Seasonal changes in plasma and aortic lipids in young rats

In young non-exercised rats, plasma triglyceride and plasma phospholipid levels increased in summer and low density lipoprotein cholesterol (LDL-C) increased in winter. As for lipids samples from the wall of the aorta, total cholesterol, cholesteryl ester and triglyceride decreased in summer and phospholipid decreased in winter. Exercise diminished the gain in body mass (delta m) and suppressed seasonal changes in the levels of LDL-C and plasma triglyceride. Seasonal changes in the aorta lipids in this case were similar to those found in non-exercised animals. The values of total energy intake (Q) and of delta m.Q-1 were found to change with season in both non-exercised and exercised rats. Seasonal changes in plasma and in aorta lipids observed in these animals ran in parallel with the respective levels of delta m.Q-1 and/or of Q. The training effect on the lipid values detected in summer and/or in winter was also found to be dependent on the reduction in delta m.Q-1 with exercise. In the non-exercised and in the exercised animals, plasma phospholipid was associated with aorta phospholipid and inversely related to aorta cholesteryl ester and aorta triglyceride. The relationship between these estimations suggests that an increase in the plasma phospholipid in summer would remove non-polar lipids from the walls of the aortae.     

The effect of silicon (Si) on lipid parameters in blood serum and arterial wall

The influence of silicon treatment on the levels of lipid parameters of blood serum and aortic wall was studied in rats. The concentrations of total cholesterol, phospholipids, triglycerides, HDL-cholesterol, LDL-cholesterol, and HDL-phospholipids were measured in sera of rats receiving per os a soluble, inorganic silicon compound--sodium metasilicate nonahydrate (Na2SiO3.9H2O)--dissolved in the drinking water. In the aortic tissue levels of total cholesterol, triglycerides and phospholipids were estimated. An increase in HDL-cholesterol and HDL-phospholipid concentrations, with a simultaneous decrease of LDL-cholesterol and triglyceride levels, was observed in the sera of the tested group. The levels of total cholesterol and phospholipids in the sera, as well as the concentrations of lipids in the aortic walls, showed no significant differences. The results obtained could provide evidence for the existence of an additional mechanism of silicon antiatheromatous action, concerning the modification of activity of enzymatic systems involved in lipids metabolism.     

Fish oil administration as a supplement to a corn oil containing diet affects arterial prostacyclin production more than platelet thromboxane formation in the rat

The administration to male rats of 5 en % fish oil (FO) as supplement to a diet containing 5 en % corn oil (CO), selectively and markedly decreased arterial parameters (6-keto-PGF1 alpha formation and platelet antiaggregatory activity) assessed in isolated aortic segments perfused with autologous platelet rich plasma (PRP). Platelet parameters (ADP-induced aggregation, TxB2 formation in thrombin-stimulated PRP and sensitivity to exogenous PGI2) were instead minimally affected. Eicosapentaenoic acid (EPA, 20:5 n-3) did not accumulate in plasma, platelet and aorta lipids and arachidonic acid (AA, 20:4 n-6) levels declined markedly only in the plasma compartment. When FO was given alone at the same 5 en % level, both arterial and platelet parameters were similarly affected. EPA accumulated in plasma cholesterol esters and was present in appreciable concentrations also in platelets and aortic walls. AA levels declined markedly in plasma lipids and appreciably also in platelet and aorta lipids. It is concluded that a) arterial and platelet parameters are differentially affected by FO administration depending upon the presence of n-6 polyunsaturated fatty acids in the diet, b) 6-keto-PGF1 alpha production by arterial tissue does not seem to be related to changes of PG precursor fatty acid levels in the phospholipid fraction.     

Association of low-density lipoprotein with particulate connective tissue matrix components enhances cholesterol accumulation in cultured subendothelial cells of human aorta

Low-density lipoproteins (LDL) were incubated with elastin particles, collagenase-resistant debris isolated from human aorta, and latex beads of 1.13 microns in diameter. As a result of incubation, insoluble LDL-associates were formed. These associates, as well as LDL-heparin-fibronectin-gelatin complexes described by other workers, were added to a 7-day primary culture of enzyme-isolated cells of human aortic subendothelial intima. The culture contained a mixed cell population made up mostly of typical and modified smooth muscle cells. 24 h later, total cholesterol, phospholipid, triacylglycerol, free cholesterol and cholesteryl ester levels were measured. Addition of insoluble LDL-complexes as well as LDL-associates to culture brought about a substantial accumulation of intracellular lipids; primarily, cholesteryl esters. The total cholesterol level in cultured cells was raised 3- to 8-fold. Addition of free LDL or LDL-free particles had no effect on the content of intracellular lipids. The results obtained allow the assumption that the occurrence of the LDL-mediated accumulation of intracellular lipids is due mainly to the LDL penetration inside the cell via 'nonspecific' phagocytosis and not through a regulated receptor-dependent pathway.     

Fish oil administration as a supplement to a corn oil containing diet affects arterial prostacyclin production more than platelet thromboxane formation in the rat

The administration to male rats of 5 en % fish oil (FO) as supplement to a diet containing 5 en % corn oil (CO), selectively and markedly decreased arterial parameters (6-keto-PGF_1α formation and platelet antiaggregatory activity) assessed in isolated aortic segments perfused with autologous platelet rich plasma (PRP). Platelet parameters (ADP-induced aggregation, TxB₂ formation in thrombin-stimulated PRP and sensitivity to exogenous PGI₂) were instead minimally affected. Eicosapentaenoic acid (EPA, 20:5 n-3) did not accumulate in plasma, platelet and aorta lipids and arachidonic acid (AA, 20:4 n-6) levels declined markedly only in the plasma compartment. When FO was given alone at the same 5 en % level, both arterial and platelet parameters were similarly affected. EPA accumulated in plasma cholesterol esters and was present in appreciable concentrations also in platelets and aortic walls. AA levels declined markedly in plasma lipids and appreciably also in platelet and aorta lipids. It is concluded that a) arterial and platelet parameters are differentially affected by FO administration depending upon the presence of n-6 polyunsaturated fatty acids in the diet, b) 6-keto-PGF_1α production by arterial tissues does not seem to be related to changes of PG precursor fatty acid levels in the phospholipid fraction.     

The effect of dietary menhaden,olive, and coconut oil fed with three levels of vitamin E on plasma and liver lipids and plasma fatty acid composition in rats

The effect of dietary fats with varying degrees of unsaturation in the presence of different concentrations of vitamin E on tissue lipid levels was studied in rats. Rats were fed either menhaden oil, olive oil or coconut oil at 15% levels with either 0.1, 0.3 or 0.6 mg/g of vitamin E as alpha-tocopherol for four weeks. Rat serum and liver were analyzed for total cholesterol, HDL-cholesterol, triacylglycerol and phospholipids. In addition, fatty acid composition of serum lipids was also analyzed. Serum total cholesterol and triacylglycerol were significantly lower in rats fed menhaden oil than in those fed olive or coconut oil, while the HDL-cholesterol was significantly higher in serum of rats fed menhaden and olive oil than in those fed coconut oil. Levels of vitamin E in the diet had only a significant effect on serum cholesterol and liver phospholipids. The Pearson correlation coefficient showed a significant positive relationship between serum triacylglycerol and total cholesterol, and a negative correlation between triacylglycerol and HDL-cholesterol, and between total and HDL-cholesterol.In the liver, total cholesterol was significantly higher in rats fed coconut oil than in rats fed menhaden oil. Total liver phospholipids were lower in rats fed either coconut oil or olive oil compared to those fed menhaden oil, especially with higher levels of vitamin E intake. Higher levels of vitamin E in the diet appear to increase triacylglycerol and phospholipids in livers of rats fed menhaden oil. In the liver a significant negative correlation was observed between phospholipids and cholesterol. The type and degree of unsaturation (polyunsaturated fatty acids in menhaden oil, monounsaturated fatty acids in olive oil and saturated fatty acids in coconut oil) significantly affected plasma and tissue lipids.     

Role of thyroid on testicular lipids in prepubertal, pubertal and adult rats. I. Hyperthyroidism

The influence of thyroxine-induced hyperthyroidism on testicular neutral and phospholipids was studied in prepubertal, pubertal and adult rats. Thyroxine treatment (25 micrograms/100 g body weight) for 1 month decreased testicular total lipids, total glyceride glycerols, total cholesterol and total phospholipids. Different classes of glyceride glycerol, cholesterol and phospholipid were also diminished due to thyroxine treatment. All classes of lipids returned to the euthyroid level after the withdrawal of thyroxine treatment. The data obtained in the present study suggest that thyroid hormones have a definite influence on testicular lipid metabolism in rats.     

Chromium Chloride Administration Causes a Substantial Reduction of Coronary Lipid Deposits,Aortic Lipid Deposits,and Serum Cholesterol Concentration in Rabbits

This experiment was carried out to test the null hypothesis that intramuscular trivalent chromium administration would not remove lipids from the heart and ascending aorta of the hyoercholesterolemic rabbits and would not lower their serum cholesterol levels. A novel computer-based method, previously described, was used to assess the sizes of the intracardiac and aortic lesions. Clinical chemistry and histopathology were performed through routine methods. The sizes of the lipid deposits in the coronary vasculature of the hypercholesterolemic rabbits were greatly reduced as a result of the intramuscular chromium chloride injections. Lipid deposits in the ascending aorta were similarly reduced, as well as the serum cholesterol concentrations. The terminal serum chromium concentrations in the chromium-treated group were in the range of 3,258–4,513 μg/L, whereas, in the untreated animals, the concentrations were 3.2 to 6.3 μg/L. The general condition of the chromium-treated animals was good and they were continuing to gain weight up to the time they were killed. However, it was found that their liver function tests had become abnormal even though there was no evidence of hepatic histopathological lesions specifically affecting the chromium-treated group. The kidney function tests and histopathology were normal. These findings suggest that a more aggressive approach than those tried hitherto might be useful in treating atherosclerotic human patients with chromium.     

Influence of high density lipoprotein (HDL), prepared from human blood, on prostanoid formation, serum and tissue lipids and development of arteriosclerosis in cholesterol rich fed rabbits

The i.v. administration of high density lipoprotein (HDL) into cholesterol fed rabbits decreased statistically significantly the serum level of total cholesterol and of low density lipoprotein cholesterol after a feeding period of 8 weeks. These diminished levels of cholesterol were associated with a statistically significant reduction in the levels of cholesterol esters in kidneys and platelets but not in hepatic tissue or in aorta. Macroscopically detectable arteriosclerosis was not statistically significantly diminished. The formation of prostanoids by the aorta remained unchanged. The atherogenic role of immunologic factors acting against the heterologous HDL may have compensated for the antiatherogenic HDL action on plasma and tissue lipids.     

Salusin-alpha and -beta expression in heart and aorta with and without metabolic syndrome

Metabolic syndrome (MetS) is a major health problem throughout the world. The role of salusins has not been investigated in heart and aortic tissues under MetS conditions. We examined the distribution of salusin alpha (sal-α) and salusin beta (sal-β) immunoreactivity in heart and aortic tissues and measured circulating salusin concentrations, glucose, insulin, triglycerides, free fatty acids, uric acid, and total cholesterol in Sprague-Dawley rats with and without MetS. Lipid, glucose, insulin and uric acid levels were determined using an autoanalyzer. Serum and tissue salusin levels were measured using ELISA. The expressions of salusins in the heart and aorta tissues were determined using immunohistochemical methods. Serum high density lipoprotein cholesterol (HDL-C), sal-α and sal-β concentrations were significantly lower in the MetS group than in the control group. Low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), total cholesterol, glucose, uric acid and insulin concentrations were higher in the MetS group than in the control group. Sal-α and sal-β were synthesized locally in the fibroblasts and smooth muscle cells of the media of the aorta and in the muscle cells of the heart. Local synthesis of sal-α and sal-β was decreased with MetS. Our findings indicate that decreased serum concentrations of salusins and HDL-C and increased uric acid, glucose and triglyceride concentrations may be indicators of MetS and could play a role in the development of cardiovascular disease.     

Effect of aflatoxin B1 on lipids of rat tissues.

The effect of aflatoxin B1 on lipids of liver, kidney, adipose and plasma of rats was studied. A single dose administration (6 mg/kg body weight) increased liver and kidney weights and their total lipids within 24 h. Increase in liver lipids was confined mainly to phospholipid and cholesterol, whereas triglycerides showed a significant decrease. Adipose tissue triglycerides were, however, increased. Plasma showed decreases in triglycerides, free fatty acids and cholesterol. Incorporation studies with palmitate-1-14C revealed increased incorporation in adipose tissue lipids and decreased incorporation in liver and plasma lipids, thereby indicating an increased synthesis of lipids in adipose. Their mobilization to plasma was, however, inhibited, hence the low levels of triglyceride in liver. But the adrenals showed hypo-activity upon aflatoxin B1 administration.     

Regression of diet-induced atherosclerosis in G?ttingen miniature swine

The regression of diet-induced atherosclerosis in G?ttingen Miniature Swine was investigated after a 6-month induction period. At 1 month after feeding a high-cholesterol and high-fat diet, levels of beta-lipoprotein, total cholesterol, free fatty acids and phospholipid had increased rapidly and the high levels were maintained throughout the 6 month induction period. Morphological features at 6 months showed fatty streaks in the thoracic aorta and fibrous plaques in the abdominal aorta. After return to the conventional diet at 6 months, serum lipids decreased rapidly and maintained the baseline level throughout the 9 month regression period. Histopathological findings showed the regression of fatty streaks but the fibrous plaques did not regress. The present study therefore confirms the regression of fatty streaks in the aorta of G?ttingen Miniature Swine by the administration of a cholesterol lowering diet.     

Early effects of feeding excess vitamin A: mechanism of fatty liver production in rats

Oral administration of vitamin A (30,000 IU daily for 2 days) to young rats caused a marked increase in hepatic glycogen, cholesterol, and glycerides, while hepatic phospholipid content remained almost unaltered. In an examination of the pathogenesis of the lipid accumulation, it was found that more glucose-(14)C was incorporated into liver lipids in vitamin A-fed rats, whereas incorporation of glucose-(14)C and dl-glycine-(14)C into liver protein remained unaltered. The increase in glucose-(14)C incorporation was confined to the glyceride-glycerol portion of the lipids; incorporation into liver fatty acids was inhibited. Plasma free fatty acid concentrations were elevated. It is postulated that in the vitamin A-fed rats, increased accumulation of lipids in the liver is caused by a stimulation of fatty acid mobilization from adipose tissue and enhanced formation of glycerophosphate through glycolysis, with consequent increase in the glyceride synthesis in the liver. The weight of the adrenals was increased, whereas cholesterol concentration in the gland was decreased, after administration of vitamin A to rats. This indicates adrenocortical stimulation. Interestingly enough, vitamin A feeding did not affect either the level of liver lipids or of plasma FFA in adrenalectomized rats.     

HDL2 and HDL3 cholesterol in hepatic cirrhosis

In order to further investigate plasma lipoproteins abnormalities secondary to serious liver damage, we studied plasma lipids and lipoproteins, and in particular HDL subfractions (HDL2, HDL3), in 12 patients with cirrhosis of the liver and in 12 sex, age and weight matched healthy volunteers. Enzymatic methods were used to determine total cholesterol and triglycerides, while the extractive method of Abell et al. was used for the determination of HDL-cholesterol levels after LDL and VLDL precipitation with polyanions (MnCl2 and Na-heparin) and of HDL3-cholesterol values after HDL2 precipitation with dextran-sulphate 15,000 m.w. Total cholesterol and HDL-cholesterol levels were significantly lower in cirrhotic patients compared to normal subjects. We must emphasize that only HDL3-cholesterol was decreased in cirrhotics, whereas HDL2-cholesterol values were normal or high. We suggest that a diminished activity of hepatic triglyceride lipase might account for the decrease in HDL3-cholesterol in liver cirrhosis.     

Cholesterol-rich Very Low Density Lipoproteins and Fatty Liver in Rats Fee Polychlorinated Biphenyls

Feeding xenobiotics such as polychlorinated biphenyls (PCB) causes hypercholesterolemia and fatty liver in rats. The hypercholesterolemia was characterized by high levels of high density lipoproteins (HDL) and apolipoprotein A-I (apo A-I), and by very low density lipoproteins (VLDL) rich in cholesterol and apo E (designated “PCB-VLDL”). The mechanisms for the generation of “PCB-VLDL” and fatty liver, and for hyper-α-lipoproteinemia in rats fed PCB were investigated. The secretion rate of VLDL-lipids was increased by PCB on day 3, while the secretion rate of only VLDL-cholesterol and phospholipid were increased by PCB on days 8 and 57. Although all liver lipids were accumulated by PCB, the accumulation of esterified cholesterol was the most drastic. These results suggested that PCB stimulated the secretion of VLDL at the early period of PCB feeding (on day 3), and that cholesterol-rich VLDL, “PCB-VLDL”, was not generated in the circulation, but was originally secreted from the liver. In spite of the stimulation of VLDL secretion, liver lipids accumulated within 8 days on the PCB diet. On days 3 and 8, serum levels of free fatty acids were not changed by PCB feeding. These data and our previous findings that PCB induced hepatic lipogenic enzymes lead us to speculate that fatty liver induced by PCB may be attributed to a stimulation of de novo synthesis of liver lipids. Even when hepatic secretion of VLDL was blocked by orotic acid, HDL-cholesterol was increased by PCB feeding, suggesting that the increase in serum level of HDL by PCB was not due to stimulation of cholesterol transport into HDL from VLDL.     

Selectively hydrogenated soybean oil with conjugated linoleic acid modifies body composition and plasma lipids in rats

The present study examined effects of a selectively hydrogenated soybean oil (SHSO) containing about 21% CLA on body composition, adipose depots and organ weights, and plasma lipid profiles in rats. Male Sprague Dawley rats were fed for 6 weeks a purified diet containing 0%, 1%, 3%, and 5% of SHSO. Different levels of SHSO supplementation did not significantly affect growth performance, although there was a trend toward decreased body weight gain with increasing dietary SHSO levels. The weights of inguinal, epididymal, and retroperitoneal adipose depot, but not mesenteric, were significantly influenced by dietary SHSO supplementation (P < 0.05, P < 0.01 and P < 0.001, respectively). Although the absolute weight of body protein in the control rats was higher in SHSO-fed rats, the effect on absolute weight of body protein is diluted and eliminated when the data are adjusted for eviscerated carcass weight as a percentage base. Therefore, as dietary SHSO level increased, body protein as a percentage of carcass weight increased (P < 0.05), although as dietary SHSO level increased, body fat proportion in carcass decreased (P < 0.01). Plasma triglycerides (TG) and total cholesterol (TC) concentrations were beneficially decreased, and HDL-cholesterol (HDL-C) to TC ratio was also beneficially increased by SHSO supplementation (P < 0.05, P < 0.001, and P < 0.01, respectively). However, plasma HDL-C concentration undesirably decreased with dietary SHSO supplementation (P < 0.05). The present study observed that body composition and plasma lipids were beneficially modulated by SHSO supplementation at least 3% levels (0.6% of CLA), and suggested that SHSO is a useful fat source because of the high level of CLA.     

Relationship between exercise-induced changes in serum and hepatic cholesterol metabolism in rats

The purpose of the present study was to determine the effects of exercise training on serum cholesterol level and hepatic cholesterol metabolism in rats. Twenty-four male Wistar strain rats, aged 6 weeks, were assigned to one of three experimental groups; control (n = 8), exercised 20 minutes a day (E20, n = 8), and exercised 60 minutes a day (E60, n = 8). Rats were sacrificed after ten weeks exercise. The levels of serum total cholesterol and HDL-cholesterol in the group E20 and group E60 were lower than that of control, 8% and 24% (p less than 0.01) for the total cholesterol and 10% and 24% (p less than 0.05) for the HDL-cholesterol, respectively. The activity of HMG-CoA reductase in liver microsome was significantly higher in the group E60 than that of control. The hepatic microsomal HMG-CoA reductase activity was negatively related to serum total (r = -0.62, p less than 0.01) and HDL (r = -0.58, p less than 0.01) cholesterol levels. From these results, we concluded that the enhancement of the cholesterol metabolism in the liver by exercise is a major course of the exercise-induced change in serum cholesterol of Wistar rats.     

Influence of fast, body weight and diet on serum cholesterol, triglycerides, and phospholipids concentrations in the aging rat

The present study was performed to document factors playing a role in the age-related increase of serum total cholesterol, triglycerides, and phospholipids in male WISTAR rats. In 59 and 122 week old rats, serum concentrations of all three parameters were significantly higher than those determined in younger rats (15-17 weeks of age). Serum triglycerides and cholesterol concentrations were higher in post absorptive than in fasting state. In mature rats of same age (59 weeks), mean concentrations of cholesterol, triglycerides, and phospholipids were significantly higher in the heavier animals than in the others. A strong correlation could be established between body weight and serum cholesterol or triglycerides of these animals. The composition of diet appears to play a role in serum cholesterol concentration but not in serum triglycerides concentration in old rats (59-65 weeks of age). This effect is demonstrated even if daily caloric intake and daily body weight gain of old rats (40-50 weeks of age) were not significantly different with both diets tested (2900 and 3250 cal/kg). In conclusion old Wistar rats develop increased concentrations of serum lipids parameters.     

Beneficial effects of alpha linolenic acid rich flaxseed oil on growth performance and hepatic cholesterol metabolism in high fat diet fed rats

The purpose of the study was to investigate the effect of flaxseed oil (FO), rich in alpha-linolenic acid (ALA) (18:3 n-3) on growth parameters and lipid metabolism of rats fed with high fat diet. High fat diet (HFD) resulted in significant alterations in hepatic lipids, increase in body weight gain and negative effect on lipoprotein metabolism. FO supplementation significantly lowered the increase in body weight gain, liver weight, plasma cholesterol, triglycerides, phospholipids, free fatty acids, high-density lipoprotein (HDL), low-density lipoprotein-cholesterol (LDL-C), very low-density lipoprotein (VLDL), LDL/HDL and TC/HDL ratio in HFD fed rats. FO significantly reduced the hepatic and plasma lipid levels indicating its hypolipidemic activity. On the other hand, oral administration of FO exhibited lower plasma lipoprotein profile as compared to HFD rats. Hepatic protection by FO is further substantiated by the normal liver histological findings in HFD fed rats. These data suggest that FO participate in the normal regulation of plasma lipid concentration and cholesterol metabolism in liver. No adverse effect of FO on growth parameters and plasma lipids in rats fed with fat-free diet. The results of the present study demonstrate that FO may be developed as a useful therapy for hyperlipidemia through reducing hepatic lipids, thereby proving its hypolipidemic activity.     

Influence of prostaglandin E1 on high density lipoprotein-fraction lipid levels in rats

Serum lipid concentrations were determined in rats treated with PGE1 and in controls. Reduced concentrations of total lipids (P less than 0.001), cholesterol (P less than 0.001), triglycerides (P less than 0.05), and phospholipids (P less than 0.002) were found in the treated rats. Furthermore, decreased concentrations of HDL-cholesterol (P less than 0.001), HDL-triglycerides (P less than 0.02), and HDL-phospholipids (P less than 0.02) were observed in the treated rats. These lipid changes could be related to the antilipolytic action of PGE1. Furthermore, these results suggest that PGE1 may exert an antiatherogenic effect modifying serum lipid levels.