Hepatic Total Lipid Research Articles

Hypolipidemic effects of hydrolyzed xyloglucan

AbstractXyloglucan is found in the primary cell walls of higher plants, where it plays important biological roles. It also exists in certain seeds, for example tamarind, as a reserve polysaccharide. Some xyloglucan oligosaccharides possess plant growth promotion activity.We prepared hydrolyzed xyloglucan from the tamarind seed xyloglucan using endo‐(1 → 4)‐ β ‐glucanase and examined its effects on lipid metabolism in rats fed a high fat diet. Among the plasma lipids, total lipid, cholesterol, triglyceride and β ‐ lipoprotein were each reduced 14 ‐ 17% by hydrolyzed xyloglucan. Hydrolyzed xyloglucan significantly reduced both adipose tissue weight and plasma GOT. Among the hepatic lipids, total lipid, cholesterol, triglyceride and phospholipid were significantly reduced by hydrolyzed xyloglucan.These hypolipidemic effects may be important for the treatment and prevention of geriatric diseases, including diabetes and cardiac disorders.

A highly toxic PCB produces unusual changes in the fatty acid composition of rat liver

The changes in lipici metabolism produced by a coplanar PCB were studied in rats. Male Wistar rats were given a single intraperitoneal injection of 3,3′,4,4′,5-pentachlorobiphenyl at a dose of 25 mg/kg. After 5 days of administration, total hepatic lipids were treated with 1 M KOH in methanoi at 75 °C and the liberated fatty acids were analyzed by HPLC after conversion to fluorescent derivatives. In comparison with free-fed and pair-fed control groups, the proportion of arachidonic acid in the PenCB-treated rats was reduced by about 50%, while oleic and linoleic acids increased significantly. We also examined the individual glycerophospholipids, separated by TLC, to see if they were affected by alteration in the fatty acid composition of the whole liver. In all glycerophospholipids, the proportion of arachidonic acid was reduced significantly to the same degree while linoleic acid increased. Changes mthe activity of desaturase isozymes have been postulated to explain this unusual lipid metabolism following administration of a toxic PCB and this may contribute to its toxicity.

Effects of hydrolyzed xyloglucan on lipid metabolism in rats

Xyloglucan is a component of the cell walls of higher plants. Hydrolyzed xyloglucan, which consists of xyloglucan heptasaccharide (Glu 4Xyl 3), octasaccharide (Glu 4Xyl 3Gal) and nona-saccharide (Glu 4Xyl 3Gal), is known to regulate plant growth. However its effects on animals are unknown. In this study we prepared hydrolyzed xyloglucan from the tamarind plant using endo-1, 4- β-glucanase and examined its effects on lipid metabolism in rats fed a high-fat diet containing corn oil (2%) and lard (15%) for 35 days. Among the plasma lipids, total lipid, cholesterol, triglyceride and β-lipoprotein were each reduced 14–17% by hydrolyzed xyloglucan. Hydrolyzed xyloglucan significantly reduced adipose tissue weight, total plasma lipid and plasma GOT. Among the hepatic lipids, total lipid, cholesterol, triglyceride and phospholipid were each significantly reduced by hydrolyzed xyloglucan. This report is the first to demonstrate the biological activity of hydrolyzed xyloglucan in animals.

Cysteine Supplementation and Reduction of Total Parenteral Nutrition—Induced Hepatic Lipid Accumulation in the Weanling Rat

SummaryTotal parenteral nutrition (TPN)‐induced hepatic steatosis is the most common complication of TPN administration to humans. The mechanism of TPN‐induced hepatic steatosis has not been studied in young mammals. The goal of this study was to determine the mechanism of TPN‐induced hepatic steatosis in the weanling rat and the effect of supplementation of TPN with choline and/or cysteine on TPN‐induced hepatic steatosis. In the weanling rat, we investigated the effect of TPN administration on histologic hepatic steatosis, total hepatic lipid, hepatic acetyl‐CoA‐carboxylase (ACC—the rate limiting enzyme in fatty acid synthesis) specific activity, and total plasma lipids. TPN administration resulted in a threefold increase in hepatic lipid as compared with control and sham animals (TPN 138 ± 12 mg/g liver versus control 57 ± 1), an increase in histologic steatosis (TPN 3.7 versus control 1.3), and a decline in total plasma lipid (TPN 2.1 ± 0.3 g/L versus control 4.1 ± 0.3). TPN‐induced hepatic steatosis in the weanling rat was not associated with an increase in ACC specific activity (TPN 2.10 ± 0.33 nmol/min/mg protein versus control 2.85 ± 0.23). Supplementation of the TPN with choline (15 mg/day) did not significantly lessen hepatic steatosis; however, supplementation of TPN with cysteine (2.5 mg/day) or with cysteine and choline did result in a significant lessening of hepatic lipid content and of histologic steatosis and a normalization of total plasma lipid. Tritiated glycerol incorporation into media lipids secreted by hepatocytes isolated from TPN‐treated animals was 45% of that from cysteine‐supplemented animals, suggesting a defect in hepatic lipid secretion associated with TPN‐induced hepatic steatosis in the weanling rat that is partially corrected by cysteine supplementation.

Cysteine Supplementation and Reduction of Total Parenteral Nutrition—Induced Hepatic Lipid Accumulation in the Weanling Rat

Total parenteral nutrition (TPN)-induced hepatic steatosis is the most common complication of TPN administration to humans. The mechanism of TPN-induced hepatic steatosis has not been studied in young mammals. The goal of this study was to determine the mechanism of TPN-induced hepatic steatosis in the weanling rat and the effect of supplementation of TPN with choline and/or cysteine on TPN-induced hepatic steatosis. In the weanling rat, we investigated the effect of TPN administration on histologic hepatic steatosis, total hepatic lipid, hepatic acetyl-CoA-carboxylase (ACC--the rate limiting enzyme in fatty acid synthesis) specific activity, and total plasma lipids. TPN administration resulted in a threefold increase in hepatic lipid as compared with control and sham animals (TPN 138 +/- 12 mg/g liver versus control 57 +/- 1), an increase in histologic steatosis (TPN 3.7 versus control 1.3), and a decline in total plasma lipid (TPN 2.1 +/- 0.3 g/L versus control 4.1 +/- 0.3). TPN-induced hepatic steatosis in the weanling rat was not associated with an increase in ACC specific activity (TPN 2.10 +/- 0.33 nmol/min/mg protein versus control 2.85 +/- 0.23). Supplementation of the TPN with choline (15 mg/day) did not significantly lessen hepatic steatosis; however, supplementation of TPN with cysteine (2.5 mg/day) or with cysteine and choline did result in a significant lessening of hepatic lipid content and of histologic steatosis and a normalization of total plasma lipid.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of highly hydrogenated soybean oil and cholesterol on plasma, liver cholesterol, and fecal steroids in rats

We investigated the relationship between dietary highly hydrogenated soybean oil (HSO) and cholesterol transport in rats. In the first study, to examine the effects on cholesterol transport of different concentrations of HSO in dietary oil, rats were given one of the three diets containing 0, 25, or 50% HSO in dietary oil with cholesterol (5 g/kg diet) or a diet without HSO and cholesterol for 22 d. Feeding the high concentration of HSO prevented the increase in plasma total cholesterol, hepatic total lipids, and cholesterol and the decrease in high-density lipoprotein-cholesterol, which were caused by dietary cholesterol. Moreover, HSO increased the fecal excretion, fecal lipids, and steroids in a dose-dependent manner. In the second study, to examine the effects on cholesterol transport of redistribution of steric acid in the triacylglycerol species contained in HSO, rats were given one of the six diets containing HSO (distearoylmonoacylglycerol and tristearoylglycerol)-rich, monostearoylglycerol-rich, or palmitic acid-rich oil with/without cholesterol (5 g/kg diet), for 30 d. Whereas the accumulation of cholesterol in the body was reduced, cholesterol excretion was enhanced effectively in rats given the HSO-rich diet compared with rats given the monostearoylglycerol-rich diet. These results suggested that not only the high concentration of stearic acid but also its uneven distribution in HSO-triacylglycerol contributed to the reduction in intestinal cholesterol absorption in rats.

The Concentration of Different Lipid Classes During Late Embryonic Development in a Randombred Turkey Population and a Subline Selected for Increased Body Weight at Sixteen Weeks of Age

Lipid changes in the yolk sac of the embryo were studied in a randombred population of turkeys (RBC2) and a subline of the RBC2 selected for increased BW at 16 wk (F line). Comparisons of yolk sac and embryonic development were made between 22 d of incubation and hatch (28 d). Poults from the F line had heavier yolk sacs from 24 to 28 d and yolk free body weight was also heavier at hatch (61.1 vs 52.8 g). Yolk sac lipid (percentage of DM) declined faster in F line embryos (69 to 39%) compared with the RBC2 line (62 to 48%). In both lines, embryonic liver dry matter and lipids (percentage of DM) were similar. Yolk sac neutral lipids increased from 22 to 28 d (70 to 80% total lipid) in both lines and there was a concomitant decline in phospholipids (30 to 20%). The direction of the changes was similar for embryonic liver lipid. At 26 and 28 d, there were significantly increased neutral lipids (94 vs 88%) and decreased phospholipids (6 vs 12%) in RBC2 compared with F line embryonic livers. The concentration of cholesterol esters (percentage of total lipid) increased in the yolk sac and embryonic liver during the course of incubation. At 26 and 28 d, livers from RBC2 embryos had increased cholesterol ester concentration compared with livers from the F line. These results suggest that selection for body weight at 16 wk of age has not changed total lipid content of the yolk, but there was a significant decline in the proportion of triacylglycerol (percentage of total lipid) and diacylglycerol (percentage of total lipid) in the F line during embryonic development. Selection also resulted in significantly increased hepatic total lipid in F line embryos but significantly decreased the proportion of hepatic neutral lipid.

Effect of dietary sodium phytate on the hepatic and serum levels of lipids and on the hepatic activities of NADPH-generating enzymes in rats fed on sucrose.

The effect was investigated of dietary 0.5% sodium phytate on the hepatic and serum lipid status in rats fed on sucrose for 29 or 30 days. The increase in hepatic weight, levels of hepatic total lipids, triglyceride, cholesterol, serum triglyceride and phospholipid, and the activities of hepatic NADPH-generating enzymes due to sucrose feeding were generally depressed by dietary sodium phytate.

Effects of protein, lipid, or carbohydrate supplementation on hepatic lipid accumulation during rapid weight loss in obese cats

Summary Effects of restricted tube-feeding (25% of energy requirements) of protein, lipid, or carbohydrates on body weight loss; hematologic and clinical chemical variables; plasma lipid and amino add concentrations; nitrogen balance; and hepatic histologic features and lipid concentrations were compared with values in voluntary-fasting cats (control, con). Twelve obese cats (6.1 ± 0.1 kg, > 40% above optimal body weight) were randomly assigned to 4 matched treatment groups (n = 3)—protein (pro), lipid (lip), carbohydrate (cho), and con—and were offered a low-palatability diet for 4 weeks. Cats of the pro, lip, and cho groups were also tube-fed isocaloric amounts (88 kcal of metabolizable energy) of a casein-soybean protein mixture, com oil, or a dextrin-dextrose mixture, respectively, during the 4 weeks. All cats fasted, rather than eat the low-palatability purified diet. Cats of the pro group lost weight at a lower rate (P < 0.05) than did cats of other groups. After 4 weeks of fasting, serum alkaline phosphatase activities were higher than reference values in all cats of the con and lip groups and in 2 cats of the cho group. At that time, 1 cat of the lip group had lethargy, hepatomegaly, and hyperbilirubinemia. Total hepatic lipid and triglyceride concentrations increased in all groups during the study, but the increase was significantly (P < 0.05) less in cats of the pro group, compared with those of the con and lip groups, and those of the cho group, compared with those of the lip group. Hepatic total lipid and triglyceride concentrations correlated well with lipid score for liver biopsy specimens when lipidosis was mild or severe, but not as well in association with the intermediate lipidosis. Cats of the PRO group were in nitrogen balance after 2 weeks of fasting. All other cats remained in negative nitrogen balance during the fast, although less nitrogen was lost by cats of the cho and lip groups than by cats of the con group. Plasma aminograms indicated that methionine and arginine might become limiting for protein synthesis during fasting in cats. Results indicate that dietary protein reduces hepatic lipid accumulation and nitrogen balance is maintained during rapid weight loss in obese cats. Ingestion of only lipids increases the risk of inducing hepatic lipidosis. Ingestion of carbohydrates reduces hepatic lipid accumulation, but is not as effective as protein in preventing all the clinical manifestations of hepatic lipidosis.

Ornithine decarboxylase, fatty acid synthetase, and lipid levels in selected organs of the postnatal developing male miniature pig

Ornithine decarboxylase (ODC) and fatty acid synthetase (FAS) activities were determined in tissues from male neonate and juvenile miniature swine (Hormel-Hanford strain) at various ages. ODC activity was measured in liver, brain, kidney, pancreas, and spleen at one day and at 1, 4, 8, 12 and between 24 and 32 weeks. Hepatic FAS activity, total lipid, triglyceride, and total cholesterol were measured at 2, 8, 16, and 32 weeks. Generally, tissue ODC activity was highest in the spleen at all ages. Three postnatal patterns of ODC activity were observed for the different organs. The mean values of FAS activity, total lipid, and cholesterol were highest at 8 weeks compared to other sampling periods.

The effects of dietary sugar-beet fibre and guar gum on lipid metabolism in Wistar rats.

This study investigates the mechanisms of action for the hypocholesterolaemic effects of sugar-beet fibre (SBF) and guar gum. Four groups of ten male Wistar rats were fed ad lib. on test diets containing either 100 g SBF or guar/kg, or control diets containing 100 g cellulose or wheat bran/kg for 28 d. Food intake, weight gain and food consumption ratios were unaffected by the diets. Circulating cholesterol and hepatic cholesterol concentrations were significantly lower in both SBF- and guar-fed groups compared with either cellulose- or bran-fed animals. Circulating triacylglycerol concentrations were significantly lower in SBF- and guar-fed animals, but total hepatic lipid concentrations and hepatic and adipose tissue lipogenesis rates were unaffected by the diets. Hepatic cholesterol-7 alpha-hydroxylase (EC 1.14.13.17) activities were significantly higher in the guar-fed animals compared with cellulose or bran control groups. Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (EC 1.1.1.88) activities were unaffected. Circulating bile acid concentrations were significantly lower in SBF- and guar-fed animals and faecal bile acid output was significantly higher in the guar-fed group compared with bran- or cellulose-fed groups. This study supports the hypothesis that guar exerts its hypocholesterolaemic effect via intraluminal bile acid binding and loss of cholesterol from increased faecal bile acid excretion. The mechanism of action for the hypocholesterolaemic effect of SBF is less clear; the results of the present study point to a mechanism involving disruption of the enterohepatic bile acid circulation, possibly via changes in the rate of absorption of dietary lipid.

Effect of dietary addition of myo-inositol on lipid metabolism in rats fed sucrose or corn starch

The effect of dietary addition of myo-inositol on lipid metabolism was examined in rats fed diets containing either sucrose or corn starch for 16–17 days. Sucrose-fed rats showed significant increases in hepatic weight, total lipids, triglyceride, cholesterol and serum triglyceride, accompanied by the activities of hepatic glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) and malic enzyme (ME, EC 1.1.1.40), compared to rats fed corn starch diet. The increases in these parameters due to sucrose feeding were clearly depressed by dietary myo-inositol. Sucrose intake also increased serum level of phospholipid, but the effect was not influenced by dietary myo-inositol. In the animals fed corn starch, dietary myo-inositol had no apparent effect on lipid metabolic parameters mentioned above. These results suggest that an exogenous source of myo-inositol may be of importance to animals fed sucrose when compared to rats fed corn starch.

Prolactin and bromocriptine induced changes in liver, adipose tissue and blood lipids of mature male bonnet monkeys, Macaca radiata (Geoffroy).

Effects of prolactin and bromocriptine on neutral and phospholipids of liver, adipose tissue and serum were studied in mature male bonnet monkeys. Hyperprolactinemia (ovine prolactin, 250 micrograms/kg body weight/day, i.p. for 30 days) elevated hepatic total lipids and phospholipids and decreased total and free cholesterol. While triacyl glycerol accumulated, mono-and diacyl glycerols diminished in liver and adipose tissues of prolactin treated monkeys. Concentrations of all phospholipid fractions, except sphingomyelin and cardiolipin in adipose tissue accrued in both tissues. Serum triacylglycerol, phosphatidyl ethanolamine, phosphatidyl choline and phosphatidyl inositol showed a significant increase in hyperprolactinaemic monkeys. Bromocriptine (1 mg/kg body weight/day for 30 days) treatment reduced serum phospholipids without altering hepatic or adipose tissue lipids. The present study indicates that hyperprolactinaemia leads to hyperlipidemia due to accretion of hepatic and adipose tissue triacyl glycerol and certain phospholipid fractions. Bromocriptine has a specific inhibitory effect on serum phospholipids.

Changes of hepatic lipid and fatty acid profiles in rats administered iron-deficient diet and ethanol

This investigation was undertaken to elucidate the effects of iron deficiency and/or ethanol ingestion on lipid metabolism of female rat liver. 40 Wistar rats (about 40 g body weight) were fed a normal diet (Fe: 40 ppm) or an iron-deficient diet (Fe: 5 ppm) for 8 wk. Half of the rats in each group were given 10% ethanol in the drinking water for the last 4 wk. In rats fed the iron-deficient diet (D), the content of total hepatic lipid was higher than that in the rats given the normal diet (N). From the gas chromatography analyses of the fatty acids in total lipids, only the proportion of 18:2n-6 was increased, whereas those of 16:1n-7 and 20:4n-6 decreased. In rats given ethanol and an iron-sufficient diet (NE), the contents of all lipids with the exception of phospholipid were significantly higher than those in the N group. The percentages of fatty acids 12:0, 14:0, 16:0, 18:1 and 20:1 in the total hepatic lipid were increased, whereas those fatty acids of 18:0, 20:4, 22:6 and 24:0 were decreased. In the rats given ethanol and an iron-deficient diet (DE), the contents of all hepatic lipid components did not differ significantly from those in the D group. The percentages of fatty acids 12:0, 14:0 and 16:1 in the total hepatic lipid were increased. These data suggest that ethanol ingestion by iron-deficient rats does not induce the same changes in their hepatic lipid components and fatty acid patterns as those seen in fatty degeneration of the liver.

13-cis-retinoic acid and hepatic steatosis in rats

The effect of administration of 13- cis-retinoic acid (100 mg/kg diet) on lipid metabolism was examined in male rats fed either a 20% casein + 0.3% methionine diet, a 20% casein diet, a 10% casein + 0.3% methionine diet, or a 10% casein + 0.6% methionine diet for 10 days. Hepatic triglyceride concentrations of rats fed either 10% casein diet were 3-fold greater than animals receiving diets containing 20% casein. The addition of 13- cis-retinoic acid to the diet further increased the total hepatic lipid (43–56%) and triglyceride (~2-fold) concentrations in rats fed the 10% casein diets. 13- cis-Retinoic acid supplementation did not alter the total liver lipid or triglyceride concentrations in rats fed either of the 20% casein diets. Thus, under specific dietary conditions, the administration of 13- cis-retinoic acid resulted in a marked accumulation of hepatic lipids which did not appear to be related to the total methionine content of the diet nor to the hepatic concentrations of S-adenosylmethionine and glutathione. In addition, all four groups of 13- cis-retinoic acid-fed rats exhibited elevations in the concentration of serum triglycerides, and 10–20% reductions in serum cholesterol concentrations.

Total Parenteral Nutrition Containing Medium- vs. Long-Chain Triglyceride Emulsions Elevates Plasma Cholesterol Concentrations in Rats , ,

Male Fischer 344 rats (235-246 g) were fed for 6-14 d by intravenous or intragastric infusion with total parenteral nutrition (TPN) solutions providing 40 or 65% of nonprotein energy as fat from long-chain triglyceride (LCT) or a 3:1 admixture of medium-chain triglyceride (MCT) and LCT emulsions. In three separate experiments, plasma cholesterol concentrations were significantly greater (24-32%) with intravenous infusion of TPN solutions containing MCT-LCT rather than LCT. Plasma cholesterol concentrations in rats were not significantly different with intragastric infusion of TPN solutions containing MCT-LCT rather than LCT. Hepatic total lipid and triglyceride concentrations were not significantly different. Hepatic total cholesterol and esterified cholesterol concentrations were significantly lower in animals given 65% of energy from MCT-LCT rather than LCT emulsions (main effects, two-way ANOVA). The concentration of individual hepatic acyl-CoA esters reflected the fatty acid profiles of the lipid emulsions infused. Total hepatic acyl-CoA concentrations suggested differences in utilization of acyl-CoA esters with intravenous infusion of MCT-LCT rather than LCT and were consistent with rapid oxidation of MCT. These data demonstrate that MCT-LCT elevates plasma cholesterol concentrations compared with LCT emulsions with intravenous, but not with intragastric, infusion of TPN solutions in rats.

Decreased mitochondrial oxidation of fatty acids in pregnant mice: Possible relevance to development of acute fatty liver of pregnancy

Severe impairment of the beta-oxidation of fatty acids, as a consequence of a single factor or a combination of different causes, leads to microvesicular steatosis of the liver. In an effort to understand the mechanism(s) leading to the development of acute fatty liver of pregnancy in some women, we determined the effects of pregnancy on the mitochondrial oxidation of fatty acids in mice. In vivo, the rate of oxidation of the whole fatty-acid chain length was determined by measuring the rate of exhalation of [14C]CO2 after intragastric administration of a tracer dose of [U-14C]palmitic acid. [14C]CO2 exhalation was not significantly decreased at 14 days of gestation, but it had declined by 40% at 18 days of gestation (i.e., 24 to 48 hr before delivery). The rate of first beta-oxidation cycle was assessed by measuring the rate of [14C]CO2 exhalation after administration of [1-14C]octanoic acid, [1-14C]butyric acid or [1-14C]palmitic acid. [14C]CO2 exhalation had declined by 60%, 46%, and 24% after administration of [1-14C]octanoic acid, [1-14C]butyric acid and [1-14C]palmitic acid, respectively, in 18-day-pregnant mice. Total hepatic lipids and triglycerides, expressed per gram of liver, remained unchanged in 18-day-pregnant mice. In vitro, the rate of mitochondrial beta-oxidation (expressed per milligram of protein) had decreased by 47% at 18 days' gestation with [U-14C]palmitic acid as substrate and by 33% with [1-14C]octanoic acid but remained unchanged with [1-14C]palmitic acid. The activity of the tricarboxylic acid cycle, assessed by the formation of [14C]CO2 from [1-14C]acetic acid, had decreased by 24%. We conclude that the mitochondrial oxidation of fatty acids decreased during late-term pregnancy in mice as a consequence of both decreased mitochondrial beta-oxidation of medium-chain fatty acids, and decreased activity of the tricarboxylic acid cycle. We suggest that this effect, in combination with other factors, may contribute to the development of fatty liver of pregnancy in some pregnant women.

Milk product and constituent protein effects on plasma and hepatic lipids and systolic blood pressure of normotensive rats

The effects of diets containing casein (C), whey protein concentrate (W), skim milk protein concentrate (MPC), and yogurt powder (Y) on plasma total cholesterol, triacylglycerides and HDL-cholesterol (HDL-C), hepatic total lipids and cholesterol levels were studied in normotensive Wistar rats. Systolic blood pressure (SBP) was recorded weekly from 6 to 10 weeks of age. Diet effects were compared to animals fed soy protein isolate (S) and rat chow (RC) diets. Animals were meal fed until 10 weeks of age, when blood and liver tissue samples were collected. All groups exhibited similar growth rates. Animals fed C, W, MPC and S diets exhibited similar plasma triacylglycerides and total cholesterol levels, which were higher ( p ≤ 0·05) than in Y and RC animals. HDL-C was higher ( p ≤ 0·05) in C, W and MPC fed animals, than those fed Y or RC. HDL-C in S fed animals only approached a significantly ( p ≤ 0·07) lower amount compared to C, W and MPC fed animals. Hepatic total lipids and cholesterol were not significantly ( p > 0·05) different between groups. The small changes in plasma lipids observed in animals fed dairy products had little effect on SBP in normotensive rats.

Effect of Taurine Levels on Liver Lipid Metabolism: An In Vivo Study in the Rat

Previous studies using guinea pigs and cats have shown that liver lipid composition is affected by intrahepatic taurine levels. The purpose of the present study was to determine whether this sulfonated amino acid could also affect lipid metabolism in the rat, an animal capable of synthesizing substantial amounts of taurine and used extensively in studies on lipid metabolism. Wide variations in the hepatic taurine content were induced by administering either 1% taurine or 1% guanidinoethane sulfonate in the drinking water for 2 weeks. These treatments increased and decreased taurine liver content, respectively, but did not affect either food or water intakes, or growth rates. The plasma concentrations of the major lipid classes in treated animals did not show any significant alteration in comparison to control animals, except for nonesterified fatty acid levels that were significantly lowered by guanidinoethane sulfonate administration. Taurine supplementation did cause a significant decrease in total hepatic lipid content that was attributable to the reduction of free and esterified cholesterol, triglyceride, and phosphatidylethanolamine hepatic concentrations. This same treatment slightly increased both bile flow and secretion of taurine-conjugated primary bile salts. In particular, the proportion of tauro-beta-muricholate significantly increased, whereas that of taurodeoxycholate greatly decreased. The administration of guanidinoethane sulfonate reduced both the bile flow and the secretion of taurine-conjugated bile salts and caused a significant alteration in the ratio between glycine- and taurine-conjugated bile salts. This did not occur after the treatment with taurine. Interestingly, we observed an inverse correlation between hepatic taurine levels and the proportion of either cholesteryl ester in hepatic lipids or taurochenodeoxycholate in biliary bile salts. These facts suggest that taurine hepatic levels influence mostly hepatic steroid metabolism, but they also affect the metabolism of other lipid classes.

Temporal changes in plasma thyroid hormone, growth hormone and free fatty acid concentrations, and hepatic 5?-monodeiodinase activity, lipid and protein content during chronic fasting and re-feeding in rainbow trout (Oncorhynchus mykiss)

Temporal changes in growth, plasma thyroid hormone, cortisol, growth hormone (GH) and non-esterified fatty acid (NEFA) concentrations, hepatic T3 content and hepatic 5'-monodeiodinase activity were measured in rainbow trout (Oncorhynchus mykiss) subjected to a sustained fast for up to eight weeks, and during a four-week re-feeding period. The purpose of the study was to examine aspects of the endocrine control of energy partitioning processes characteristic of short-term (acute; fasting) and long-term (chronic; starvation) food-deprivation states in fish, and to explore the role of the thyroid hormones, cortisol and GH in the energy repartitioning that takes place during an acute anabolic (re-feeding) state following chronic food deprivation.Differences in growth rate between fed and fasted groups were evident after two weeks, but significant weight loss by the fasted groups was not evident until between four and six weeks into the fast. Hepatosomatic indices (HSIs) were significantly reduced in the fasted fish within seven days, and as early as two days in one study; recovery of the HSI in fasted fish was evident within three days of re-feeding. Liver protein content (expressed as % wet weight) was consistently depressed in the fasted fish in only one of the three studies. Liver total lipid content (expressed as % wet weight) was depressed in the fasted fish within two days of food deprivation. Because of the rapid and sustained decrease in the HSI of fasted fish, the hepatic total protein and lipid reserves, when considered on a body weight basis, were markedly lowered within the first few days of the fast. Plasma GH concentrations exhibited a bi-modal pattern of change, with a transient fall in levels, followed by a sustained increase in fasted fish. The indicators of interrenal activity were suggestive of a depressed pituitary-interrenal axis in fasted animals; plasma cortisol levels were elevated to levels of fed animals within one day of re-feeding. The indicators of thyroid hormone economy (plasma thyroid hormone levels, liver triiodothyronine content, hepatic 5'-monodeiodinase (MD) activity, thyroid epithelial cell height) were similarly indicative of a depressed pituitary-thyroid axis in fasted animals, with recovery to levels of the fed animals within one week. Despite the compensatory changes in accumulation of reserves (as indicated by a compensatory increase in HSI), there were no apparent compensatory changes in any of the endocrine parameters evident during the re-feeding period.