Objectives: Any uptake of I-131 after total thyroidectomy means the remant thyroid tissue or distant metastasis of the thyroid cancer. However diffuse hepatic uptake of I-131 without abnormal uptake was showen in many cases on I-131 whole body scan. The aim of this study was to classify the liver uptake after I-131 scan and to evaluate the analysis of this finding. Materials and Methods: Between 1982 and 1998, 104 patients(l4 males, 90 females) with normal liver function underwent I-131 scan after total thyroidectomy. Prospectively we reviewed the films of the whole body scan and analysed the correlations between results of radioiodine uptake, pathologic diagnosis, prognostic factors, lymphatic metastasis, and thyroid function test. Result: Diffuse hepatic uptake was found in 44 of 104(42%) patients. 10 of 39(26%) patients on I-131 100mCi, and 34 of 63(54%) on I-131 150mCi showed hepatic uptake. 52 of 104(50%) patients was locally invasive thyroid cancer. The rate of the hepatic uptake was no significant differences with the thyroid hormone levels(T3, Free T4) and thyroglobulin between uptake group and non-uptake group. Conclusion: The rate of I-131 uptake was high in high-dose radioiodine treatment group. However, we can not find any correlation among the thyroid functions, the extent of metastasis or the extent of local invasion. We need further study to find out the causes of the hepatic uptake of I-131 after total thyroidectomy, besides liver metabolism of I-131 attached thyroid hormones.
In order to independently examine the effects of long-chain saturated fatty acids and dietary cholesterol levels on plasma and hepatic cholesterol concentrations, six different diets were fed to male Mongolian gerbils (14 gerbils pes grcup) for an 8-week period. Purified diets contained 36% energy as fat (each saturated fatty acid tested comprised about 20% of the total fat energy) and 0.06% (w/w) cholesterol, corresponding to typical human consumption patterns in Western diets. Fat blends were formulated with natural fat sources. To determine the effects of different saturated fatty acids on plasma and liver cholesterol levels, four of the six diets contained constant levels of all nutrients except for the amounts of lauric acid (12 0), myristic acid (14 : 0), palmitic acid (16 0), and stearic acid (18 : 0). Dietary cholesterol effects were tested using 16 : 0-enriched diets containing 0, 0.006, and 0.06% (w/w) cholesterol. None of the plasma lipids were influenced by fatty acid treatment, including triglycerides, plasma total-, VLDL+LDL-, and HDL-cholesterol. However, hepatic esterified cholesterol concentrations were increased in the palmitic and stearic arid diet groups compared to the lauric and myristic acid diet group. The molar ratios of hepatic EC/FC were the highest in the palmitic acid diet (12.2 $\pm$0.6) and the lowest in the myristic acid diet (6.4$\pm$0.2). Dietary cholesterol significantly (p<0.001) increased the plasma total cholesterol which was due to the increase of both HDL-and VLDL+LDL-cholesterol. In the absence of dietary cholesterol and compared to other species, the gerbil exhibited a high molar ratio of hepatic EC/FC, which was funker elevated by dietary cholesterol feeding (0.06%). The results from this study indicate that hepatic cholesterol concentrations are sensitive to both low levels of dietary cholesterol and saturated fatty acid chain length and also, that plasma cholesterol concentrations are sensitive to low levels of dietary cholesterol .
Baik, Myunggi;Nguyen, Trang Hoa;Jeong, Jin Young;Piao, Min Yu;Kang, Hyeok Joong
Asian-Australasian Journal of Animal Sciences
/
제28권1호
/
pp.127-134
/
2015
Castration induces the accumulation of body fat and deposition of intramuscular fat in Korean cattle, resulting in improved beef quality. However, little is known about the metabolic adaptations in the liver following castration. To understand changes in lipid metabolism following castration, hepatic expression levels of lipid metabolism genes were compared between Korean bulls and steers. Steers had higher (p<0.001) hepatic lipids contents and higher (p<0.01) mRNA levels of lipogenic acetyl-CoA carboxylase. This differential gene expression may, in part, contribute to increased hepatic lipid content following the castration of bulls. However, we found no differences in the hepatic expression levels of genes related to triglyceride synthesis (mitochondrial glycerol-3-phosphate acyltransferase, diacylglycerol O-acyltransferase 1 and 2) and fatty acid (FA) oxidation (carnitine palmitoyltransferase 1A, C-4 to C-12 straight chain acyl-CoA dehydrogenase, very long chain acyl-CoA dehydrogenase) between bulls and steers. No differences in gene expression for very-low-density lipoprotein (VLDL) secretion, including apolipoprotein B mRNA and microsomal triglyceride transfer protein (MTTP) protein, were observed in the liver although MTTP mRNA levels were higher in steers compared to bulls. In conclusion, FA synthesis may contribute to increased hepatic lipid deposition in steers following castration. However, hepatic lipid metabolism, including triglyceride synthesis, FA oxidation, and VLDL secretion, was not significantly altered by castration. Our results suggest that hepatic lipid metabolism does not significantly contribute to increased body fat deposition in steers following castration.
It is known that dehydroepiandrosterone (DHEA) shows a dual effect, prooxidant or antioxidant, depending on the do-sage or physiological status of animals. The purpose of this study was to determine the effects of DHEA administration at low dose on lipid peroxidation, protein carbonylation and fatty acid composition in liver. Sprague Dawley male rats were fed either com oil diet containing $15\%$ com oil or fish oil diet containing $2\%$ corn oil + $13\%$ sardine oil, with or without $0.2\%$ DHEA for 9 weeks. Atherogenic index and hepatic triglyceride and cholesterol levels were significantly reduced by DHEA administration in rats fed with fish oil diet. Hepatic lipid peroxide product (TBARS) and protein carbonyl levels were significantly higher in rats fed with fish oil diet than in rats fed with corn oil diet. However, DHEA administration significantly reduced the hepatic thiobarbituric acid-reactive substance (TBARS) and conjugated diene levels in rats fed with fish oil diet. Contents of C16 : 0, C16 : 1, C20 : 5 and C22 : 6 in hepatic microsome were higher in rats fed with fish oil diet than in rats fed with corn oil diet, and contents of C18 : 2 and C20 : 4 were lower than in rats fed with com oil diet. DHEA administration significantly increased C16 : 0 and C18 : 3 contents and reduced C18 : 2 content in rats fed with com oil diet, while it increased C16 : 0 and C18 : 1 and reduced C20 : 5 and C22 : 6 in rats fed with fish oil diet. On overall, DHEA administration increased saturated fatty acid (SFA) and reduced polyunsaturated fatty acid (PUFA) in hepatic microsome, thereby PUFA/SFA ratio was significantly (p < 0.0001) reduced without the change of n-3/n-6 ratio. Taken together, low dose of DHEA administration lowered PUFA/SFA ratio in hepatic microsomal membranes and also showed antioxidative effect especially in fish oil-induced highly oxidative stress condition through blocking increases of C20 : 5 and C22 : 6 contents.
Mostly, hypercholesterolemia has been focused on atherosclerosis and coronary heart disease and can be produced by intake of high cholesterol diet. However, toxic effects of cholesterol itself on liver and relationship between intake of high cholesterol diet and hepatic fibrosis have not been clearly investigated. Male Wistar rats were fed diet supplemented with 1.0 % cholesterol and 0.3 % sodium cholate for 12 weeks. Rats were sacrificed at 0, 3, 6, 9 and 12, respectively. Histopathological and blood chemical studies were performed on these animal sets. Total cholesterol, AST, ALT and LDH levels increased from week 3 and maintained around that level throughout the experiment compared to control. However, TG and albumin levels were the same or lower than those of control. Intake of high cholesterol and sodium cholate diet caused hepatic necrosis, macrophage infiltration, steatosis and fibrosis. Following feeding this diet to rats, hepatic necrosis, macrophage infiltration and steatosis markedly increased throughout the experiment, comparing to control. Collagen deposition and myofibroblasts were detected from at week 9 to 12 in the liver. Mast cell increased in proportion to the degree of hepatic damages. In conclusion, these results suggest that intake of high cholesterol diet is a risk factor on hepatic steatosis and fibrosis as well as atherosclerosis and coronary heart disease. Furthermore, this animal model for hepatic fibrosis can be use for application of anti-fibrogenic agents screening in vivo.
This study was designed to determine the effects of larval extracts from Protaetia brevitarsis seulensis shade dried larva from Korea and China on liver tissues of hepatic injury groups. The experimental groups are divided into five groups; Normal, carbon tetrachloride single injection ($CCl_4$), Pb-CHI ($CCl_4$ + P. brevitarsis shade dried larva from China), Pb-KOR ($CCl_4$ + P. brevitarsis shade dried larva from Korea) and SIL ($CCl_4$ + 0.35% silymarin) groups. Sprague Dawley rats were oral injected with $CCl_4$ at a dose l mg/kg (20% in corn oil) for induction of liver damage for 4 weeks. Each experimental group was fed with a dose 50 mg/kg of larval extracts based on medicinal preparations from 3 weeks to 4 weeks after $CCl_4$ treatment. At the end of 4 weeks, we evaluated the serum levels of glutamate-oxaloacetate transaminase (GOT), glutamate-pyruvate transferase (GPT), alkaline phosphatase (ALP) and blood urea nitrogen (BUN) in serum and the cytokine levels of tumor necrosis factor-${\alpha}$) (TNF-${\alpha}$) and transforming growth factor-${\beta}$ (TGF-${\beta}$) in the cells isolated from spleen and liver. The histological analysis was also conducted. The $CCl_4$ injection reduced body weight, induced congestion of middle lobe and hepatocytic degeneration, resulting in disintegration of hepatic cords, and increased biochemical markers of blood related to hepatic injury. On the other hand, the Pb-CHI and Pb-KOR group decreased the levels of biochemical markers in blood and cytokine levels in spleen and liver. Especially, the Pb-KOR group facilitated the recovery of biochemical values of blood related to hepatic injury, hepatic lesions and fibrosis. Taken together, larval extract from P. brevitarsis might prevent acute hepatotoxicity and enhance the recovery of liver fibrosis and cirrhosis induced by $CCl_4$, and the ingredients could be a promising candidate for the prevention and treatment of hepatic disorders.
A number of toxicants have been incriminated as a causing hepatic disease. Among many detrimental injury, alcohol has been noted for hepatitis, fatty liver, fibrosis, and hepatic cirrhosis. The purpose of this study was to develop animal model for hepatic fibrosis in pigs fed ethanol, and to search for a new anti-fibrogenic agent via this model. Twelve male Landrace pigs were divided into 3 groups of 4 animals each. Group 1, 2 and 3 were fed with active ceramic water only, ceramic water + liquid diet containing 15% ethanol and normal tap water + liquid diet containing 15% ethanol for 12 weeks, respectively. At week 12, all pigs were immediately sacrificed for collection each tissue and blood. Serologically, serum ALT and AST levels were significantly reversed in group 2, as compared to group 3. They were normal range in pigs of group 1. Microscopically, macrovesicular lipid droplets and moderate hepatocellular necrosis were evident in the tap water + ethanol fed group 3. However, the active ceramic water treated group 1 showed normal architecture. Moreover, in group 2, mild fatty changes and necrosis were observed in hepatocytes. Collagen fibers were increased in spaces surrounding periportal and interlobular connective tissues in the group 3 of tap water + ethanol, but collagen synthesis and its thickness of fibrotic septa connecting portal tracts were markedly reduced in the group 2 of ceramic water + ethanol. Myofibroblasts were detected mainly in the interlobular connective tissues of pig liver of group 3 treated ethanol and tap water. Few to no myofibroblasts were observed in groups 1 and 2. CYP2E1 was not or rarely detected in group 1 fed ceramic water. However, group 2 showed slightly activation of CYP2E1 in the area of pericentral vein, while CYP2E1 was significantly activated in group 3 fed tap water and ethanol. Based on the above data, we believe that we have developed a unique alcohol induced fibrosis model in pig, which will be useful in developing anti-fibrotic agents and drugs. Furthermore, the active ceramic water used in our study had an inhibitory and may be protective against ethanol induced hepatic toxicity and fibrosis.
The focus of this study was to investigate the influences of enzymatic scavengers of active oxygen metabolites and phospholipase $A_2$ inhibitor on hepatic secretory and microsomal function during hepatic ischemia/reperfusion. Rats were pretreated with free radical scavengers such as superoxide dismutase (SOD), catalase, deferoxamine and phospholipase $A_2$ inhibitor such as quinacrine and then subjected to 60 min. no-flow hepatic ischemia in vivo. After 1, 5 hr of reperfusion, bile was collected, blood was obtained from the abdominal aorta, and liver microsomes were isolated. Serum aminotransferase (ALT) level was increased at 1 hr and peaked at 5 hr. The increase in ALT was significantly attenuated by SOD plus catalase, deferoxamine and quinacrine especially at 5 hr of reperfusion. The wet weight-to-dry weight ratio of the liver was significantly increased by ischemia/reperfusion. SOD and catalase treatment minimized the increase in this ratio. Hepatic lipid peroxidiltion was elevated by ischemia/reperfusion, and this elevation was inhibited by free radical scavengers and quina crine. Bile flow and cholate output, but not bilirubin output, were markedly decreased by ischemia/reperfusion and quinacrine restored the secretion. Cytochrome $P_{450}$ content was decreased by ischemia/reperfusion and restored by free radical scavengers and quinacrine to the level of that of the sham operated group. Aminopyrine N-demethylase activity was decreased and aniline p-hydroxylase was increased by ischemia/reperfusion. The changes in the activities of the two enzymes were prevented by free radical scavengers and quinacrine. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory functions as well as microsomal drug metabolizing systems by increasing lipid peroxidation, and in addition to free radicals, other factors such as phospholipase $A_2$ are involved in pathogenes of hepatic dysfunction after ischemia/reperfusion.
This study was performed to establish the recovery effect of So Si Ho Tang on hepatic injury in dogs. Clinically healthy eight dogs (1-3 yrs old, 3-5 kg) were divided into control group (n=3) and experimental group (50 mg/kg, n=5). Hepatic injury was induced by administration of $CCl_4$ in all groups. Control group was received no treatment after hepatic injury and experimental group was orally administered with So Si Ho Tang at a dose of 50 mg/kg. The change of serum ALT and AST activities was examined before hepatic injury and on day 0, day 5 and day 12 after administration of So Si Ho Tang. Histopathologic examinations were performed on day 12. As a result, significant changes in serum ALT were found on day 5(p<0.05) and day 12(p<0.05), compared with those of control group, respectively. In addition, significant change in serum AST was found on day 1 (p<0.05) and day 5 (p<0.05), compared with those of control group, respectively. In histopathologic examination, mild hemorrhage and fatty degeneration and vacuolization were observed in experimental group in contrast to those of control group. Accordingly, it was suggested that administration of So Si Ho Tang was effective for hepatic injury induced by $CCl_4$ in dogs.
After Triton WR-1339 (TX; 600mg/kg) intraperitoneal injection, hepatic tissues of ICR mice were intragastric injected with Hyulboochucketang extract(HCE; 3.3ml/kg/day) were observed to investigate the suppressive effect of lipid accumulation that evoke by the antihyperlipidemic effect of HCE. These hepatic tissues were fixed in fromol-calcium solution and were cryocut. These tissues stained by H&E for general morphology, sudan black B for lipid and perchloric acid-naphthoquinone(PAN) method for cholesterol. After TX treatment, the increase of hepatocyte having meshlike cytoplasm(HHMC) were shown in all hepatic lobules and the hepatic plates were disappeared in the aggregative region of HHMC. The number of blue black colored lipid drop and dark green colored asterisk shaped cholesterol particle in hepatic cytoplasm were increased and the size of lipid drop and cholesterol particle were enlarged. But, in HCE-treated mice, the HHCM were disappeared and hapatic plate were rearranged. The number of lipid drop and cholesterol particle were decreased than TX-treated mice and the size of lipid drop and cholesterol particle were diminished. As results indicated that the HCE work on the suppression of lipid accumulation in hepatic tissue of hyperlipidemic mice caused by disturbance of lipid metabolism.
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