Effects of atorvastatin on progression-regression of renal injury in hyperlipidemic chickens

Complex interrelationships exist between hyperlipidemia and the progression of renal injury. The aim of this study was to evaluate the impact of high plasma cholesterol and triglyceride levels on renal structure and the effects of atorvastatin on progression-regression of renal injury. One-hundred chickens were divided into five groups: Group A: Standard diet (SD) for 6 months; Group B: Hyperlipidemic diet (HD) for 6 months; Group C: HD for three months and SD during the next 3 months; Group D: HD for 3 months and SD during the next 3 months, when they received oral atorvastatin (3 mg/kg/d); Group E: HD for the whole 6 months, and atorvastatin (3 mg/kg/d) during the last 3 months. Increased alpha-actine immunostaining was found in glomeruli of groups B and C. An important decrease of immunostaining was observed in glomeruli of atorvastatin treated groups. Group D showed the lowest value for presence of lipids, and significant differences were found with respect to the rest of the groups. The glomeruli of group B presented the highest damage grades and those of group D showed the lowest grades and presented significant differences from the rest of the groups. The combination of atorvastatin therapy and proper diet proved to be effective in promoting renal disease regression. However, the study of several parameters indicates that neither only diet nor atorvastatin in the progression group resulted completely effective in decreasing the progression of the disease.     

Effects of dietary conjugated linoleic acids on lipid metabolism and antioxidant capacity in laying hens

To examine the effects of dietary conjugated linoleic acids (CLA) on lipid metabolism and antioxidant capacity in laying hens, Hy-Line Brown layers (n = 384, 52 weeks old) were randomly allocated to one of four dietary treatments. Each treatment had six replicates of 16 hens each. All birds were assigned to a corn-soybean meal-based diet containing a mixture of CLA at 0%, 1%, 2% or 4% for six weeks. With increasing dietary CLA, egg weight and feed intake decreased, and yolk colour was darkened. Feed efficiency was improved at 1% and 2% dietary CLA. Serum triglyceride concentration was significantly reduced by CLA in a dose dependent manner. A linear decrease in total cholesterol and low-density lipoprotein cholesterol, and an increase in high-density lipoprotein cholesterol levels were observed after CLA supplementation. With increasing dietary CLA, the deposition of two major isomers of CLA (c9, t11; t10, c12) in yolk lipids increased linearly, the proportion of saturated fatty acids increased and monounsaturated fatty acids decreased significantly. The proportion of polyunsaturated fatty acids was highest at 1% CLA. Compared to the control, CLA supplementation significantly increased the activities of superoxide dismutase and glutathione peroxidase, inhibited hydroxyl radicals and superoxide anion production, and decreased the malonaldehyde concentrations in both serum and liver. The results demonstrated that dietary CLA meliorated serum lipid profiles and enhanced the antioxidant capacity of laying hens.     

Effect of gamma-linolenic acid on lipid metabolism in laying hens.

1. Single comb white leghorn laying hens were given diets with additional mould, Mucus circineloides, containing gamma-linolenic acid (GLA) at levels of 0, 2.59 and 5.06 g GLA/kg diet ad lib. for 2 weeks and serum lipid contents were determined in experiment 1. 2. Serum low density lipoprotein and chylomicron levels were significantly reduced with the increase of dietary GLA levels. Serum triglyceride and cholesterol tended to be lowered by dietary GLA, but not significantly different. 3. Effects of mould GLA and extracted oil GLA on the egg yolk cholesterol concentration and fatty acid composition were compared in experiment 2. Both mould GLA and extracted oil GLA diets containing 5.32 and 4.71 g GLA/kg diet were given ad lib. for 2 weeks. 4. Yolk cholesterol content was not affected by dietary GLA sources. Content of GLA in the yolk was not altered, although that of arachidonic acid was enhanced by dietary GLA supplementation, particularly by the extracted oil GLA. 5. It is suggested that GLA is rapidly metabolized to arachidonic acid in the body and incorporated into the yolk.     

Effects of zopiclone on blood glucose level, serum lipid concentration and clot lysis time in normoglycemic and normolipidemic rats

In normoglycemic and normolipidemic rats the i.p. injection of zopiclone induced an acceleration of fibrinolysis in a dose-dependent bell shaped manner and various changes of the blood glucose level. Total lipids, total cholesterol and triglyceride serum levels remained unaffected by doses of 1.25, 2.5 and 15.0 mg/kg, with the exception of the medium dose (5.0 mg/kg) and the next dose (10.0 mg/kg) which lowered them very significantly.     

Concentration and distribution of apolipoproteins A-I and E in normolipidemic, WHHL and diet-induced hyperlipidemic rabbit sera.

Two sandwich-type enzyme immunoassays have been developed to measure apolipoproteins A-I and E in rabbit serum. Specific goat antibodies were purified by affinity chromatography and used both for coating and for preparing antibody-peroxydase conjugates. The sensitivity of these assays is sufficient to allow studies of apo A-I and E distribution in lipoproteins fractionated by gel filtration from 50 microliters of serum. In WHHL rabbits, apo A-I is 5-fold lower (5.2 +/- 2.5 mg/dl) and apo E is 8-fold higher (9.9 +/- 3.5 mg/dl) than in normolipidemic rabbits (29 +/- 4.3 mg/dl and 1.3 +/- 0.5 mg/dl, respectively). In hyperlipidemic rabbits, fed 2 months on a 0.5% cholesterol diet, the apo A-I level was similar (32 +/- 12 mg/dl) to that of normolipidemic rabbits, but the apo E level is 12-fold higher (15.1 +/- 5.5 mg/dl). In addition, HDL particles were enriched with cholesterol and apo E. The bulk of apo E and cholesterol is located in large beta-VLDL in diet-induced hyperlipidemia, whereas they are mainly located in smaller size beta-VLDL in WHHL rabbits. In normolipidemic rabbits apo E occurs mainly in HDL, and cholesterol is distributed in the main three lipoprotein fractions VLDL, LDL and HDL. Interestingly, HDL of WHHL rabbit are deficient in apo A-I. These results are compatible with profound perturbations of lipoprotein composition and metabolism in atherogenic hyperlipidemia.     

Measurement of fasting serum apoB-48 levels in normolipidemic and hyperlipidemic subjects by ELISA

The present study was designed to evaluate the metabolism of chylomicron and chylomicron remnants by measuring serum apolipoprotein B-48 (apoB-48) levels in 335 normolipidemic and 253 hyperlipidemic subjects using a novel ELISA system. The distribution of fasting serum apoB-48 levels in normolipidemic subjects varied widely, ranging from <1 to >24 microgram/ml (mean, 5.2 +/- 3.8 microgram/ml; median, 3.9 microgram/ml). Serum apoB-48 levels correlated with serum triglyceride (TG) concentrations (r = 0.45, P < 0.001), but not with total cholesterol levels. Serum apoB-48 levels were 7 to 18 times higher in patients with Type I, Type V, and Type III hyperlipidemia, and only slightly higher in patients with Type IIa, Type IIb, and Type IV hyperlipidemia, compared with normolipidemic subjects. The calculated apoB-48/TG ratio was elevated only in patients with dysbetalipoproteinemia (apoE2/2 phenotype). In normolipidemic subjects, oral fat loading resulted in about 2-fold increase in serum apoB-48 levels, with a peak level recorded at 3-4 h postloading, and then returned to the baseline level within 6 h. On the other hand, in patients with dysbetalipoproteinemia, serum apoB-48 levels did not change considerably. Our results indicate that serum apoB-48 is a very useful parameter for evaluating lipoprotein metabolism in exogenous pathways.     

Effects of ethanol on lipid metabolism.

Alcohol promotes accumulation of fat in the liver mainly by substitution of ethanol for fatty acids as the major hepatic fuel. The degree of lipid accumulation depends on the supply of dietary fat. Progressive alteration of the mitochondria, which occurs during chronic alcohol consumption, decreases fatty acid oxidation by interfering with citric acid cycle activity. This block is partially compensated for by increased ketone body production, which results in ketonemia. Thus, mitochondrial damage perpetuates fatty acid accumulation even in the absence of ethanol oxidation. Alcohol facilitates esterification of the accumulated fatty acids to triglycerides, phospholipids, and cholesterol esters, all of which accumulate in the liver. The accumulated lipids are disposed of in part as serum lipoprotein, resulting in moderate hyperlipemia. In some individuals with pre-existing alterations of lipid metabolism, small ethanol dose may provoke marked hyperlipemia which responds to alcohol withdrawal. Inhibition of the catabolism of cholesterol to bile salt may contribute to the hepatic accumulation and hypercholesterolemia. The capacity of lipoprotein production and hyperlipemia development increases during chronic alcohol consumption, probably as a result of the concomitant hypertrophy of the endoplasmic reticulum and Golgi apparatus. However, this compensation is relatively inefficient in ridding the liver of fat. This inefficiency may be linked to alterations of hepatic microtubules induced by ethanol or its metabolites, which interfere with the export of protein from liver to serum, promoting hepatic accumulation of proteins as well as fat. As liver injury aggravates, hyperlipemia wanes and liver steatosis is exaggerated. Derangements of serum lipids similar to those found in other types of liver disease also become apparent. The changes in serum lipids may be a sensitive indicator of the progression of liver damage in the alcoholic.     

Effects of octreotide on lipid metabolism in acromegaly.

Hypertriglyceridemia is the most frequent modification of lipid metabolism observed in acromegaly. The somatostatin analog, octreotide (Sandostatin), widely used in the treatment of acromegaly, is able to produce a decrease in levels of growth hormone (GH), insulin, and Insulin-like Growth Factor 1 (IGF1). We have attempted to evaluate the influence of this treatment on the lipid status of acromegalic patients. Seventeen patients with active acromegaly were treated with octreotide, 100 to 500 micrograms/injection subcutaneously three times daily. The levels of fasting serum triglycerides (TG), total cholesterol, High Density Lipoprotein (HDL) cholesterol and IGF1, as well as mean plasma GH and insulin levels during a diurnal profile, were evaluated before and after three months of octreotide therapy. GH, insulin and IGF1 decreased by 61%, 42% and 36% respectively (p less than 0.05). Mean levels (+/- SEM) of TG and total cholesterol fell from 2.2 +/- 0.4 mmol/l to 1.6 +/- 0.3 mmol/l (p less than 0.05) and 6.4 +/- 0.39 mmol/l to 5.6 +/- 0.27 mmol/l (p greater than 0.05), respectively. There was no correlation between triglyceride decrease and hormonal changes or clinical status (BMI, age, sex). In conclusion, the administration of octreotide over a three month period to acromegalic patients is associated with a decrease in TG levels.     

Effects of castor oil on lipid metabolism in rats

Weanling rats were given diets contained castor oil (CAO-diet), coconut oil (CO-diet), or high-oleic safflower oil (HO-diet) each 10% (wt). No growth retardations were observed on the CAO-diets. The CAO-diet group showed significantly lower serum cholesterol and hepatic triacylglycerols than the HO-diet group. Ricinoleic acid was found at an extremely low level in perirenal adipose tissue.     

Effects of genetic and diet-induced obesity on lipid metabolism

C57BL/6J obese (ob/ob) and lean mice fed ad libitum on a normal mouse chow diet (Normal), were compared with lean mice of the same age and strain fed ad libitum on a high-fat diet, consisting of the Normal diet with the addition of beef lard (Lard), from age 3 months for 34 days. The lard-fed mice were seen to have significantly higher (P<0.05) body weight in this 34-day period than that of the other two groups fed on the Normal diet. Epididymal fat depot and adipocyte cell size were significantly larger (P<0.05) in the Lard-fed lean mice and in the obese (ob/ob) mice than were those of the Normal-fed lean mice. Dietary Lard intake did not significantly affect concentrations of plasma triglyceride although those of plasma cholesterol were significantly increased (P<0.05). The development of obesity in these Lard-fed mice appeared to be accelerated and significant.     

Effects of dexamethasone on lipid metabolism in rat organs

Injecting of dexamethasone (10 mg/kg body weight) for 8 days to rats decreased the body weight and feed intake by 29 and 50%, respectively. The increase in weights of liver, heart, kidneys and testes per 100 g body weight was 55, 37, 33 and 13%, respectively. Though, in general, the triglyceride content increased in all the organs, maximum increase (9-fold) was observed in the liver. The plasma showed elevated levels of triglycerides, cholesterol and phospholipids. In hepatic mitochondrial membranes, the content of protein, phospholipids and cholesterol decreased/g tissue. The percent 14C distribution, as a part of total incorporation in nonpolar lipids, of [14C]acetate into triglycerides of liver, kidneys and testes increased significantly. The increased turnover of phospholipids in liver and heart was mainly due to increased turnover of phosphatidyl choline (PC) and phosphatidyl ethanolamine in liver and PC in heart. Turnover of phospholipids of testes was not affected.     

取食蜂蜜对棉铃虫齿唇姬蜂体内主要代谢物质的影响

为揭示食物在齿唇姬蜂Campoletis chlorideae Uchida生命中所起的作用,测定分析饱食蜂蜜和只取食清水的齿唇姬蜂体内糖类、脂肪和蛋白质随日龄增加的变化趋势。结果显示,取食蜂蜜对齿唇姬蜂体内主要代谢物质影响显著。10%蜂蜜水和清水饲养的齿唇姬蜂的雌蜂和雄蜂在刚羽化时体内都含有较高水平的糖原、总糖、脂肪和蛋白质。但随着日龄的增加,用清水饲养的雌、雄蜂体内的糖原和总糖含量迅速下降并达到最低水平;而用蜂蜜水饲养的雌、雄蜂随日龄的增加体内的糖原含量没有显著变化,并且与清水饲养的雌、雄蜂相比,其体内总糖含量反而有所上升。用蜂蜜水饲养的齿唇姬蜂的寿命显著长于用清水饲养的齿唇姬蜂。由于蜂蜜中含有丰富的果糖,所以冷蒽酮反应测定显示,用蜂蜜水饲养的齿唇姬蜂体内果糖含量较高,但却不能在清水饲养的齿唇姬蜂体内测出。2种食物处理的齿唇姬蜂在羽化后体内脂肪含量均有下降;并且随日龄的增加,清水饲养的齿唇姬蜂体内脂肪含量的下降速度明显快于蜂蜜水饲养的齿唇姬蜂。取食蜂蜜水的齿唇姬蜂体内蛋白质含量随日龄无显著变化;而用清水饲养的齿唇姬蜂在羽化后体内蛋白质含量随日龄的增长迅速下降并达到最低水平。     

Effects of ethanol and methanol on lipid metabolism in Bacillus subtilis

In Bacillus subtilis, the fatty acid moiety of the phospholipids was affected differently during growth in the presence of 1.1 M-methanol or 0.7 M-ethanol, though at these concentrations methanol and ethanol had the same effects on growth rate and completely inhibited sporulation. Synthesis of phosphatidylglycerol was also strongly inhibited and the amount of total cell phospholipids was reduced by 50% by both alcohols. The composition of fatty acids, especially the relative concentration of 12-methyltetradecanoic acid, was modified only by ethanol; in bacteria grown in the presence of methanol, changes in fatty acid composition were negligible. In non-sporulating mutants, synthesis of phosphatidylglycerol was much less affected than in the wild-type and synthesis of phosphatidylethanolamine was increased. In these strains, fatty acid composition was also modified by ethanol but unaffected by methanol.     

微量元素对糖尿病大鼠糖脂代谢的影响

目的观察微量元素铬对糖尿病大鼠糖脂代谢的影响。方法选糖尿病大鼠经灌胃给予有机铬水溶液治疗12周后,分别观察口服有机铬200μg/d及400μg/d的糖尿病大鼠空腹血糖及血脂水平(血清总胆固醇、甘油三酯、低密度脂蛋白和高密度脂蛋白)。实验分为4组:1组为正常对照组;2组为铬200μg/d组;3组为铬400μg/d组;4组为糖尿病对照组。结果有机铬具有明显降低血糖、血清总胆固醇、低密度脂蛋白和甘油三酯及升高高密度脂蛋白的作用(P0.05~P0.01)。结论有机铬能明显改善糖尿病大鼠的糖脂代谢。     

High density lipoprotein metabolism in normolipidemic and cholesterol-fed rabbits.

New Zealand white rabbits were used to determine the compositional and metabolic changes induced in high density lipoproteins (HDL, rho = 1.063--1.21 g/ml) in response to cholesterol feeding. There was no change in total HDL cholesterol in plasma due to cholesterol feeding (12 weeks), but the triglyceride level was decreased to 29% of pretreatment values. Total protein content of HDL was decreased in response to cholesterol feeding, resulting in a significant increase in the cholesterol/protein ratio. There was a decrease in some isomer of the major apolipoproteins (A-I2) of HDL. The decay of radioactivity in HDL or its apolipoproteins was biphasic in both normolipidemic and hypercholesterolemic rabbits. The first phase was much more rapid than the second. The decay rates for the radioactivity in HDL depended upon the dietary status of the recipient animal.