pigs are fatter when they are heat-stressed, it was hypothesized that lipid metabolism is enhanced in heat-stressed pigs. To test this hypothesis, an experiment was conducted to determine the influence of a high ambient temperature on the level of plasma lipids, thyroid hormones, lipoprotein lipase activity, and on the composition of very low density lipoproteins (VLDL) and chylomicrons in the growing pig. Twelve Large White x Landrace castrated male pigs with an initial weight of 20 +/- 0.6 kg were allotted to one of the following treatments: 1) ambient temperature of 31 degrees C, with ad libitum access to feed or 2) ambient temperature of 20 degrees C and fed the amount consumed by those kept at 31 degrees C until 35 kg BW. Ambient temperature did not affect piglet performance. Compared to that in pigs kept at 20 degrees C, in pigs kept at 31 degrees C the lipid content of backfat was 26% higher and the proportion of flare fat was increased by more than twofold (P < 0.001). Lipoprotein lipase activity was increased more than twofold in backfat and nearly twofold in leaf fat at 31 vs 20 degrees C (P < 0.001). In warmth-exposed (31 degrees C), feed-restricted pigs, the plasma level of triiodothyronine was 30% lower than at 20 degrees C (P < 0.001), whereas VLDL-lipid concentration was more than fourfold higher, and plasma concentrations of NEFA and triglycerides were 2.6- and 3.6-fold higher, respectively (P < 0.001). In conclusion, the chronic exposure of growing pigs to a high ambient temperature enhances lipid metabolism in both the liver (VLDL production) and the adipose tissue (lipoprotein lipase activity). Consequently, plasma triglyceride uptake and storage are facilitated in the adipose tissue, which results in greater fatness. (+info)
In addition to the high-density lipoprotein fraction, apolipoprotein C-III is detected in chylomicrons and the very low-density lipoprotein fraction from serum of normolipidemic cows.
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Apolipoprotein (apo) C-III is a low-molecular-mass protein that is involved in the regulation of the triglyceride metabolism. Except for the hyperlipidemic calf, cattle apoC-III is mainly detected in the high-density lipoprotein (HDL) fraction, and the distribution in chylomicrons (CM) and the very low-density lipoprotein (VLDL) fraction has not yet been clarified. The purpose of the present study was to detect apoC-III in concentrated CM and VLDL fractions to examine whether apoC-III is distributed in the two fractions even in normolipidemic cattle. ApoC-III could be detected by immunoblot analysis in both concentrated cow CM and VLDL fractions, but not in the corresponding calf fractions. These results suggest that apoC-III is distributed in the CM and VLDL fractions, at least in cows, although the concentrations in these fractions are considerably lower than in the HDL fraction. (+info)
The effect of estrogen on the lipoprotein lipase activity of rat adipose tissue.
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The effect of 17beta-estradiol or progesterone administration on adipose tissue lipoprotein lipase activity was studied in male and ovariectomized female rats. Lipoprotein lipase activity was measured in acetone-ether-extracted preparations of adipose tissue with doubly labeled (14C-fatty acid, 3H-glyceryl) chylomicron triglyceride as substrate. Administration of 17beta-estradiol to male rats lowered adipose tissue lipoprotein lipase activity from 8.22 plus or minus 1.8 U/g (1 U = 1 mumol triglyceride hydrolyzed per h) to 4.96 plus or minus 0.5 U/g in the treated group. Ovariectomy increased adipose tissue lipoprotein lipase activity from 10.4 plus or minus 1.8 U/g in controls to 22.7 plus or minus 4.3 U/g. 17beta-Estradiol administration to ovariectomized rats cuased a marked fall in adipose tissue lipoprotein lipase activity: 17beta-estradiol (2.5 mug/day) lowered the enzyme activity to 9.00 plus or minus 1.2 U/g, whereas 25 mug/day further decreased lipoprotein lipase activity to 3.2 plus or minus 0.6 U/g. Blood triglyceride levels increased from 0.8 plus or minus 0.05 mumol/ml in ovariectomized rats to 1.4 plus or minus 0.09 mumol/ml in 25 mug/day 17beta-estradiol-treated rats. Progesterone administration did not affect adipose tissue lipoprotein lipase activity in either male or ovariectomized rats. Heart and lung lipoprotein lipase activity was unaffected by hormone treatment. We suggest that the rise in blood triglyceride concentrations, which accompanies high palsma estrogen levels, could be due to the marked inhibition of adipose tissue lipoprotein lipase activity. (+info)
7-Ketocholesterol delivered to mice in chylomicron remnant-like particles is rapidly metabolised, excreted and does not accumulate in aorta.
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Cholesterol oxidation products (oxysterols) have been implicated in atherogenesis due to their presence in atherosclerotic tissue and their potent effects in vitro. One of the major oxysterols currently of interest is 7-ketocholesterol (7K) and it has been suggested that the diet is an important source of this oxysterol. This investigation tested the hypothesis that 7K, delivered in a physiologically relevant vehicle, chylomicron remnant-like emulsion (CMR), would be metabolised and excreted by mice in a similar manner and to a similar extent as previously observed in rats when delivered in a chemically modified lipoprotein, acetylated low-density lipoprotein (acLDL). Indeed, the metabolism of 14C-7K delivered in CMR mirrored that of acLDL and was much more rapid than (3)H-cholesterol delivered simultaneously. The 7K-derived (14)C was cleared from the liver, appeared in the intestine and was excreted in the faeces. A substantial proportion of the 7K-derived (14)C in the intestine and faeces was aqueous-soluble, indicating metabolism to polar products, presumably bile acids. Moreover, while cholesterol-derived (3)H increased in the aorta, (14)C appeared transiently and there was no observable accumulation within 24 h. The data confirm our previous findings of rapid hepatic metabolism of 7K when delivered in acLDL and demonstrate that 7K delivered in a vehicle of dietary significance is similarly metabolised and excreted. Indeed, the data encourage further investigation into the contribution that dietary oxysterols may or may not make to atherogenesis. (+info)
Reduced hepatic triglyceride secretion in rats fed docosahexaenoic acid-rich fish oil suppresses postprandial hypertriglyceridemia.
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To evaluate the mechanisms of suppression of postprandial hypertriglyceridemia by fish oil rich in docosahexaenoic acid, the effect on the intestinal absorption of triglyceride, activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) and metabolism of chylomicrons (CM) and CM remnants were compared with that of safflower oil in Sprague-Dawley rats in a series of studies. The feeding of fish oil for 3 wk suppressed postprandial hypertriglyceridemia (study 1). Dietary fish oil did not alter the rate of lymphatic absorption of triglyceride (study 2). The activities of LPL and HTGL were measured at 5 h after the beginning of feeding, when serum triglyceride concentrations were highest in both dietary groups. The activities of LPL in adipose tissue and heart were greater (P < 0.05) and those of HTGL were lower (P < 0.05) in the rats fed fish oil (study 3). In contrast, there were no differences in the activities of LPL and HTGL in postheparin plasma between the fish and safflower oil groups (study 4). The clearance rates of CM and CM remnants were measured by injecting intravenously CM collected from rats fed safflower or fish oils with [14C]triolein and [3H]cholesterol (study 5). Dietary oil did not influence the half-lives of CM or CM remnants. The secretion of triglyceride from the liver of rats injected with Triton WR-1339 was lower (P < 0.05) in the rats fed docosahexaenoic acid, a major component of fish oil, than those fed linoleic acid, a major component of safflower oil (study 6). These observations strongly support the hypothesis that in rats, the principal cause of the suppression of postprandial hypertriglyceridemia by fish oil is the depression of triglyceride secretion from the liver. (+info)
Vitamin A intake affects the contribution of chylomicrons vs. retinol-binding protein to milk vitamin A in lactating rats.
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To investigate the influence of vitamin A intake on the contribution of chylomicrons vs. holo retinol-binding protein to milk vitamin A, female rats were fed diets containing either 10 (n = 6) or 50 micromol vitamin A/kg body (n = 4) during pregnancy and through d 13 of lactation. [3H]Vitamin A was incorporated into each diet beginning on d 6 of lactation. Vitamin A concentrations on d 13 were significantly higher in dam liver (x 3), pup liver (x 2.6), milk (x 2.5) and mammary tissue (x 1.3) in rats consuming the higher level of vitamin A. In both groups, vitamin A specific activities in plasma and milk reached apparent plateaus by 2.33 d after addition of [3H]vitamin A to the diets. Vitamin A specific activity in milk was higher than in plasma at all times in both groups. The estimated minimum contribution of chylomicrons to milk vitamin A was 32 +/- 3% in rats fed the lower level of vitamin A vs. 52 +/- 10% at the higher level (P = 0.014). We concluded that dietary vitamin A, like triglycerides, may be directed to mammary tissue during lactation for preferential secretion into milk; thus, increasing vitamin A intakes will increase the contribution of dietary vitamin A to milk. In contrast to milk, mammary tissue vitamin A turns over very slowly. (+info)
Effects of prior moderate exercise on exogenous and endogenous lipid metabolism and plasma factor VII activity.
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Moderate exercise reduces postprandial triacylglycerol concentrations, which are a risk marker for coronary heart disease. The present study sought to determine the qualitative nature of exercise-induced changes in lipid metabolism and their association (if any) with changes in factor VII activation. Eleven normotriglyceridaemic men, aged 51.7+/-6.1 years (mean+/-S.D.), participated in two oral fat tolerance tests after different pre-conditions: control (no exercise), and exercise (90 min of brisk walking the day before). Venous blood samples were obtained in the fasted state and for 8 h after ingestion of a high-fat meal (1.32 g of fat, 1.36 g of carbohydrate, 0.30 g of protein and 10 mg of [1,1,1-(13)C] tripalmitin x kg(-1) body mass). Prior exercise reduced postprandial plasma triacylglycerol concentrations by 25+/-3% (mean+/-S.E.M.), with lower concentrations in the Svedberg flotation rate (Sf) 20--400 (very-low-density lipoprotein) fraction accounting for 79+/-10% of this reduction. There was no effect on plasma factor VII coagulant activity or on the concentration of the active form of factor VIIa. Prior exercise increased postprandial serum 3-hydroxybutyrate and plasma fatty acid concentrations, decreased serum postprandial insulin concentrations and increased exogenous (8 h (13)C breath excretion of 15.1+/-0.9% of ingested dose compared with 11.9+/-0.8%; P=0.00001) and endogenous postprandial fat oxidation. These data raise the possibility that reduced hepatic secretion of very-low-density lipoprotein plays a role in the attenuation of plasma triacylglycerol concentrations seen after exercise, although it is possible that increased triacylglycerol clearance also contributes to this effect. (+info)