共查询到20条相似文献,搜索用时 11 毫秒
1.
Klaus Eder 《Lipids》1999,34(7):717-725
This study was carried out to investigate the effects of a dietary oxidized oil on lipid metabolism in rats, particularly
the desaturation of fatty acids. Two groups of rats were fed initially for a period of 35 d diets containing 10% of either
fresh oil or thermally treated oil (150°C, 6d). The dietary fats used were markedly different for lipid peroxidation products
(peroxide value: 94.5 vs. 3.1 meq O2/kg; thiobarbituric acid-reactive substances: 230 vs. 7 μmol/kg) but were equalized for their fatty acid composition by using
different mixtures of lard and safflower oil and for tocopherol concentrations by individual supplementation with dl-α-tocopherol acetate. In the second period which lasted 16 d, the same diets were supplemented with 10% linseed oil to study
the effect of the oxidized oil on the desaturation of α-linolenic acid. During the whole period, all the rats were fed identical
quantities of diet by a restrictive feeding system in order to avoid a reduced food intake in the rats fed the oxidized oil.
Body weight gains and food conversion rates were only slightly lower in the rats fed the oxidized oil compared to the rats
fed the fresh oil. Hence, the effects of lipid peroxidation products could be studied without a distortion by a marked reduced
food intake and growth. To assess the rate of fatty acid desaturation, the fatty acid composition of liver and heart total
lipids and phospholipids was determined and ratios between product and precursor of individual desaturation reactions were
calculated. Rats fed the oxidized oil had reduced ratios of 20∶4n−6/18∶2n−6, 20∶5n−3/18∶3n−3, 20∶4n−6/20∶3n−6, and 22∶6n−3/22∶5n−3
in liver phospholipids and reduced ratios of 20∶4n−6/18∶2n−6, 22∶5n−3/18∶3n−3, and 22∶6n−3/18∶3n−3 in heart phospholipids.
Those results suggest a reduced rate of desaturation of linoleic acid and α-linolenic acid by microsomal Δ4-, Δ5-, and Δ6-desaturases.
Furthermore, liver total lipids of rats fed the oxidized oil exhibited a reduced ratio between total monounsaturated fatty
acids and total saturated fatty acids, suggesting a reduced Δ9-desaturation. Besides those effects, the study observed a slightly
increased liver weight, markedly reduced tocopherol concentrations in liver and plasma, reduced lipid concentrations in plasma,
and an increased ratio between phospholipids and cholesterol in the liver. Thus, the study demonstrates that feeding an oxidized
oil causes several alterations of lipid and fatty acid metabolism which might be of great physiologic relevance. 相似文献
2.
Male Sprague-Dawley rats four weeks or eight months of age were fed purified diets containing 10% fat, either as a blend of
safflower oil and palm olein (polyunsaturated fatty acids, PUFA, 34%), a blend of linseed oil and palm olein (PUFA, 33%) or
sardine oil (PUFA, 33%) for four weeks. In other trials, sterol contents were made equivalent by supplementing cholesterol
to a blend of corn oil and palm olein (PUFA, 30%) or phytosterol to sardine oil (PUFA, 30%). Fish oil was hypolipidemic in
rats of different ages, but it tended to increase liver cholesterol in adult animals and this was not improved by the addition
of phytosterol. The age-dependent increase in liver cholesterol was not duplicated in rats fed a vegetable fat blend supplemented
with cholesterol. At both ages, liver 3-hydroxy-3-methylglutaryl coenzyme A reductase activity was lower in the sardine oil
than in the other groups. There were no significant age- or diet-related differences in the activity of liver cholesterol
7α-hydroxylase. Fecal steroid excretion was comparable in age-matched rats fed diets supplemented either with cholesterol
or phystosterol. Sardine oil reduced the Δ6-desaturase activity markedly as compared with linseed oil, and age-dependent reduction
of the desaturase activity was observed in all dietary groups examined. Thus, the results showed a specific effect of fish
oil on lipid metabolism. 相似文献
3.
Male Sprague-Dawley rats were fed a cholesterol-free (Exp. 1) or cholesterol-supplemented (Exp. 2) diet containing 20% casein
(control group) or 15% defatted squid and 5% casein (defatted squid group), as protein, for 14 d. Serum and hepatic cholesterol
concentrations were lower in rats fed defatted squid than in those fed casein in both cholesterol-free (−20%, P<0.05 and −15%, P<0.05, respectively) and cholesterol-supplemented (−25%, P<0.05 and −15%, P<0.05, respectively) diets. Hepatic triglyceride concentration was lower in the defatted squid than in the control groups
in both cholesterol-free (−51%, P<0.05) and cholesterol-supplemented diets (−38%, P<0.01). The activities of cytosolic fatty acid synthase and the NADPH-generating enzymes, malic enzyme and glucose-6-phosphate
dehydrogenase, in the liver were lower in the defatted squid than in the control groups in both cholesterol-free (−21%, P<0.01, −33%, P<0.05, and −33%, P<0.01, respectively) and cholesterol-supplemented diets (−34%, P<0.05, −57%, P<0.05, and −67%, P<0.05, respectively). The activity of mitochondrial carnitine palmitoyltransferase in the liver was comparable between the
control and defatted squid groups. The activity of Mg2+-dependent phosphatidate phosphohydrolase in the liver cytosol was lower in the defatted squid (−9%, P<0.05) than in the control groups only in the cholesterol-free diet. Fecal excretion of total steroids was stimulated by the
feeding of defatted squid in both cholesterol-free (+77%, P<0.005) and cholesterol-supplemented diets (+29%, P<0.01). These results suggest that the nonlipid fraction of squid exerts a hypocholesterolemic effect by increasing the excretion
of total steroids in feces. The fraction also induces a triglyceride-lowering activity in the liver by decreasing hepatic
lipogenesis. 相似文献
4.
The effect of dietary fish oil on serum lipid levels was studied by comparing it with dietary corn oil in Donryu rats subcutaneously
implanted with an ascites hepatoma cell line (AH109A). The hepatoma-bearing rats exhibited hyperlipidemia charactarized by
a rise in both serum cholesterol and triglyceride levels. Increased cholesterogenesis in the host liver and decrease steroid
excretion into feces are suggested to be responsible for the hepatoma-induced hypercholesterolemia, and increased fatty acid
mobilization from peripheral adipose tissues and decreased triglyceride clearance from the blood circulation are considered
causes for the hepatoma-induced hypertriglyceridemia. Dietary fish oil reduced the hyperfipidemia in these animals, suppressed
the hepatoma-induced increase in hepatic cholesterogenesis and fatty acid mobilization from adipose tissue. Dietary fish oil
also tended to increase fatty acid oxidation in the liver. Such diverse effects of fish oil may lead to the reduction of the
hepatoma-induced hyperlipidemia. These results suggest that studies on dietary fish oil may be warranted in patients with
cancer-related hyperlipidemia. 相似文献
5.
6.
The purpose of this study was to determine the responsiveness of alveolar type II cells to dietary fish oil and the consequent
effects on alveolar and lung surfactant. Rats were fed a corn oil or a fish oil diet for four weeks. Dietary n−3 fatty acids
were readily incorporated into the type II cell phospholipids as indicated by higher levels of eicosapentaenoic acid (2.77±0.10%)
and docosahexaenoic acid (1.63±0.10%) in the group receiving the fish oil diet. The elevated levels of n−3 fatty acids were
accompanied by concomitant reduction in arachidonic acid and linoleic acid. Neither eicosapentaenoic acid nor docosahexaenoic
acid was incorporated into type II cell triacylglycerols. Feeding a fish oil containing diet increased surfactant phospholipids,
particularly 1,2-disaturated acyl phosphatidylcholines in whole lung compared to a corn oil diet. However, the amount of surfactant
found in the alveolus was not different between the two diet treatment groups. The results suggest that dietary n−3 fatty
acids stimulate synthesis and/or inhibit degradation of lung surfactant without altering surfactant secretion in alveoli. 相似文献
7.
Sprague-Dawley rats were fed purified diets varying in both protein (20%) and lipid (11%) content for 28 d to verify the independent
and interactive effects of dietary proteins and lipids on serum and hepatic lipids, and on tissue lipoprotein lipase (LPL)
activity in both fasted and postprandial states. These diets consisted of either casein-menhaden oil, casein-coconut oil,
soy protein-menhaden oil (SPMO), soy protein-coconut oil, cod protein-menhaden oil, or cod protein-coconut oil. A randomized
3×2 factorial design was used. A significant protein-lipid interaction was seen on serum triglyceride levels: menhaden oil,
compared with coconut oil, induced a decrease in serum triglyceride levels when combined with soy protein but not when combined
with cod protein and casein. The lower serum triglyceride concentrations observed in the SPMO-fed rats could be the result
of decreased hepatic triglycerides when soy protein was compared with casein and when menhaden oil was compared with coconut
oil. Total LPL activity in the heart was higher in menhaden oil-fed rats than in coconut oil-fed rats in the postprandial
state. The higher LPL activity in the heart could, however, explain only 10% of the reduction of serum triglycerides, contributing
slightly to the lowering effects of SPMO diet on serum triglycerides. Therefore, the present results indicate that dietary
proteins can modulate the effects of fish oil on triglyceridemia in the rat, and that could be mainly related to specific
alterations in hepatic lipid concentrations. 相似文献
8.
Effects of dietary triolein and sunflower oil on insulin release and lipid metabolism in zucker rats
Obese and lean male Zucker rats were fed ad libitum on diets containing either 50 (L) or 200 (H) g/kg diet of either triolein
(T) or sunflowerseed oil (S). The specific activity of the hepatic microsomal Δ9 desaturase enzyme was depressed in both lean
and obese rats fed the HS diet compared with the other three diets. The fatty acid composition of liver and subcutaneous white
adipose tissue lipids were consistent with a lower Δ9 desaturation activity in rats fed the H diets, particularly for the
HS diet. In both genotypes, microsomal Δ9 desaturase activity and the ratio of 16∶1/(16∶0+16∶1) fatty acids in liver lipids
were inversely related to the proportion of 18∶2 in liver lipid. Plasma insulin concentrations and rates of glucose-stimulated
insulin release in vivo were higher in obese rats compared with lean rats, and plasma insulin levels were higher in rats fed
S compared with T. There was no relationship between Δ9 desaturase activity and either plasma insulin concentration or rates
of insulin release in vitro. These findings suggest that hepatic Δ9 desaturase activity of Zucker rats is responsive to changes
in the proportion of 18∶2 in liver lipids but is not affected by changes in insulin secretion. 相似文献
9.
Male rats were fed on a fat-free diet for 8 weeks and then switched to diets containing 10% hydrogenated coconut oil (HCO),
safflower oil (SFO) or evening primrose oil (EPO). Half of each group was also given 1% of cholesterol in the diet. After
5 further weeks, plama, red cell and liver fatty acids were measured in the various lipid fractions. Plasma and liver cholesterol
also were estimated. In almost all fractions and on all three diets, feeding cholesterol led to accumulation of the substrates
of desaturation reactions and to deficits of the products of these reactions. The results were consistent with inhibition
of Δ-6, Δ-5 and Δ-4 desaturation of n−6 essential fatty acids. Since the diets were deficient in n−3 fatty acids, levels were
very low but were also consistent with inhibition of desaturation. In contrast, cholesterol had relatively less consistent
effects on 20∶3n−9, suggesting that desaturation of n−9 fatty acids was less inhibited. Plasma cholesterol levels rose sharply
in the HCO and SFO groups but not at all in the EPO group. EPO contains the product of Δ-6 desaturation, 18∶3n−6, suggesting
that conversion of linoleic acid to 18∶3n−6 and possibly to further metabolites may be important for the cholesterol-lowering
effect of polyunsaturates. 相似文献
10.
Pieter C. Dagnelie Jimmy D. Bell Steve C. R. Williams Timothy E. Bates Paul D. Abel Christopher S. Foster 《Lipids》1994,29(3):195-203
The aim of this study was to investigate whether tumor-induced cachexia and aberrations in host liver metabolism, induced
by the MAT-LyLu variant of the Dunning prostate tumor, could be prevented by ω3 fatty acids from fish oil. On day 0, adult
Copenhagen-Fisher rats fed normal chowad libitum were inoculated with 106 MAT-LyLu cells (n=14) or saline (n=9). On day 7, when tumors were palpable, four tumor-bearing (TB) and four nontumorbearing
(NTB) rats were put on isocaloric diets with 50% of total energy as fish oil. The introduction of fish oil-enriched diets
caused a reduction in energy intake to less than half of the energy intake by animals fed normal diets during days 7–14 (difference
by dietary group: NTB,P<0.001; TB,P<0.001). During days 14–21, energy intake in fish oil-fed animals returned to approximately 75% of energy intake by animals
fed normal diets (difference by dietary group: NTB,P<0.003; TB,P=0.001). Carcass weight of animals on day 21, when the study was terminated, was significantly related to initial weight (P=0.05) and mean food intake during the study (P=0.01). When data were adjusted for these variables using analysis of covariance, with NTB animals on normal diets being the
reference group, significant loss of carcass weight was observed in TB animals on normal diets only (mean ±SEM 58±10 g loss,P<0.001), but not in TB animals on fish oil diets (8±18 g loss,P=0.67). This positive effect of fish oil diets on carcass weight in TB animals was statistically significant (50±19 g,P<0.02), implicating that the fish oil enriched diet inhibited tumor-induced weight loss by more than 85%. No effect of fish
oil diets on tumor growth was detected. In all TB animals, regardless of diet, hepatic [Pi]/adenosine triphosphate] ratios measured by31P magnetic resonance spectroscopy (MRS)in vivo andin vitro were elevated, and absolute concentrations of phosphocholine, glycerophosphocho-line, glycerophosphoethanolamine and glucose-6-phosphate
as determined by31P MRSin vitro were reduced. Ultrastructural studies of liver tissue revealed increased numbers of mitochondria and increased amounts of
endoplasmic reticulum in the host liver of TB animals, without differences between dietary group. In conclusion, fish oil
supplementation partially inhibited MAT-LyLu tumor-induced cachexia, but did not prevent the majority of31P MRS-detectable alterations in host liver metabolism. 相似文献
11.
We have reported that dietary fish oil (FO) rich in n-3 PUFA modulates gut contractility. It was further demonstrated that the gut of spontaneously hypertensive rats (SHR) has a depressed contractility response to prostaglandins (PG) compared with normotensive Wistar-Kyoto (WKY) rats. We investigated whether feeding diets supplemented with n-3 PUFA increased gut contractility and restored the depressed prostanoid response in SHR gut. Thirteen-week-old SHR were fed diets containing fat at 5 g/100 g as coconut oil (CO), lard, canola oil containing 10% (w/w) n-3 FA as alpha-linolenic acid (1 8:3n-3), or FO (as HiDHA, 22:6n-3) for 12 wk. A control WKY group was fed 5 g/100 g CO in the diet. As confirmed, the SHR CO group had a significantly lower gut response to PGE2 and PGF2alpha compared with the WKY CO group. Feeding FO increased the maximal contraction response to acetylcholine in the ileum compared with all diets and in the colon compared with lard, and restored the depressed response to PGE2 and PGF2alpha in the ileum but not the colon of SHR. FO feeding also led to a significant increase in gut total phospholipid n-3 PUFA as DHA (22:6n-3) with lower n-6 PUFA as arachidonic acid (20:4n-6). Canola feeding led to a small increase in ileal EPA (20:5n-3) and DHA and in colonic DHA without affecting contractility. However, there was no change in ileal membrane muscarinic binding properties due to FO feeding. This report confirms that dietary FO increases muscarinic- and eicosanoid receptor-induced contractility in ileum and that the depressed prostanoid response in SHR ileum, but not colon, is restored by tissue incorporation of DHA as the active nutrient. 相似文献
12.
In the rat, both fish oil diet and thyroid hormone replacement are reported to augment bile cholesterol secretion out of proportion
to bile flow or secretion of other bile lipids. We sought common mechanisms for these effects and evaluated the role of phospholipid
fatty acid composition in the process. Methimazole-treated hypothyroid rats were fed low-fat chow or chow supplemented with
10% corn oil or fish oil, and were studied before and after thyroid hormone treatment. Serum, hepatic, and bile lipids were
measured, phospholipid fatty acid composition determined, and hepatic 3-hydroxy-3-methylglutaryl CoA reductase activity assayed.
Fish oil diet stimulated cholesterol secretion into bile only after thyroid hormone was given, and this action was synergistic
with that of thyroid hormone. Reduced serum cholesterol in fish oil-treated rats was associated with increased biliary cholesterol
secretion and diminished hepatic cholesterol content. This suggests that augmented biliary cholesterol secretion may contribute
to the fish oil-induced reduction of serum cholesterol. No definite relationship between hepatic or biliary phospholipid fatty
acid composition and biliary secretion was apparent, although high bile cholesterol secretion was associated with a low percentage
of hepatic and bile phospholipid linoleic acid. 相似文献
13.
The activity of lipoprotein lipase (LPL) in the adipose tissue and skeletal muscle of rats fed glucose- or fructose-based
diets containing fish oil, corn oil or tallow was examined. In addition, heart LPL activity was measured in rats fed a glucose-based
diet containing either corn oil or fish oil. Adipose tissue LPL activity was unaffected by dietary fat. In both heart and
skeletal muscle, LPL activity was higher in rats fed the fish oil diet. These results suggest that increased removal of triglyceride
by muscle may contribute to the blood triglyceride lowering effect of dietary fish oil. 相似文献
14.
Peanut oil has been shown to be unexpectedly atherogenic for cholesterol-fed rats, rabbits and rhesus monkeys. However, randomization
(rearrangement of fatty acids to random distribution) of peanut oil significantly reduced its atherogenicity for rabbits and
monkeys. This study was conducted to investigate whether the absorption and transport of dietary cholesterol was altered in
the presence of peanut oil or randomized peanut oil, thereby accounting for the difference in the atherogenicity of the two
diets. Intestinal lymph fistula rats were infused intraduodenally with a lipid emulsion at a rate of 3 ml/hr. The lipid emulsion
contained either peanut oil (control) or randomized peanut oil (experimental) (10 mM),14C-cholesterol (1.3 mM) and sodium taurocholate (19 mM) in phosphate-buffered saline, pH 6.4. Lymph triglyceride, cholesterol
and phospholipid outputs were similar in both groups of rats during fasting and subsequently during lipid infusion. Comparable
recovery of14C-cholesterol from the intestinal lumen and the intestinal mucosa of the control and the experimental rats showed that the
absorotion and transport of dietary cholesterol were similar in both groups of rats. Analyses of thefatty acid of both lymph
and intestinal mucosal lipid again failed to reveal a difference between the 2 groups of rats. It is concluded that the difference
in the atherogenicity between the peanut oil and the randomized peanut oil is probably caused by events subsequent to the
release of cholesterol containing chylomicrons and very low density lipoproteins by the small intestinal epithelial cells. 相似文献
15.
The comparative effects of dietary α-linolenic acid and fish oil on eicosanoid metabolism was studiedin vivo. Resident murine peritoneal cells were stimulatedin vivo with opsonized zymosan in animals maintained on diets containing increasing amounts of α-linolenic acid or fish oil concentrate
with projected n−3/n−6 ratios of 0.2, 0.4 and 1.0. While fish oil feeding resulted in significant changes in eicosapentaenoate
tissue levels, α-linolenic acid was preferentially metabolized to docosahexaenoate. High performance liquid chromatographic
analysis revealed the formation of leukotriene E5 (LTE5) in all the fish oil groups (19.8±3.5 ng/mouse to 83.3±13 ng/mouse), but only in the highest linolenic acid group (6.0±3.2
ng/mouse). Concomitantly, the 4-series sulfidopeptide leukotrienes and PGI2 were significantly reduced in the two highest fish oil containing dietary groups. Similar reductions were observed in the
highest linolenic acid group, but the changes were not statistically different from the control values. In summary, this paper
reports thede novo synthesis of 5-series sulfidopeptide leukotrienes in animals consuming α-linolenic acid. It also reveals that dietary fish
oil is 2.5 to 5 times more effective than α-linolenic acid in modulating eicosanoid metabolism and altering tissue phospholipid
fatty acid composition.
Presented, in part, at the 74th annual meeting of the Federation of American Societies for Experimental Biology, Washington,
D.C., March, 1990;FASEB J. 4(3): 4227 (1990). 相似文献
16.
Maud Cansell Noredine Moussaoui Alain Pierre Petit Alain Denizot Nicole Combe 《European Journal of Lipid Science and Technology》2006,108(6):459-467
Two n‐3 polyunsaturated fatty acid (PUFA)‐rich diets differing in their chemical and physical forms were given to rats during 2 wk. Liposomes [phospholipids (PL) organized in bilayer structures] made from a natural marine lipid extract or a mixture of fats containing fish oil [similar fatty acids esterified in triacylglycerols (TAG)] were used. The influence of n‐3 PUFA dietary sources on plasma parameters, i.e. TAG, cholesterol and PL concentrations, was investigated. A similar hypotriglyceridemic effect of n‐3 PUFA from liposomes or fish oil was observed. In contrast, feeding rats with liposomes led to different PL and cholesterol patterns. In the plasma of rats fed liposomes, total cholesterol amounts were positively correlated with PL levels. Liposome and fish oil feedings caused a marked increase in the amounts of n‐3 PUFA, which occurred mainly at the expense of n‐6 PUFA. However, the enrichment in n‐3 PUFA in the different plasma lipid classes differed substantially when ingested in the form of fish oil or liposomes. These results were interpreted in terms of different lipid bioavailability and metabolic fate during the digestive steps and in the liver, with the dietary source. 相似文献
17.
Rats red ad lib. for 12 weeks either a fat-free diet, a diet containing 15% cottonseed oil, or a diet containing 15% cuttlefish
liver oil, with or without exogenous (1%) cholesterol, were studied to evaluate and compare the effect of polyunsaturated
fatty acids of cuttlefish liver oil and cottonseed oil on cholesterol metabolism. The results indicate that the longer chain
polyunsaturated fatty acids contained in the fish oil cannot substitute for the essential fatty acid, linoleic, either as
far as effect on various aspects of cholesterol metabolism are concerned or in the ability to form arachidonic acid. The observed
interference of cuttlefish liver oil with the absorption of exogenous cholesterol may be caused by the presence in this oil
of the highly unsaturated long chain fatty acids. 相似文献
18.
Polyoxyethalated cholesterol (POEC) is a water soluble derivative of cholesterol which decreases cholesterol absorption in
rats without affecting body weight, fatty acid excretion, or intestinal histology. In the present study rat feces were analyzed
for cholic, deoxycholic, chenodeoxycholic, muricholic and lithocholic acid following 3 months of feeding a standard or a 2%
enriched cholesterol diet with or without 1.5% POEC. In rats maintained on the cholesterol free diet, POEC increased total
bile acids (mg/day) by 50% from 14±3 to 21±3 (mean ±SEM) but only the increase in chenodeoxycholic acid was significant (P<0.05).
The corresponding POEC effect in the 2% cholesterol diet was 31% (70±8 to 93±3, P<0.01). Fecal nitrogen and serum cholesterol
did not vary among groups. Comparing these data with neutral steroid excretion previously determined showed that POEC in the
cholesterolfree diet increased the negative cholesterol balance more than three-fold (34±7vs 118±13 P<0.01). In rats fed 2% cholesterol, POEC caused a negative cholesterol balance of 222±8 compared to the control of
27±52 (P<0.01). The data indicate that POEC exerts complex effects in the intestinal tract which increase both bile acid and
cholesterol excretion. 相似文献
19.
Substitution of casein for soybean protein in the diet causes high degrees of hypercholesterolemia in rabbits. When rats or
humans were fed exactly the same diets, no response of the concentration of serum cholesterol to the type of protein was observed.
The hypothesis is put forward that, in rabbits, dietary casein and peptides derived from it—because of their high degree of
phosphorylation—inhibit the binding of glycine-conjugated bile acids to insoluble calcium phosphate in the intestinal lumen.
As a result, feeding of casein causes an increase in the availability of bile acids, which leads to enhanced absorption of
bile acids and cholesterol. Eventually, the concentration of serum cholesterol will be increased. In rabbits this cascade
of events occurs because these animals have a relatively low activity of intestinal alkaline phosphatase, and a high ratio
of glycine to taurine in conjugated bile acids. Unlike glycine conjugates, taurine-conjugated bile acids do not effectively
bind to the intestinal calcium-phosphate sediment. The low activity of intestinal alkaline phosphatase in rabbits secures
the high degree of phosphorylation of casein and its peptide products in the small intestine. In contrast with rabbits, rats
and humans have high activities of intestinal alkaline phosphatase and a low glycine-to-taurine ratio in conjugated bile acids.
Thus the hypothesis presented would explain why rabbits, but not rats and humans, are susceptible to dietary casein with respect
to the concentration of serum cholesterol. The relevance of the hypothesis as to the mechanisms underlying the hypercholesterolemic
effect of some other dietary proteins is discussed. 相似文献
20.
R. N. Redinger 《Lipids》1979,14(3):277-284
The effect of 1.7–2.2 mg/day oral phenobarbital over short (1 MO) and long term (6–24 MO) treatment on primary bile acid (BA)
secretion, composition, synthesis, pool size, and enterohepatic cycling rates as well as phospholipid (PL) and cholesterol
(C) secretion rates and biliary composition was determined in 12 asymptomatic cholesterol gallstone subjects while 5 normals
had only short term studies. Phenobarbital enhanced BA and C secretion (BA-636±166 to 2110±382 mg/hr, p<0.001 and C-42±5 to
224±48 mg/hr, p<0.001) and BA cycling rate in all subjects studied during stimulated enterohepatic circulation but, during
fasting, it only enhanced BA secretion (451±129 vs. 759±159 mg/hr, p<0.05) in gallstone subjects. Cholic acid (CA) production
rate (171±28 to 395±9 mg/hr, p<0.05) and pool size (727±80 to 1209±132 mg/hr, p<0.05) were increased during long term treatment
of gallstone subjects, while the proportion of CA in bile and deoxycholic acid (DCA) in feces increased. Treatment decreased
biliary cholesterol from supersaturated to saturated levels (9.5±0.6 vs. 6.1±0.9 moles%, p<0.02) in all fasting gallstone
subjects and decreased cholesterol crystal loads during long term treatment; but, while prohibiting gallstone growth, it did
not affect stone dissolution over 24 month's treatment. Phenobarbital also failed to affect biliary lipid composition or bile
acid pool size in short term treatment of normals. Thus, phenobarbital affected hepatic metabolism of CA by enhancing production
rate, secretion, and pool size; and in testinal metabolism of both CA and chenodeoxycholic (CDC) acids by increasing their
cycling rates. Phenobarbital may have failed to produce stone dissolution by enhancing CA production and pool size more than
that of CDC.
Portions of this work were presented at the National Meeting of the American Federation of Clinical Research, Atlantic City,
April 29, 1973 and at the Annual Meeting of the Canadian Society of Clinical Investigation, Winnepeg, Manitoba, January 21,
1975 as well as that of the Royal College of Physicians and Surgeons of Canada, January 27, 1977 at Toronto, Canada. 相似文献