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.     

Changes in serum lipids in rats treated with PGF2 alpha

Serum lipid concentrations were determined in rats treated with PGF2 alpha, PGE1, and controls. Administration of PGF2 alpha in rats influenced only the HDL lipid composition. HDL-cholesterol decreased while HDL-triglycerides increased. No significant difference was observed in the levels of serum total cholesterol, triglycerides, and phospholipids between animals treated with PGF2 alpha and controls. Reduced concentrations of serum lipid levels and especially of HDL-cholesterol, HDL-triglycerides, and HDL-phospholipids were found in the rats treated with PGE1. These results suggest that PGF2 alpha and PGE1 could modify serum lipid levels influencing lipoprotein metabolism.     

Sex differences in gastric mucosal protection after 16, 16-dimethyl PGE2 and lithium chloride

While the incidence of duodenal ulcer disease has been documented to be greater in men than in women, this observation has not been previously noted in animal studies of the upper gastrointestinal tract. In this study, we questioned whether the cytoprotective properties of 16, 16-dimethyl PGE2 were sex-related by comparing the degree of ethanol-induced hemorrhagic gastritis in male and female rats pretreated with 16,16-dimethyl PGE2 or lithium chloride. Animals receiving 16,16-dimethyl PGE2 or lithium chloride had significantly less ethanol-induced hemorrhagic gastritis (1.17 +/- 0.15 and 1.24 +/- 0.13, respectively, p less than 0.001) when compared with controls (2.69 +/- 0.10). Female rats treated with 16,16-dimethyl PGE2 had 59% less hemorrhagic gastritis than male rats treated similarly (0.76 +/- 0.14 vs 1.86 +/- 0.19 respectively, p less than 0.001). This sex-related difference in hemorrhagic gastritis was not noted in male and female rats receiving lithium chloride (1.24 +/- 0.15 vs 1.23 +/- 0.27, respectively). However, female rats treated with 16, 16-dimethyl PGE2 had significantly less hemorrhagic gastritis when compared with female rats receiving lithium chloride (0.76 +/- 0.14 vs 1.24 +/- 0.15 respectively, p less than 0.05).     

Inhibition of prostaglandin synthesis and contractility in the rabbit and rat uterus by ibuprofen

Sixty uterine strips were excised from 8 pregnant and 7 post partum rabbits andstimulated electrically in vitro until they developed maximum isometric tension. The non-steroidal anti-inflammatory agent, Ibuprofen, at concentrations of 125, 250 and 500 μg/ml, signidicantly reduced tension of the 55 experimental uteri (P<0.001) within 7.5 minutes, in comaparison with the pretreatment value. Tension in 15 solvent-treated controls remained stable during the same observation period. The reduction in tension was greater in the post partum than the pregnant uteri (P<0.05). Sixteen additional uterine strips, excised from 4 preganant and 4 post partum rabbits were treated either with 500 μg Ibuprofen or solvent for 7.5 minutes. Radioimmunoassay showed that Ibuprofen significantly reduced the uterine levels of PGE (P<0.001) and PGE (P<0.001 post partum; P<0.05 pregnant) and again the effect was greater in the post partum unteri. These findings suggest that the suppression of uterine function by Ibuprofen is mediated by inhibition of PG-synthesis.In a subsequent study, 36 rats were treated with Ibuprofen on days 20 and 21 of pregnancy, at the ineffective dose level of 4 mg/day and the effective levels of 12, 20 and 30 mg/day, In comparison with the first group. Spontaneous labor was significantly delayed in the other three groups (P<0.05, P<0.01 and P<0.001, respectively). In addition, 7 rats were treated with 30 mg/day Ibuprofen and 7 with solvent on days 19 and 20 of pregnancy. In day 21, the Ibuprofen-treated rats showed a significant (P<0.001) reduction in the uterine PGF and PGE concentrations, indicating that the prolongation of pregnancy is mediated by an inhibition of uterine PG-synthesis.     

High Levels of Both n-3 and n-6 Long-Chain Polyunsaturated Fatty Acids in Cord Serum Phospholipids Predict Allergy Development

Background

Long-chain polyunsaturated fatty acids (LCPUFAs) reduce T-cell activation and dampen inflammation. They might thereby counteract the neonatal immune activation and hamper normal tolerance development to harmless environmental antigens. We investigated whether fatty acid composition of cord serum phospholipids affects allergy development up to age 13 years.

Methods

From a population-based birth-cohort born in 1996/7 and followed until 13 years of age (n = 794), we selected cases with atopic eczema (n = 37) or respiratory allergy (n = 44), as well as non-allergic non-sensitized controls (n = 48) based on diagnosis at 13 years of age. Cord and maternal sera obtained at delivery from cases and controls were analysed for proportions of saturated, monounsaturated and polyunsaturated fatty acids among serum phospholipids.

Results

The cord serum phospholipids from subject who later developed either respiratory allergy or atopic eczema had significantly higher proportions of 5/8 LCPUFA species, as well as total n-3 LCPUFA, total n-6 LCPUFA and total LCPUFA compared to cord serum phospholipids from controls who did not develop allergy (P<0.001 for all comparisons). Conversely, individuals later developing allergy had lower proportion of the monounsaturated fatty acid 18∶1n-9 as well as total MUFA (p<0.001) among cord serum phospholipids. The risk of respiratory allergy at age 13 increased linearly with the proportion of n-3 LCPUFA (P_trend<0.001), n-6 LCPUFA (P_trend = 0.001), and total LCPUFA (P_trend<0.001) and decreased linearly with the proportions of total MUFA (P_trend = 0.025) in cord serum phospholipids. Furthermore, Kaplan-Meier estimates of allergy development demonstrated that total LCPUFA proportion in cord serum phospholipids was significantly associated with respiratory allergy (P = 0.008) and sensitization (P = 0.002), after control for sex and parental allergy.

Conclusion

A high proportion of long-chain PUFAs among cord serum phospholipids may predispose to allergy development. The mechanism is unknown, but may involve dampening of the physiologic immune activation in infancy needed for proper maturation of the infant''s immune system.     

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.     

Effects of lysine clonixinate on cyclooxygenase I and II in rat lung and stomach preparations

Lysine clonixinate (LC) is a drug of antiinflammatory antipyretic and analgesic activity that produces minor digestive side-effects. This fact induced us to think that LC is possibly a weak COX-1 inhibitor. In order to investigate our hypothesis we inhibited cyclooxygenase activity with LC or indomethacin (INDO) in rat lung and stomach obtained from rats treated with lipopolysacharide (LPS) and control rats. Rat lung preparations incubated with 14C-arachidonic acid synthesise mainly PGE2. LC at 2.5 and 4.1 x 10(-5) M does not modify the basal production of PGE2 (probably COX-1) but at 6.8 x 10(-5) M significantly inhibited PGE2 production (approximately 48.5% inhibition, P<0.001). On the other hand, INDO at 10(-6) inhibited the basal production of PGE2 by around 73%. In LPS-treated rats, the production of PGE2 was significantly higher than in the lungs of control rats, probably due to the induction of COX-2. The addition of LC at 2.7 and 4.1 x 10(-5) M recovered the control values of PGE2 inhibiting, probably only from COX-2 activity. LC at higher concentrations (6.8 x 10(-5) M) and INDO 10(-6) M inhibited PGE2 formed by COX-2 and also partly by COX-1 activity.     

Serum levels of IL-6 type cytokines and soluble IL-6 receptors in active B-cell chronic lymphocytic leukemia and in cladribine induced remission

We have investigated the serum concentrations of interleukin-6 (IL-6) and two IL-6 family cytokines-oncostatin M (OSM) and leukemia inhibitory factor (LIF)-in 63 patients with B-cell chronic lymphocytic leukemia (B-CLL) and 17 healthy controls using the enzyme-linked immunosorbent assay (ELISA) method. Simultaneously, we measured the serum levels of the soluble forms of two subunits of the IL-6 receptor complex-ligand binding glycoprotein 80 (sIL-6R) and glycoprotein 130 (sgp130). The cytokines and receptors were evaluated in 25 untreated patients and 38 patients treated with cladribine (2-CdA), as well as in 17 healthy controls. We have correlated the serum levels of these proteins with Rai's clinical stage of the disease, the response to 2-CdA treatment and some hematological parameters. We have also evaluated the correlation of the IL-6 serum level with the concentration of OSM and IL-6 soluble receptors. IL-6 was measurable in 62/63 (98.4%), OSM in 20/25 (80%) of untreated and 14/38 (37.8%) of the treated patients. sIL-6R and sgp130 were detectable in all 63 patients and LIF in none of the CLL patients. IL-6 serum level in untreated patients was not significantly different as compared to its concentration in the control group (P>0.05). However, in the patients treated with 2-CdA the IL-6 level was significantly lower (P<0.02), and the lowest concentration was found in the patients with complete remission (CR; median 1.4pg/ml; P<0.02). The concentration of sIL-6R was significantly higher in untreated (median 61.8 ng/ml) and treated (median 50.1 ng/ml) CLL patients when compared to normal persons (median 41.2 ng/ml; P=0.04; P<0.001, respectively). There was no difference between the sIL-6R levels in the patients with CR and the healthy controls. In non-responders sIL-6R concentration was the highest and similar to its level in the untreated patients. OSM level was higher in the untreated patients (median 1.8pg/ml) than in the normal controls (median 0.0pg/ml; P<0.001) and in the CR patients (median 0.0pg/ml; P<0.03). The serum concentration of sgp130 was similar in the untreated (median 480 pg/ml) and treated (median 470 pg/ml) patients, as well as in the healthy persons (median 420 pg/ml; P>0.05). We have found significant positive correlation between the levels of sIL-6R and the lymphocytes count in CLL patients (p=0.423; P<0.001). In addition, sIL-6R and OSM serum concentrations correlated also with CLL Rai stage. In conclusion, the serum level of IL-6, OSM and sIL-6R, but not LIF and sgp130, are useful indicators of CLL activity.     

Elevation of red cell sodium-lithium countertransport in hyperlipidemias

Red cell Na-Li countertransport was measured in 78 normal subjects, 64 patients with essential hypertension, and 67 patients with hyperlipidemias. Both hypertensive and hyperlipidemic patients had elevated Na-Li countertransport compared to normal controls (p less than 0.001). Subjects with hyperlipidemia and hypertension had higher countertransport (p less than 0.02) than patients with only hyperlipidemia. Normotensive hyperlipidemic subjects had higher countertransport than normotensive and normolipidemic controls (p less than 0.02). This suggest that hypertension and high plasma lipids can influence independently the Na-Li countertransport. In another group of 52 normotensive subjects, Na-Li countertransport was positively correlated with serum total and free (unesterified) cholesterol, phospholipids and triglycerides. No correlations were found with HDL-cholesterol or HDL-phospholipids. A very high positive correlation was found between Na-Li countertransport and plasma acetylcholinesterase (p less than 0.005). These findings suggest that plasma lipids, probably through membrane lipids, can affect the maximal rate of the Na-Li exchange in red cells. The relationship between plasma or membrane lipids and cation transport should be further studied in erythrocytes and other cells.     

Effect of dietary fish oil on tumor-induced hyperlipidemia and tumor growth in rats implanted with a methylcholanthrene-induced sarcoma

Male Fischer 344 rats implanted with a methylcholanthrene-induced sarcoma (MCS), along with normal (or control) animals, were fed diets containing either 10% com oil (CO) or 2% CO + 8% fish oil (FO), designated as diets CO and FO, respectively, in a study designed to determine the effect of dietary FO on serum lipids (in the presence or absence of a tumor) and the growth and fatty acid composition of the MCS. For both diets, MCS-bearing rats had significantly (p < 0.05) higher serum levels of triglycerides, cholesterol, phospholipids, and total lipids than controls. For both controls and tumor-bearers, serum levels of all these lipids were, with the exception of cholesterol for the tumorbearers, significantly lower in rats receiving the FO diet than for the corresponding groups receiving the CO diet. Relative to rats fed the CO diet, those fed the FO diet had significantly higher serum levels of some fatty acids (e.g., 20:5n-3) but significantly lower levels of others (e.g., 18:2n-6), regardless of tumor status. For the tumor-bearers, differences in the levels of fatty acids in MCS tissue reflected differences in the fatty acid composition of total serum lipids. Sarcoma growth was unaffected by diet. Thus, feeding dietary FO resulted in changes in the lipid status of both control and tumor-bearing rats. Since sarcoma growth was unaffected by diet, the reduction in the severity of MCS-induced hyperlipidemia by FO appears to be due to an effect of the oil per se.     

Decreased production of interleukin-6 and prostaglandin E2 associated with inhibition of delta-5 desaturation of omega6 fatty acids in mice fed safflower oil diets supplemented with sesamol

The differences in the immune responses in mice fed sesame oil diets and those fed sesamin may be attributed to the presence of other lignans in the non-fat portion of the oil. The fatty acid composition (mean +/- SD mol. %) of liver membrane phospholipids and the levels of endotoxin-induced prostaglandin (PG) E2, interleukin (IL)-6, IL-10, IL-12 and tumor necrosis factor (TNF)-alpha were determined in mice fed diets supplemented with 5% safflower oil (SO) in the absence or presence of 1% sesamol. The levels of dihomo-gamma-linolenic acid (20:3omega6) were markedly higher (P<0.025) in the livers from mice fed sesamol supplemented SO diets (1.6 +/- 0.1) compared to the controls (1.4 +/- 0.1). These data suggest that sesamol or its metabolite could inhibit the in vivo delta-5 desaturation of omega6 fatty acids. Further, in animals fed sesamol supplemented SO diets, the levels of PGE2 (228 +/- 41 pg/ml) were markedly lower (P<0.01) compared to those fed SO diet alone (1355 +/- 188 pg/ml). Concomitantly, the concentrations of IL-6 were also lower (P<0.01) in mice fed sesamol diet (63 +/- 11 ng/ml) compared to the controls (143 +/- 22 ng/ml). A marked reduction in the levels of PGE2 in animals fed sesamol diets suggests that sesamol or its metabolite could inhibit the activity of cyclooxygenase enzyme.     

Effect of testosterone on serum immunoactive inhibin concentrations in intact and hypophysectomized male rats

Intact and hypophysectomized rats were treated with graded doses of testosterone via subcutaneous Silastic implants over a 13-week period. Serum inhibin concentrations fell 50% (P less than 0.001) after 2 weeks of hypophysectomy, remaining suppressed at this level for 13 weeks. The administration of testosterone to hypophysectomized rats (serum testosterone values 2-12 ng/ml; control values 5.5 ng/ml) was without effect on serum inhibin values. In contrast, administration of testosterone to intact animals for 7 weeks resulted in an initial fall (P less than 0.05) in inhibin levels to 50-70% of controls then increasing to reach control levels at higher doses. Serum FSH concentrations were similarly biphasic with increasing dose of testosterone and values for these two hormones were significantly correlated (r = 0.44, P less than 0.01). Segments of seminiferous tubules in culture from rats after various times of hypophysectomy showed a partly suppressed secretion of inhibin. The administration of testosterone did not modify inhibin production although inhibin production was sensitive to FSH. It is concluded that (1) serum inhibin concentrations are partly suppressed after hypophysectomy and testosterone has no effect on serum inhibin values; and (2) the suppression of serum inhibin in intact rats treated with increasing doses of testosterone is attributable to the concomitant fall in serum FSH concentrations.     

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.     

Th 细胞因子IL-17、IFN-γ、IL-4 在狼疮性肾炎中的表达及意义

目的:探讨T辅助细胞(Th)相关细胞因子在狼疮性肾炎发病中的免疫机制作用。方法:64例系统性红斑狼疮患者和28例健康体检者作为对照,采用酶联免疫吸附测定法(ELISA法)检测所有受试者血清IL-17、IFN-γ、IL-4水平,并对其与SLEDAI、SDI、24小时尿蛋白量相关性进行研究。结果:狼疮性肾炎组血清IL-17水平显著高于狼疮无肾炎组和健康对照组(P<0.001),狼疮性肾炎组血清IFN-γ水平显著高于狼疮无肾炎组(P<0.05)和健康对照组(P<0.01),血清IL-4水平在狼疮性肾炎组、狼疮无肾炎组均显著高于健康对照组(P<0.01)。狼疮性肾炎组IFN-γ/IL-4比值显著高于狼疮无肾炎组(P<0.01)和健康对照组(P<0.05);狼疮无肾炎组IFN-γ/IL-4比值显著低于健康对照组(P<0.01)。SLE患者血清IFN-γ表达水平与SLEDAI积分呈正相关(r=0.402,P<0.05),血清IL-17、IL-4表达水平与SLEDAI、SDI、抗ds-DNA抗体、C3、24小时尿蛋白量均无相关性。结论:狼疮性肾炎患者外周血中IL-17、IFN-γ、IL-4等促炎细胞因子均有不同程度升高促起炎症发生及组织损伤,参与了狼疮性肾炎的免疫发病过程。     

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.     

Long‐term effects of calorie restriction on serum sex‐hormone concentrations in men

Calorie restriction (CR) slows aging and consistently reduces circulating sex hormones in laboratory animals. However, nothing is known regarding the long‐term effects of CR with adequate nutrition on serum sex‐hormone concentration in lean healthy humans. In this study, we measured body composition, and serum total testosterone, total 17‐β‐estradiol, sex hormone–binding globulin (SHBG), and dehydroepiandrosterone sulfate (DHEA‐S) concentrations in 24 men (mean age 51.5 ± 13 years), who had been practicing CR with adequate nutrition for an average of 7.4 ± 4.5 years, in 24 age‐ and body fat–matched endurance runners (EX), and 24 age‐matched sedentary controls eating Western diets (WD). We found that both the CR and EX volunteers had significantly lower body fat than the WD volunteers (total body fat, 8.7 ± 4.2%; 10.5 ± 4.4%; 23.2 ± 6.1%, respectively; P = 0.0001). Serum total testosterone and the free androgen index were significantly lower, and SHBG was higher in the CR group than in the EX and WD groups (P ≤ 0.001). Serum 17β‐estradiol and the estradiol:SHBG ratio were both significantly lower in the CR and EX groups than in the WD group (P ≤ 0.005). Serum DHEA‐S concentrations were not different between the three groups. These findings demonstrate that, as in long‐lived CR rodents, long‐term severe CR reduces serum total and free testosterone and increases SHBG concentrations in humans, independently of adiposity. More studies are needed to understand the role of this CR‐mediated reduction in sex hormones in modulating the pathogenesis of age‐associated chronic diseases such as cancer and the aging process itself.     

Effects of infusion of some prostaglandins in essential fatty acid-deficient and normal rats

Infusion of 1 mg/kg per day of prostaglandin E(1) (PGE(1)) for 2 and 7 wk failed to correct the dermal signs of essential fatty acid (EFA) deficiency in rats despite the known conversion of EFA to certain prostaglandins. PGE(1) caused no significant changes in serum cholesterol, triglycerides, or phospholipids or in liver neutral lipids in EFA-deficient or normal rats. In normal rats epinephrine-induced lipolysis was greater in fat pads from infused than from untreated rats. The effect on epinephrine-induced lipolysis was greater after the 7 wk infusion than after the 2 wk infusion. The 7 wk infusion also lowered plasma free fatty acid (FFA) concentrations. Infusion of PGE(2) and PGF(2alpha) in combination for 4 wk had no significant effect on either dermal signs of EFA deficiency, lipolysis, or plasma FFA concentrations.     

高原鼢鼠、高原鼠兔和大鼠肺表面活性物质组成和含量的比较

本研究通过分析肺表面活性物质(pulmonary surfactant,PS)组成和含量探讨高原鼢鼠(Myospalax baileyi)和高原鼠兔(Ochotona curzoniae)的低氧适应机制.高原鼢鼠和高原鼠兔各36只,捕捉于海拔3 600 m左右的青海省海南州贵德县拉脊山地区,36只Sprague-Daw...     

Gender-based differences in the effect of dietary cholesterol in rats

Male and female rats were fed diets supplemented with cholesterol and palm fat at 10 and 50 g/kg, respectively; serum, hepatic tissue and faeces were analysed. Cholesterol supplementation significantly increased serum and hepatic cholesterol both in male and female rats. Male and female rats fed the cholesterol-containing diet differed significantly in serum cholesterol concentration (2.48 ??mol/mL vs 2.92 ??mol/mL), concentration of serum triacylglycerols, but not in hepatic cholesterol concentration. The serum and hepatic cholesterol concentrations correlated non-significantly in male rats (r=0.491; P=0.063) and significantly in female rats (r=0.818; P<0.001). Cholesterol supplementation non-significantly decreased relative expression of the hepatic LDL receptor gene and significantly increased relative expression of the hepatic cholesterol 7??-hydroxylase gene in rats of both genders. The faeces of control rats contained similar amounts of cholesterol and bile acids. Cholesterol supplementation increased cholesterol concentration 10 times in the faeces of male rats and 12 times in faeces of female rats. The corresponding increases of bile acid concentration were much lower (83% in male rats and 108% in female rats). It can be concluded that the effects of cholesterol supplementation were more pronounced in female than in male rats.     

In vivo intra-luteal implants of prostaglandin (PG) E(1) or E(2) (PGE(1), PGE(2)) prevent luteolysis in cows. I. Luteal weight, circulating progesterone, mRNA for luteal luteinizing hormone (LH) receptor, and occupied and unoccupied luteal receptors for LH

Previously, it was reported that chronic intra-uterine infusion of PGE(1) or PGE(2) every four hours inhibited luteolysis in ewes. However, estradiol-17β or PGE(2) given intra-uterine every 8h did not inhibit luteolysis in heifers, but infusion of estradiol+PGE(2) inhibited luteolysis in heifers. The objective of this experiment was to determine whether and how intra-luteal implants containing PGE(1) or PGE(2) prevent luteolysis in Angus or Brahman cows. On day-13 post-estrus, Angus cows received no intra-luteal implant and corpora lutea were retrieved or Angus and Brahman cows received intra-luteal silastic implants containing Vehicle, PGE(1), or PGE(2) and corpora lutea were retrieved on day-19. Coccygeal blood was collected daily for analysis for progesterone. Breed did not influence the effect of PGE(1) or PGE(2) on luteal mRNA for LH receptors or unoccupied or occupied luteal LH receptors did not differ (P>0.05) so the data were pooled. Luteal weights of Vehicle-treated Angus or Brahman cows from days-13-19 were lower (P<0.05) than those treated with intra-luteal implants containing PGE(1) or PGE(2). Day-13 Angus luteal weights were heavier (P<0.05) than Vehicle-treated Angus cows on day-19 and luteal weights of day-13 corpora lutea were similar (P>0.05) to Angus cows on day-19 treated with intra-luteal implants containing PGE(1) or PGE(2). Profiles of circulating progesterone in Angus or Brahman cows treated with intra-luteal implants containing PGE(1) or PGE(2) differed (P<0.05) from controls, but profiles of progesterone did not differ (P>0.05) between breeds or between cows treated with intra-luteal implants containing PGE(1) or PGE(2). Intra-luteal implants containing PGE(1) or PGE(2) prevented (P<0.05) loss of luteal mRNA for LH receptors and unoccupied or occupied receptors for LH compared to controls. It is concluded that PGE(1) or PGE(2) alone delays luteolysis regardless of breed. We also conclude that either PGE(1) or PGE(2) prevented luteolysis in cows by up-regulating expression of mRNA for LH receptors and by preventing loss of unoccupied and occupied LH receptors in luteal tissue.