Effects of force-feeding and dietary cellulose on liver lipid accumulation and lipid composition of liver and plasma in growing chicks

Changes of content and composition of lipid in liver and plasma affected by force-feeding and dietary cellulose were investigated in 14-day old Single-Comb White Leghorn male chicks. They were given a purified high energy diet (starch-casein diet without fiber) supplemented with or without dietary cellulose. Chicks were fed ad libitum or force-fed the experimental diet. Force-feeding of excess food improved the growth rate of chicks and feed efficiency, but feeding of cellulose did not affect body weight gain and feed efficiency, though a slight improvement in nitrogen retention was observed. Liver weight and lipid content in liver and plasma were markedly elevated by force-feeding, and were markedly depressed by dietary cellulose in the force-fed chicks. It is suggested that changes of liver lipid by force-feeding and dietary cellulose are mainly originated from the changes of triglyceride in the liver lipid. No marked changes were observed in fatty acid composition of abdominal fat and liver lipid in the cellulose-fed chicks. These results suggest that dietary cellulose may affect lipid metabolism in growing chicks.     

Hepatic iron accumulation in copper-deficient rats

Studies of anaemia and tissue iron distribution were carried out in copper-deficient rats and pair-fed control animals given Fe orally or parenterally in varying doses. The anaemia of Cu deficiency was partially but incompletely corrected by oral Fe supplementation of one- to five-fold normal dietary levels or by intramuscular Fe supplementation. Serum Fe increased in Cu-deficient animals as the dose of supplemental Fe was increased. Hepatic Fe accumulation occurred in Cu-deficient rats which were administered with either oral Fe in two- to five-fold excess or low doses of intramuscular Fe. This difference was not seen in animals receiving high doses of intramuscular Fe, but similar relative differences were seen in Cu-deficient and Cu-replete rats which had been given no Fe supplementation. Duodenal Fe was not increased in Cu deficiency. Bone marrow Fe was present in Cu-deficient animals receiving either parenteral or oral Fe supplementation. Present studies suggest that a decrease in caeruloplasmin (EC 1.16.3.1) activity does not wholly explain the anaemia of Cu deficiency. Fe accumulation may be restricted to the liver, suggesting that Cu may be required for normal intracellular Fe metabolism.     

Increased lipid accumulation in liver and white adipose tissue in aging in the SAMP10 mouse

The population of elderly persons has increased worldwide. However, few studies have examined age-dependent changes in lipid and carbohydrate metabolism related to age-related diseases. The number of cases of metabolic syndrome is increasing worldwide and prevention of lifestyle diseases may lead to prolongation of lifespan. In this study, we examined age-dependent changes in lipid and carbohydrate metabolism in the senescence-accelerated (SAM) P10 mouse. Tissue weights and biochemical parameters in plasma and liver were examined in SAMP10 mice aged 3, 6, 9, and 12 mo. White adipose tissue weight and the levels of liver triacylglycerol, plasma free fatty acids, and plasma insulin all showed increases with aging of the mice. To examine this mechanism in detail, aging-related changes in mRNA expression of genes related to lipid and carbohydrate metabolism were examined by DNA microarray analysis. The mRNA level for Hsd11b1 (hydroxysteroid 11-beta dehydrogenase 1), which increases insulin secretion and resistance, was elevated with aging in the liver of SAMP10 mice. These results show that lipid accumulation in liver and white adipose tissue is promoted by aging in SAMP10 mice through an increase in plasma insulin levels.     

Hepatic lipid peroxidation and aldehyde dehydrogenase activity in alcoholic and non alcoholic liver disease

It has been suggested that lipid peroxidation plays a role in the pathogenesis of chronic alcoholic liver disease (CALD). However, whether or not CALD differs from chronic non alcoholic liver disease (CLD) in lipid peroxidation, is still questionable. Thirty-eight patients affected by CALD and CLD who were matched for age, sex, nutrition and liver function tests (LFTs) and 17 controls (C) took part in this study. The following tests were performed: serum and liver malondialdehyde (MDA) determination by the TBA test, liver total glutathione (GSH) estimate, mitochondrial (ALDH2) and cytosolic (ALDH1) aldehyde dehydrogenase activity determinations. Patients who showed signs of malnutrition were excluded from this study. Serum and hepatic TBA-reactive substances resulted in a slight increase in chronic liver patients compared to controls but did not show any difference between CALD and CLD groups. Liver total glutathione did not show any change. Hepatic ALDH2 activity was significantly (P less than 0.01) higher in CALD than in CLD and control patients whereas ALDH1 did not show any difference. These results suggest that the increased lipid peroxidation in CALD and in CLD is probably secondary to liver damage rather than being the pathogenic factor.     

Dietary curcuminoids prevent high-fat diet-induced lipid accumulation in rat liver and epididymal adipose tissue.

Curcumin and its structurally related compounds (curcuminoids), the phenolic yellowish pigments of turmeric, display antioxidative, anticarcinogenic and hypocholesterolemic activities. In this study, we investigated the effects of dietary supplemented curcuminoids [commercial grade curcumin: a mixture of curcumin (73.4%), demethoxycurcumin (16.1%) and bisdemethoxycurcumin (10.5%)] on lipid metabolism in rats. Male Sprague-Dawley rats were assigned to three diet groups (n = 6) and fed a moderately high-fat diet (15 g soybean oil/100 g diet) for 2 wk. One diet group did not receive supplements (CONT), while the others were supplemented with 0.2 g curcuminoids/100 g diet (CUR0.2) or 1.0 g curcuminoids/100 g diet (CUR1.0). Liver triacylglycerol and cholesterol concentrations were significantly lower in CUR1.0 rats than in CONT rats. Plasma triacylglycerols in the VLDL fraction were also lower in CUR1.0 rats than in CONT rats (P < 0.05). Hepatic acyl-CoA oxidase activity of both the CUR0.2 and CUR1.0 rats was significantly higher than that of CONT rats. Furthermore, epididymal adipose tissue weight was significantly reduced with curcuminoid intake in a dose-dependent manner. These results indicate that dietary curcuminoids have lipid-lowering potency in vivo, probably due to alterations in fatty acid metabolism.     

Hepatic fat accumulation in man with excess parenteral glucose

The threshold for the conversion of parenterally administered glucose to hepatic fat was estimated by measuring the amount of fat accumulated in the liver of malnourished cancer patients. Patients were given 7–10 days of TPN with glucose (47 kcal/kg/d) as the sole non-protein calorie source. The derived threshold, 42 kcal/kd/day) is in reasonable accord with the value for the glucose oxidation capacity derived from indirect methods. Most of the newly synthesized fat accumulates in the liver.     

Hepatic lipid profiles in miniature pigs after alcohol feeding

Changes in lipid profiles have not been reported for the known increases in total lipid content in livers of alcoholics. We have reported a lowering of the β-oxidative capacity of alcoholic livers, and therefore would expect a lower turnover of fatty acids in these livers, and thus a change in lipid profile. The percentage composition of saturated and unsaturated fatty acids in the liver of alcohol-fed miniature pigs versus the controls, as well as the function of distance from the main hepatic vein, have both been determined in this study involving the feeding of ethanol for one year. Livers of alcohol-fed miniature pigs contained more total lipids than those of controls. Results also indicated significantly higher percentages of free fatty acids and triglycerides in the alcohol-fed miniature pigs, and also an increase in percentage total neutral lipids. The effect of distance from the main blood source (and therefore oxygenation) gave a fatty acid profile that showed an increase in the ratio of saturated to unsaturated fatty acids with increasing distance from the right hepatic vein. This change in ratio was independent of alcohol feeding.     

2型糖尿病大鼠氧化应激介导肝脏和骨骼肌细胞内脂肪堆积的差异

目的观察2型糖尿病大鼠高脂饮食后肝脏和骨骼肌氧化应激及脂质堆积的差异。方法10只雄性Goto Kakisaki（GK）大鼠随机分为两组：糖尿病对照组和糖尿病硫辛酸治疗组（α-硫辛酸35mg／kg隔天腹腔内注射1次），健康Wistar大鼠4只为正常对照组，高脂饮食12周。测定各组大鼠肝、骨骼肌匀浆中的GSH、SOD和MDA及脂质谱水平，以及观察其组织病理形态学改变。结果糖尿病对照组肝组织GSH、SOD和MDA及脂质谱水平较正常对照组明显异常，经α-硫辛酸治疗后有明显改善，且GSH、SOD和MDA水平与甘油三酯水平相关；骨骼肌组织中除SOD外，GSH和MDA以及脂质谱水平在3组之间的变化，差异无统计学意义（P〉0．05）。糖尿病对照组有明显的肝细胞脂肪变性、坏死及炎性细胞浸润，硫辛酸治疗后有明显改善，而骨骼肌组织病理形态学无明显变化。结论12周高脂饮食可导致明显的氧化应激状态和细胞内脂肪堆积，但肝脏和骨骼肌两者之间存在一定差异，α-硫辛酸通过改善氧化应激状态而对细胞脂质代谢异常有明显的缓解作用。     

全氟辛酸对大鼠肝细胞BRL-3A脂质蓄积的影响

目的 探讨全氟辛酸(perfluorooctanoic acid,PFOA)对大鼠肝细胞BRL-3A细胞活力及对转录因子核因子E2相关因子2(nuclear factor erythroid 2-related factor 2,Nrf2)和精氨酸琥珀酸合酶(arginosuccinate synthase 1,Ass...     

Medium-chain fatty acid reduces lipid accumulation by regulating expression of lipid-sensing genes in human liver cells with steatosis

Accumulation of lipids in the liver can lead to cell dysfunction and steatosis, an important factor in pathogenesis causing non-alcoholic fatty liver disease. The mechanisms related to lipid deposition in the liver, however, remain poorly understood. This study was aimed to investigate the effects of medium-chain fatty acid (MCFA) on the lipolysis and expression of lipid-sensing genes in human liver cells with steatosis. A cellular steatosis model, which is suitable to experimentally investigate the impact of fat accumulation in the liver, was established in human normal liver cells (LO2 cells) with a mixture of free fatty acids (oleate/palmitate, 2:1) at 200?μm for 24?h incubation. MCFA was found to down-regulate expression of liver X receptor-α, sterol regulatory element binding protein-1, acetyl-CoA carboxylase, fatty acid synthase, CD 36 and lipoprotein lipase in this cellular model, and have positive effects on adipose triglyceride lipase and hormone-sensitive lipase. These results suggest that MCFA may reduce lipid accumulation by regulating key lipid-sensing genes in human liver cells with steatosis.     

Chitosan reduces plasma adipocytokines and lipid accumulation in liver and adipose tissues and ameliorates insulin resistance in diabetic rats

Chitosan is a natural product derived from chitin. To investigate the hypoglycemic and anti-obesity effects of chitosan, male Sprague-Dawley rats were divided into four groups: normal control, diabetic, and diabetic fed 5% or 7% chitosan. Diabetes was induced in rats by injecting streptozotocin/nicotinamide. After 10 weeks of feeding, the elevated plasma glucose, tumor necrosis factor-α, and interleukin-6 and lower adiponetin levels caused by diabetes were effectively reversed by chitosan treatment. In addition, 7% chitosan feeding also elevated plasma glucagon-like peptide-1 levels and lowered the insulin resistance index (homeostasis model assessment) in diabetic rats. Lower adipocyte granular intensities and higher lipolysis rates in adipose tissues were noted in the 7% chitosan group. Moreover, chitosan feeding reduced hepatic triglyceride and cholesterol contents and increased hepatic peroxisomal proliferator-activated receptor α expression in diabetic rats. Our results indicate that long-term administration of chitosan may reduce insulin resistance through suppression of lipid accumulation in liver and adipose tissues and amelioration of chronic inflammation in diabetic rats.     

Endotoxin-mediated hepatic lipid accumulation during parenteral nutrition in rats

OBJECTIVE: To assess the effect of endotoxemia on hepatic lipid content during parenteral nutrition (PN) in rats. METHODS: Twenty male Sprague-Dawley rats (185-230 gm) were randomized to receive PN (n=9) or PN plus a continuous infusion of E. coli 026:B6 lipopolysaccharide (LPS; n= 11). All animals received isocaloric (170 kcal/kg/day), isonitrogenous (1.1 g N/kg/day), glucose-based PN for the next 78 hours. After 30 hours of adaptation to TPN, the animals were randomized to receive PN or PN plus LPS at 6 mg/kg/day for the remaining 48 hours of study. The animals were euthanized and the livers were harvested. RESULTS: Liver weight increased significantly (by 60%) from 7.5+/-0.6 g to 12.1+/-2.4 g (p < or = 0.01) in the animals who received PN versus LPS, respectively. The proportion of liver water remained the same for PN and LPS groups (72.9+/-3.2% versus 72.3+/-3.8%, respectively, p = N.S.). However, liver fat increased disproportionately (by about 130%) from 0.20+/-0.05 g to 0.46+/-0.20 g (p < or = 0.01) total fat weight or from 9.6+/-1.8% to 13.6+/-4.1% (p < or = 0.02) lipid content (g/g) of the dry liver weight for the PN and LPS groups, respectively. CONCLUSION: Endotoxin, when given concomitantly with parenteral nutrition, increases hepatic lipid accumulation and thus augments the development of parenteral nutrition-associated fatty liver in rats.     

Hepatic lipid metabolism in domestic fowl as influenced by dietary cereal

The influence of dietary cereal on hepatic lipid metabolism was studied in adult Japanese quail and mature female chickens fed isoenergetic and isonitrogenous corn-soy and wheat-soy diets ad libitum. Hepatic lipid accumulation and rate of biosynthesis were significantly higher in birds fed the corn-soy diet. The differential response to the cereals was seen in ovipositing females but not in mature male quail. There were no significant concomitant changes in body composition, egg production, egg weight, body weight, feed, and energy intake. Results of sequential changes in hepatic lipid metabolism showed that reduction in liver fat was significant 2 to 3 weeks after feeding the wheat diet and was due to a significant reduction in rate of lipogenesis and the amount of triacylglycerols deposited. Plasma levels of free fatty acids and glucose were not significantly altered by the dietary regimes in laying hens. In Japanese quail fed the corn-soy diet, plasma glucose was elevated and there was evidence of impaired glucose tolerance. In vitro rate of oxidation of labeled palmitate was significantly higher in liver homogenates from birds fed the corn-soy diet. Addition of carnitine to the incubation mixtures resulted in an increase of equivalent magnitude for both treatments. Liver hemorrhages were observed in laying hens but not in Japanese quail. Addition of myo-inositol to the corn diet for Japanese quail failed to significantly alter hepatic lipid accumulation. These studies show that differences in liver lipid accumulation due to corn and wheat diets are related to changes in rate of lipogenesis.     

Enzymatically synthesized glycogen reduces lipid accumulation in diet-induced obese rats

Based on a recent study indicating that enzymatically synthesized glycogen (ESG) possesses a dietary, fiber-like action, we hypothesized that ESG can reduce the risk of obesity. In this study, the antiobesity effects of ESG were investigated in a model of diet-induced obesity. Male Sprague-Dawley rats were divided into 4 groups and fed a normal or high-fat diet, with or without 20% ESG, for 4 weeks. Body weight, food intake, lipid deposition in the white adipose tissues and liver, fecal lipid excretion, and plasma lipid profiles were measured. At week 3, the body fat mass was measured using an x-ray computed tomography system, which showed that ESG significantly suppressed the high-fat diet–induced lipid accumulation. Similar results were observed in the weight of the adipose tissue after the experiment. Moreover, ESG significantly suppressed the lipid accumulation in the liver but increased fecal lipid excretion. The plasma concentrations of triacylglycerol and nonesterified fatty acid were lowered after a high-fat diet, whereas the total bile acid concentration was increased by ESG. However, the hepatic messenger RNA (mRNA) levels of enzymes related to lipid metabolism were not affected by ESG. Conversely, the mRNA levels of long-chain acyl-CoA dehydrogenase and medium-chain acyl-CoA dehydrogenase were up-regulated by ESG in the muscle. These results suggest that the combined effects of increased fecal lipid excretion, increased mRNA levels of enzymes that oxidize fatty acids in the muscle, and increased total bile acid concentration in the plasma mediate the inhibitory effect of ESG on lipid accumulation.