scholarly journals Adzuki resistant starch lowered serum cholesterol and hepatic 3-hydroxy-3-methylglutaryl-CoA mRNA levels and increased hepatic LDL-receptor and cholesterol 7α-hydroxylase mRNA levels in rats fed a cholesterol diet

2005 ◽  
Vol 94 (6) ◽  
pp. 902-908 ◽  
Author(s):  
Kyu-Ho Han ◽  
Miharu Iijuka ◽  
Ken-ichiro Shimada ◽  
Mitsuo Sekikawa ◽  
Katsuhisa Kuramochi ◽  
...  
Keyword(s):  
Bile Acid ◽  
Serum Cholesterol ◽  
Resistant Starch ◽  
Mrna Level ◽  
Ldl Receptor ◽  
Mrna Levels ◽  
Cholesterol Diet ◽  
Receptor Mrna ◽  
Reductase Mrna ◽  
Coa Reductase

We examined the effects of adzuki bean resistant starch on serum cholesterol and hepatic mRNA in rats fed a cholesterol diet. The mRNA coded for key regulatory proteins of cholesterol metabolism. The control rats were fed 15 % cornstarch (basal diet, BD). The experimental rats were fed BD plus a 0·5 % cholesterol diet (CD), or a 15 % adzuki resistant starch plus 0·5 % cholesterol diet (ACD) for 4 weeks. The serum total cholesterol and VLDL + intermediate density lipoprotein + LDL-cholesterol levels in the ACD group were significantly lower than those in the CD group throughout the feeding period. The total hepatic cholesterol concentrations in the CD and ACD groups were not significantly different. The faecal total bile acid concentration in the ACD group was significantly higher than that in the BD and CD groups. Total SCFA and acetic acid concentrations in the ACD group were significantly higher than those in the CD group but there were no significant differences in the concentrations between the ACD and BD groups. The hepatic LDL-receptor mRNA and cholesterol 7α-hydroxylase mRNA levels in the ACD group were significantly higher than those in the CD group and the hepatic 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase mRNA level in the ACD group was significantly lower than in the CD group. The results suggest that adzuki resistant starch has a serum cholesterol-lowering function via enhancement of the hepatic LDL-receptor mRNA and cholesterol 7α-hydroxylase mRNA levels and faecal bile acid excretion, and a decrease in the hepatic HMG-CoA reductase mRNA level, when it is added to a cholesterol diet.

scholarly journals Exercise-induced changes in β-adrenergic-receptor mRNA level measured by competitive RT-PCR

1997 ◽  
Vol 82 (6) ◽  
pp. 1926-1931 ◽  
Author(s):  
Nobuharu Fujii ◽  
Takeshi Shibata ◽  
Sachiko Homma ◽  
Haruo Ikegami ◽  
Kazuo Murakami ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Human Lymphocytes ◽  
Mrna Level ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Receptor Mrna ◽  
Exercise Induced ◽  
Induced Changes ◽  
Receptor Mrna Level

Fujii, Nobuharu, Takeshi Shibata, Sachiko Homma, Haruo Ikegami, Kazuo Murakami, and Hitoshi Miyazaki. Exercise-induced changes in β-adrenergic-receptor mRNA level measured by competitive RT-PCR. J. Appl. Physiol. 82(6): 1926–1931, 1997.—Competitive reverse transcription-polymerase chain reaction (RT-PCR) analysis was used to clarify whether dynamic exercise-induced increases in β-adrenergic-receptor (β-AR) number in human lymphocytes are accompanied by increases in the β-AR mRNA level. Sixteen healthy subjects performed cycle ergometry until exhaustion. Before and immediately after exercise, peripheral blood was drawn from a forearm vein for preparation of lymphocytes. Both the β-AR mRNA level and the β-AR number were significantly increased by exercise. The changes in β-AR mRNA level and β-AR number were significantly correlated ( r = 0.63, P < 0.01). This finding suggests that a rapid increase in β-AR mRNA level might be an early adaptive response of the sympathetic nervous system to dynamic exercise. In vitro incubation of lymphocytes with epinephrine had no effect on β-AR mRNA levels, nor did adenosine 3′,5′-cyclic monophosphate, protein kinase C, or intracellular Ca2+ increase the β-AR mRNA level in vitro. Therefore, it appears that other mechanisms underlie the exercise-induced elevation of β-AR mRNA levels in human lymphocytes.

scholarly journals High Cholesterol Diet-Induced Changes in Oxysterol and Scavenger Receptor Levels in Heart Tissue

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Erdi Sozen ◽  
Burak Yazgan ◽  
Ali Sahin ◽  
Umit Ince ◽  
Nesrin Kartal Ozer
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Unsaturated Fatty Acids ◽  
Scavenger Receptor ◽  
Heart Tissue ◽  
High Cholesterol Diet ◽  
Mrna Levels ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Receptor Mrna

Involvement of high cholesterol and oxidative stress in cardiovascular diseases is well studied, as it can be hypothesized that various products originated from lipid peroxidation, such as oxysterols, or affected protein expression might lead to cardiomyocyte damage followed by the pathological modifications. Although oxidation of excessive cholesterol to oxysterols in elevated stress conditions is identified by a number of studies, the role of a high cholesterol diet in regulating fatty acid and oxysterol accumulation, together with scavenger receptor mRNA levels, in the heart remains little investigated. Our study provides a detailed analysis of the changes in fatty acid, oxysterol, and scavenger receptor profiles and its relation with histological alterations in the heart tissue. We evaluated alterations of fatty acid composition, by the GC-MS method, while 4β-, 25-, and 27-hydroxycholesterol and 7-ketocholesterol levels by means of LC-MS/MS in high cholesterol diet-fed rabbits. Additionally, a number of proteins related to lipid metabolism and scavenger receptor mRNA expressions were evaluated by Western blotting and RT-PCR. According to our in vivo results, a high cholesterol diet enhances a number of unsaturated fatty acids, oxysterols, and LXRα, in addition to CD36, CD68, CD204, and SR-F1 expressions while α-tocopherol supplementation decreases LXRα and SR expressions together with an increase in 27-hydroxycholesterol and ABCA1 levels. Our results indicated that the high cholesterol diet modulates proteins related to lipid metabolism, which might result in the malfunction of the heart and α-tocopherol shows its beneficial effects. We believe that this work will lead the generation of different theories in the development of heart diseases.

scholarly journals Endotoxin suppresses rat hepatic low-density lipoprotein receptor expression

1996 ◽  
Vol 313 (3) ◽  
pp. 873-878 ◽  
Author(s):  
Wei LIAO ◽  
Mats RUDLING ◽  
Bo ANGELIN
Keyword(s):  
Time Course ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Receptor Expression ◽  
Plasma Lipoproteins ◽  
Low Density ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Receptor Mrna

Endotoxin induces hyperlipidaemia in experimental animals. In the current study, we investigated whether endotoxin alters hepatic low-density lipoprotein (LDL) receptor expression in rats. Endotoxin treatment suppressed hepatic LDL receptor expression in a dose- and time-dependent manner. Eighteen hours after intraperitoneal injection of increasing amounts of endotoxin, LDL receptor and its mRNA levels were determined by ligand blot and solution hybridization respectively. LDL receptor expression was inhibited by about 70% at a dose of 500 μg/100 g body weight. However, LDL receptor mRNA levels were markedly increased in all endotoxin-treated groups at this time point (by 83–136%; P < 0.001). Time-course experiments showed that LDL receptor expression was already reduced by 48% 4 h after endotoxin injection and was maximally reduced (by 63–65%) between 8 and 18 h. Changes in hepatic LDL receptor mRNA showed a different pattern. By 4 h after endotoxin injection, LDL receptor mRNA had decreased by 78% (P < 0.001). However, by 8 h after endotoxin injection, LDL receptor mRNA had returned to levels similar to controls, and 18 and 24 h after endotoxin injection, they were increased by about 60% (P < 0.05). Separation of plasma lipoproteins by FPLC demonstrated that endotoxin-induced changes in plasma triacylglycerols and cholesterol were due to accumulation of plasma apolipoprotein B-containing lipoproteins among very-low-density lipoprotein, intermediate-density lipoprotein and LDL. It is concluded that endotoxin suppresses hepatic LDL receptor expression in vivo in rats.

scholarly journals Modulation of glomerular endothelin and endothelin receptor gene expression in aminonucleoside-induced nephrosis.

1995 ◽  
Vol 5 (8) ◽  
pp. 1585-1590
Author(s):  
T Nakamura ◽  
I Ebihara ◽  
M Fukui ◽  
S Osada ◽  
Y Tomino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Mrna Level ◽  
Experimental Period ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Puromycin Aminonucleoside ◽  
Receptor Mrna ◽  
Etb Receptor ◽  
Receptor Gene Expression

This study assessed glomerular endothelin (ET)-1, ET-3, and ET-receptor A and B mRNA levels in puromycin aminonucleoside (PAN)-induced nephrosis. During the nephrotic stage, 8 days after PAN injection, ET-1 and ETB receptor mRNA were elevated by 2.8 +/- 0.8-fold (P < 0.01) and 2.4 +/- 0.9-fold (P < 0.01), respectively, as compared with controls. These mRNA levels decreased to control levels by Day 20, when the nephrosis was in remission. In contrast, glomerular ETA receptor mRNA levels did not change in PAN nephrosis or control rats during the experimental period. ET-3 mRNA was not detected in the glomeruli of PAN nephrosis or control rats. Additionally, plasma ET concentration and glomerular ET production were measured in PAN nephrosis and control rats by radio-immunoassay. Eight days after PAN injection, ET-1 levels in plasma and glomeruli were not significantly altered in rats with PAN-induced nephrosis (glomeruli, 104.68 +/- 16.46 pg/mg of protein versus 98.24 +/- 13.68 pg/mg of protein; plasma, 2.68 +/- 1.10 versus 2.52 +/- 0.98 pg/mL). The administration of methylprednisolone to PAN rats resulted in the rapid disappearance of proteinuria and partially attenuated the increased ET-1 and ETB receptor gene expression in the glomeruli. These data indicate that glomerular ET-1 and ETB receptor expression in PAN nephrosis in increased at the mRNA level and that methylprednisolone treatment results in an attenuated increase.

Short-term effects of ACTH on the low-density lipoprotein receptor mRNA level in rat and hamster adrenals

1991 ◽  
Vol 6 (3) ◽  
pp. 223-230 ◽  
Author(s):  
J.-G. Lehoux ◽  
A. Lefebvre
Keyword(s):  
Cholesterol Metabolism ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Cholesterol Content ◽  
Low Density ◽  
Short Term ◽  
Hmg Coa Reductase ◽  
Receptor Mrna ◽  
Coa Reductase

ABSTRACT Low-density lipoprotein (LDL) receptor mRNA was found in both rat and hamster adrenals. Within 30 min after ACTH administration a significant increase in the levels of both LDL receptor and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) mRNAs was observed in rat adrenals; these levels remained increased for up to 240 min. The increase in the levels of LDL receptor and HMG-CoA reductase mRNAs produced by ACTH was reduced by co-administration of aminoglutethimide while, at the same time, the adrenal cholesterol content of rats treated with both aminoglutethimide and ACTH was significantly increased compared with that in groups treated with ACTH alone. Cycloheximide also induced increased levels of rat adrenal mRNAs for LDL receptor and HMG-CoA reductase, but this effect was not additive with that of ACTH. These results suggest that, in the rat, the short-term effect of ACTH on the levels of mRNAs for the LDL receptor and HMG-CoA reductase is similarly controlled and might be mediated through changes in the adrenal cholesterol content. In the hamster adrenal, however, no significant fluctuations were found in the level of LDL receptor mRNA, although a marked increase was found in the level of HMG-CoA reductase mRNA, 2 h after ACTH administration. This indicates that an important effect of ACTH on cholesterol metabolism in the hamster adrenal is at the level of HMG-CoA reductase. In the hamster, therefore, where the main source of cholesterol for the adrenal gland is de-novo synthesis, it seems that a complex mechanism is involved in the control of LDL receptor gene expression.

scholarly journals Identification of liver CYP51 as a gene responsive to circulating cholesterol in a hamster model

2016 ◽  
Vol 5 ◽  
Author(s):  
Haiqiu Huang ◽  
Zhuohong Xie ◽  
Wallace Yokoyama ◽  
Liangli Yu ◽  
Thomas T. Y. Wang
Keyword(s):  
High Fat Diet ◽  
Cholesterol Metabolism ◽  
Ldl Receptor ◽  
High Fat ◽  
Hamster Model ◽  
Hmg Coa Reductase ◽  
Cholesterol Levels ◽  
Reductase Mrna ◽  
Coa Reductase ◽  
The Relationship

AbstractHypercholesterolaemia is a risk factor for CVD, which is a leading cause of death in industrialised societies. The biosynthetic pathways for cholesterol metabolism are well understood; however, the regulation of circulating cholesterol by diet is still not fully elucidated. The present study aimed to gain more comprehensive understanding of the relationship between circulating cholesterol levels and molecular effects in target tissues using the hamster model. Male golden Syrian hamsters were fed with chow or diets containing 36 % energy from fat with or without 1 % cholesteyramine (CA) as a modulator of circulating cholesterol levels for 35 d. It was revealed that the expression of lanosterol 14α-demethylase (CYP51) instead of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase mRNA expression was responsive to circulating cholesterol in hamsters fed hypercholesterolaemic diets. The high-fat diet increased circulating cholesterol and down-regulated CYP51, but not HMG-CoA reductase. The CA diet decreased cholesterol and increased CYP51 expression, but HMG-CoA reductase expression was not affected. The high-fat diet and CA diet altered the expression level of cholesterol, bile acids and lipid metabolism-associated genes (LDL receptor, cholesterol 7α-hydroxylase (CYP7A1), liver X receptor (LXR) α, and ATP-binding cassette subfamily G member 5/8 (ABCG5/8)) in the liver, which were significantly correlated with circulating cholesterol levels. Correlation analysis also showed that circulating cholesterol levels were regulated by LXR/retinoid X receptor and PPAR pathways in the liver. Using the hamster model, the present study provided additional molecular insights into the influence of circulating cholesterol on hepatic cholesterol metabolism pathways during hypercholesterolaemia.

scholarly journals Dietary acetic acid reduces serum cholesterol and triacylglycerols in rats fed a cholesterol-rich diet

2006 ◽  
Vol 95 (5) ◽  
pp. 916-924 ◽  
Author(s):  
Takashi Fushimi ◽  
Kazuhito Suruga ◽  
Yoshifumi Oshima ◽  
Momoko Fukiharu ◽  
Yoshinori Tsukamoto ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Bile Acid ◽  
Total Cholesterol ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Mrna Level ◽  
Serum Total Cholesterol ◽  
Free Access ◽  
Mrna Levels ◽  
Atp Citrate Lyase

To investigate the efficacy of the intake of vinegar for prevention of hyperlipidaemia, we examined the effect of dietary acetic acid, the main component of vinegar, on serum lipid values in rats fed a diet containing 1% (w/w) cholesterol. Animals were allowed free access to a diet containing no cholesterol, a diet containing 1% cholesterol without acetic acid, or a diet containing 1% cholesterol with 0·3% (w/w) acetic acid for 19 d. Then, they were killed after food deprivation for 7 h. Cholesterol feeding increased serum total cholesterol and triacylglycerol levels. Compared with the cholesterol-fed group, the cholesterol and acetic acid-fed group had significantly lower values for serum total cholesterol and triacylglycerols, liver ATP citrate lyase (ATP-CL) activity, and liver 3-hydroxy-3-methylglutaryl-CoA content as well as liver mRNA levels of sterol regulatory element binding protein-1, ATP-CL and fatty acid synthase (P<,0·05). Further, the serum secretin level, liver acyl-CoA oxidase expression, and faecal bile acid content were significantly higher in the cholesterol and acetic acid-fed group than in the cholesterol-fed group (P<0·05). However, acetic acid feeding affected neither the mRNA level nor activity of cholesterol 7a-hydroxylase. In conclusion, dietary acetic acid reduced serum total cholesterol and triacylglycerol: first due to the inhibition of lipogenesis in liver; second due to the increment in faecal bile acid excretion in rats fed a diet containing cholesterol.

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