This study was conducted to investigate the effects of mulberry fruit, mulberry leaves and silkworm powder with different mixing ratios on hepatic antioxidative system and lipid metabolism in streptozotocin-induced diabetic rats. Sprague-Dawley male rats weighing $100{\pm}10g$ were induced diabetic by 50 mg/kg bw streptozotocin and randomly assigned to following experimental groups; normal diet group (DM), 0.3% and 0.6% mulberry fruit diet groups (F and 2F), 0.3% mulberry leaves diet group (M), 0.3% silkworm powder diet group (S), 0.15% mulberry fruit+0.15% mulberry leaves diet group (FM), 0.15% mulberry fruit+0.15% silkworm powder diet group (FS), 0.1 % mulberry fruit+0.1 % mulberry leaves+0.1% silkworm powder diet group (FMS). The experimental diets were fed for 4 weeks. Hepatic SOD activity was not changed significantly by any of single or combined supplementations of mulberry fruit, leaves and silkworm powder but GSH-px and catalase activities were increased by the groups supplemented with two or three of the test ingredients (FM, FS, FMS) as compared with the DM group. Hepatic TBARS value was not reduced significantly by any of the supplementations but lipofuscin contents were significantly reduced in the FM, FS and FMS groups as compared with the DM group. Hepatic mitochondria and microsomal carbonyl values were reduced by the single and combined supplementations of the test ingredients. Hepatic HMG-CoA reductase activities were increased in the all supplementation groups as compared with the DM group. Hepatic total lipid and triglyceride contents were increased but cholesterol contents reduced in the supplemented groups. The effects on the enzyme activities, peroxide or its products and lipid contents were most remarkable in the FMS group. In conclusion, mulberry fruit, mulberry leaves and silkworm powder have the favorable effects on antioxidative system and lipid metabolism in the diabetic liver and the mulberry fruit, leaves and silkworm powder with equal ratio exert the synergistic effect expectedly to prevent diabetic complications.
Objective: This study was conducted to investigate the effects of age and diet forms on growth-development patterns, serum metabolism indicators, and parameters of body fat deposition in Cherry Valley ducks. Methods: According to the hatching age and initial weight, a total of 150 1-day-old male SM3 Cherry Valley ducks were randomly assigned to two diet forms (pellet vs powder form). Each treatment had with 5 replicates per treatment and 15 meat ducks per replicate. The study lasted 42 d, which was divided into two periods (1 to 21 vs 22 to 42 d). Results: Our results showed that compared with powder group, ducks in pellet group had greater growth performance during different period (p<0.05). The inflection point was 24 d and was not numerically affected by diet forms. Increasing age (42 vs 21 d) significantly increased the weight of body fat and hepatic fat metabolism related enzyme activities in ducks (p<0.05), meanwhile, increasing age (42 vs 21 d) improved serum metabolism indicators and decreased mRNA expression levels of fat metabolism-related genes in liver (p<0.05). Ducks fed different diets (pellet vs powder form) increased growth performance as well as the weight of body fat and improved serum metabolism indicators (p<0.05). In addition, interactions were found between age and diet forms on the levels of serum metabolism indicators in ducks (p<0.05). Conclusion: In conclusion, powder feed reduced growth performance of ducks, and the day of inflection point was 24 days old. Ducks with higher age or fed with pellet diet showed higher fat deposition. The effect of age and feed forms on body fat deposition might result from changes in the contents of serum metabolism indicators, key enzyme activity of lipid production, and hepatic gene expressions.
This study was designed to examine the effect of estrogen deficiency on the metabolism of ethanol in ovariectomized rats. Female rats were assigned to an ovariectomy (OVX) and a sham (SHAM) surgery group. Gain body weight was greater in incresed in OVX group and especially uterus weight significantly decrease depending on the concentration of estrogen after 3 month of ovariectomy. Ethanol at the tolerative dose (6 g/kg) was injected to rats by oral administration to measure the concentration of ethanol in blood. The area under the blood concentration time curve (AUC) was significantly lower in OVX group than SHAM group. The significant decrease in AUC in OVX group indicates that the estrogen deficiency leads to changes of the factors related to ethanol metabolism. Activity of hepatic alcohol dehydrogenase was not significantly influenced by the ovariectomy and also the ethanol elimination rate in vivo was not different. Cytochrome P450 isozymes did not show any changes except CYP 1A1 and 2E1. Level of hepatic glutathione in OVX group was higher after treatment of ethanol. Therefore the reduction of AUC appears not to be directly associated with the difference of ethanol metabolizing enzyme, but to be related with the physical factors like body weight.
This study was done to investigate effects of n-s fatty acids and vitamin E supplement on the preneoplastic hepatic enzyme altered foci and cholesterol metabolism in experimental hepatocarcinogenesis system. Weaning male Sprague-Dawley rats were fed the diet containing either 15% corn oil(CO) or sardine oil(SO) with or without vitamin E 800IU supplementation for 12 weeks. After two weeks of feeding, rats were intraper-itoneally injected with a single dose of diethylnitrosamine(DEN:200mg/kg, BW). At the 4th week, rats were given the diet containing 0.02% acetylaminofluorene(AAF) for next 4 weeks. At the 6th Week, 0.05% pheno-barbital was incorporated into diet for 6 weeks. At the end of 12th week, rats were sacrificed and hepatic glutathions S-transferase placental form positive(GST_{TEX}$P^{+}${/TEX}) foci and serum and liver cholesterol levels were determined. GST_{TEX}$P^{+}${/TEX} formation was significantly decreased by SO feeding when compared with Co feeding but it tended to be enhanced by vitamin E supplementation. Histopathological changes were similar to patterns of GST_{TEX}$P^{+}${/TEX} formation in almost all dietary groups. Serum and hepatic cholesterol levels of SO fed groups were significantly lower than those of CO fed groups. Carcinogen treatments significantly increased serum and liver cholesterol levels in CO fed groups but not in SO fed groups. Correlation data showed a positive correlation(${\gamma}$=0.83, p<0.01) between serum cholesterol level GST_{TEX}$P^{+}${/TEX} foci area. These results indicate that sardine oil as a m-3 fatty acid source may have a reducing effect in rat hepatocarcinogenesis by the altheration of cholesterol metabolism.
Ginseng may have antioxidant and pharmacologic effects similar to those of vitamin E. The interactive effect of ginseng and vitamin E was studied with respect to cholesterol metabolism and the antioxidant status. A ginseng supplement (0.1%, wt/wt) with comparable levels of vitamin E was provided with a high-cholesterol (1%, wt/wt) diet to rats for 5 weeks. The amount of vitamin E included in the ginseng-free and ginseng diets was either a low (low-E) or a normal (normal-E) level. The ginseng supplements significantly (p<0.05) altered the concentrations of plasma triglycerides in both the low-vitamin E group and normal-vitamin E group compared to the each ginseng-free group. The hepatic triglyceride and cholesterol content were not significantly (p>0.05) different between groups regardless of the vitamin E level in the diet. The hepatic HMG-CoA reductase activity was significantly (p<0.05) lowered by the ginseng supplement in both the low-vitamin E and the normal-vitamin E groups compared to the ginseng-free group. The HMG-CoA reductase activity was also significantly (p<0.05) lowered with in increase of the dietary vitamin E in the ginseng-free group. The excretion of fecal neutral sterol was significantly (p<0.05) lower in the normal-E ginseng group than th low-E ginseng-free group. Neither dietary ginseng nor vitamin E significantly changed the hepatic antioxidant enzymes activity. This data indicates that ginseng supplements lower the concentration of plasma triglyceride and hepatic HMG-CoA reductase activity regardless of eh dietary vitamin E level. This information may contribute to understanding the interactive effect of ginseng and vitamin E on cholesterol biosynthesis in high cholesterol-fed rats.
Purpose: Sour cherry (Prunus cerasus L.) contains abounding phytochemicals, such as polyphenols and anthocyanins, and has antioxidative effects. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator in enhancing the lipid metabolism. This study hypothesized that the intake of sour cherry affects AMPK signaling. Therefore, this study examined whether sour cherry regulates AMPK to balance the hepatic lipid metabolism and exert ameliorating effects. Methods: Male C57BL/6J mice had obesity induced with a 45% fat diet. The mice were divided into four groups: control (CON), high-fat diet (HFD), low percentage sour cherry powder (LSC), and high percentage sour cherry powder (HSC). The mice in the sour cherry groups were fed 1% sour cherry or 5% sour cherry in their respective diets for 12 weeks. Results: The body weight, visceral fat weight, and lipid droplet size significantly decreased in the treatment groups. The serum and hepatic triglyceride and total cholesterol levels improved significantly in the HSC group. The low-density lipoprotein cholesterol levels were also reduced significantly, whereas the high-density lipoprotein cholesterol levels were increased significantly in both treatment groups. The sterol regulator binding protein-1c and fatty acid synthase expression levels as fatty acid synthesis-related enzymes were significantly lower in the treatment groups than in the high-fat diet group. Furthermore, the adipose triglyceride lipase and hormone-sensitive lipase expression levels as lipolytic enzyme activity and AMPK/acetyl-CoA carboxylase/carnitine palmitoyltransferase-1 as fatty acid β-oxidation-related pathway were upregulated significantly in both sour cherry groups. Conclusions: These results show that sour cherry intake improves hepatic lipid synthesis and chronic diseases by activating AMPK signaling. Therefore, this study suggests that phytochemical-rich sour cherry can be developed as a healthy functional food.
Pharmacokinetic characteristics of Acebutolol and its main metabolite, diacetolol, following a single 10 mg/kg oral dose, were investigated in rabbits with carbon tetrachloride-induced hepatic failure. Plasma concentrations of acebutolol and diacetolol were determined by a high performance liquid chromatography assay. The area under the plasma concentration-time curves (AUC) and maximum plasma concentration ($C_{max}$) of acebutolol were significantly increased in moderate and severe carbon tetrachloride-induced hepatic failure rabbits. The ratio of the diacetolol to total acebutolol in plasma (i.e., metabolite percentage rate) was significantly decreased in moderate and severe carbon tetrachloride-induced hepatic failure rabbits. Volume of distribution ($V_{d}$) and total body clearance ($CL_{t}$) of acebutolol were significantly decreased in moderate and severe carbon tetrachloride-induced hepatic failure rabbits. Slope of terminal phase ($\beta$) of acebutolol was significantly decreased in hepatic failure rabbits. These findings suggest that the $V_{d},{\;}CL_{t}$ and $\beta$ of acebutolol were significantly decreased as a result of inhibition of the hepatic metabolism in moderate to severe hepatic failure rabbits. Therefore, dose adjustment may be necessary for acebutolol in hypertensive patients with hepatic damage.
BACKGROUND/OBJECTIVES: Changes in nutritional status during gestation and lactation have detrimental effects on offspring metabolism. Several animal studies have shown that maternal high-fat diet (HFD) can predispose the offspring to development of obesity and metabolic diseases, however the mechanisms underlying these transgenerational effects are poorly understood. Therefore, we examined the effect of maternal HFD consumption on metabolic phenotype and hepatic expression of involved genes in dams to determine whether any of these parameters were associated with the metabolic outcomes in the offspring. MATERIALS/METHODS: Female C57BL/6 mice were fed a low-fat diet (LFD: 10% calories from fat) or a high-fat diet (HFD: 45% calories from fat) for three weeks before mating, and during pregnancy and lactation. Dams and their male offspring were studied at weaning. RESULTS: Dams fed an HFD had significantly higher body and adipose tissue weights and higher serum triglyceride and cholesterol levels than dams fed an LFD. Hepatic lipid levels and mRNA levels of genes involved in lipid metabolism, including $LXR{\alpha}$, SREBP-2, FXR, LDLR, and ABCG8 were significantly changed by maternal HFD intake. Significantly lower total liver DNA and protein contents were observed in dams fed an HFD, implicating the disturbed liver adaptation in the pregnancy-related metabolic demand. HFD feeding also induced significant oxidative stress in serum and liver of dams. Offspring of dams fed an HFD had significantly higher serum cholesterol levels, which were negatively correlated with liver weights of dams and positively correlated with hepatic lipid peroxide levels in dams. CONCLUSIONS: Maternal HFD consumption induced metabolic dysfunction, including altered liver growth and oxidative stress in dams, which may contribute to the disturbed cholesterol homeostasis in the early life of male mice offspring.
Objective: Ramulus mori (RM) has been known to be effective for the treatment of obesity. To show the effectiveness of RM in a more scientific way, RM extract was prepared and evaluated in high fat diet rats by measuring the changes of body weight and lipid metabolism as described briefly below. Methods: 200 g of crushed RM was extracted withmethyl alcohol. The extract was evaporated under reduced pressure to give 33.4 g. For 10 weeks, control group rats were fed a high fat diet, while the test group rats were fed with the same diet plus RM extract. The normal group was fed with a normal diet. 150 mg of RM extract per 1 kg of body weight was added to the diet in the test group rats. Results: The control group rats on the high fat diet gained weight significantly, whereas the test group rats on the high fat diet plus RM extract gamed less weight. The significant increase of liver weight caused by the high fat diet was also inhibited by the RM extract treatment. Total lipid, triglyceride and total cholesterol levels of serum in the high fat diet rats were remarkably increased, whereastheir levels on the high fat diet plus RM extract were less increased. While serum HDL-cholesterol levels were remarkably decreased in the high fat diet, its level was less decreased in the high fat diet plus RM extract. Furthermore, we observed that the activities of hepatic acetyl-CoA carboxylase and fatty acid synthetase increased under the high fat diet, while their activities under the high fat diet plus RM extract were getting back nearly to the normal levels of the normal diet rats. Conclusions: These result show that the obesity caused by a high fat diet was effectively inhibited by an RM extract. Our results also showed that the abnormal lipid metabolism caused by a high fat diet was effectively cured by adding RM extract.
The purpose of this study was to investigate the effects of altering relative intakes of fat and carbohydrates on serum lipid profiles, hepatic acyl-CoA synthetase (ACS), carnitine palmitoyltransferase-I (CPT-I), and the acetyl-CoA carboxlyase (ACC) mRNA level in Sprague-Dawley rats. For four weeks the rats were fed either an AIN-76 diet or one of its modified diets that were supplemented with 20% beef tallow (high-fat diet, HF) and 66.3% sucrose (highsucrose diet, HS). The HS group had significantly higher serum triglyceride and total cholesterol concentrations when compared with the other groups. Serum LDL-cholesterol concentrations in the HS and HF groups were significantly higher when compared to the normal diet (ND) group. Serum HDL-cholesterol levels of the ND and HS groups were significantly higher than those of the HF group. The hepatic total lipid level of the HF group was significantly higher than those of other groups; triglyceride levels of the HS and HF groups were significantly higher than those of the ND group. Hepatic ACS mRNA levels of the HF group were significantly higher than those of the ND group. Hepatic CPT-I mRNA levels were higher in the HF group than other groups. Also, ACC mRNA levels in the liver increased in the HF group. In conclusion, changes in the composition of dietary fat and carbohydrates could affect the hepatic ACS, CPT-I, and ACC mRNA levels. These results facilitate our understanding of the coordinated regulation of the ACS, CPT-I, and ACC mRNA levels and will serve to enhance our understanding of the molecular mechanisms that underlie the regulation of fatty acid metabolism.
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