scholarly journals Anti-atherogenic effect of soya and rice-protein isolate, compared with casein, in apolipoprotein E-deficient mice

2003 ◽  
Vol 90 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Weihua Ni ◽  
Yasuyuki Tsuda ◽  
Shinichiro Takashima ◽  
Hiroyoshi Sato ◽  
Masao Sato ◽  
...  

Our objective was to determine whether dietary plant proteins such as soya-protein isolate (SPI) and rice-protein isolate (RPI) compared with animal proteins, such as casein, could afford beneficial effects on atherosclerosis development in apolipoprotein E-deficient mice. In experiment 1, male and female mice were fed on a purified diet containing either casein, SPI or RPI for 9 weeks. The en face lesion area in the aorta (P < 0·05) and the lesion size in the aortic root (P < 0·05) in mice fed the casein-based diet were greater than those in the SPI or RPI groups. The plant protein groups had an increased concentration of serum l-arginine (P < 0·05) and NO metabolites (NO2 plus NO3) (P < 0·05) than did the casein group. The inhibitory effect of the plant proteins on the lesion formations was unrelated to gender and total serum cholesterol. In experiment 2, the l-arginine and l-methionine contents were the same in the l-arginine-supplemented casein-based and SPI-based diets, and between the l-methionine-supplemented SPI-based and the casein-based diets. Male mice were fed on the diets for 15 weeks. There were no significant differences in the en face lesion area and the lesion size between the casein group and the l-arginine-supplemented group, although the serum l-arginine (P < 0·05) and NO2 plus NO3 (P < 0·05) concentrations in the supplemented group were higher than those in the casein group. There were no significant effects of l-methionine supplementation on the lesion formations. In experiment 3, male mice were given the casein-based diet or the l-arginine-supplemented casein-based diet together with water or water containing an NO synthesis inhibitor for 9 weeks. When given the casein-based diet, the inhibitor drinking, compared with water drinking, resulted in a reduction of the serum NO2 plus NO3 concentration (P < 0·01) and an increase in the en face lesion area (P < 0·05) and the lesion size (P < 0·01). When given the l-arginine-supplemented diet, the inhibitor drinking, compared with water drinking, resulted in no increase in the lesion area and size. These results demonstrate anti-atherogenic potentials of SPI- as well as RPI-derived proteins, but their l-arginine and l-methionine contents were not sufficient enough to explain the underlying mechanism(s).

Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5428-5437 ◽  
Author(s):  
Johan Bourghardt ◽  
Anna S. K. Wilhelmson ◽  
Camilla Alexanderson ◽  
Karel De Gendt ◽  
Guido Verhoeven ◽  
...  

The atheroprotective effect of testosterone is thought to require aromatization of testosterone to estradiol, but no study has adequately addressed the role of the androgen receptor (AR), the major pathway for the physiological effects of testosterone. We used AR knockout (ARKO) mice on apolipoprotein E-deficient background to study the role of the AR in testosterone atheroprotection in male mice. Because ARKO mice are testosterone deficient, we sham operated or orchiectomized (Orx) the mice before puberty, and Orx mice were supplemented with placebo or a physiological testosterone dose. From 8 to 16 wk of age, the mice consumed a high-fat diet. In the aortic root, ARKO mice showed increased atherosclerotic lesion area (+80%, P &lt; 0.05). Compared with placebo, testosterone reduced lesion area both in Orx wild-type (WT) mice (by 50%, P &lt; 0.001) and ARKO mice (by 24%, P &lt; 0.05). However, lesion area was larger in testosterone-supplemented ARKO compared with testosterone-supplemented WT mice (+57%, P &lt; 0.05). In WT mice, testosterone reduced the presence of a necrotic core in the plaque (80% among placebo-treated vs. 12% among testosterone-treated mice; P &lt; 0.05), whereas there was no significant effect in ARKO mice (P = 0.20). In conclusion, ARKO mice on apolipoprotein E-deficient background display accelerated atherosclerosis. Testosterone treatment reduced atherosclerosis in both WT and ARKO mice. However, the effect on lesion area and complexity was more pronounced in WT than in ARKO mice, and lesion area was larger in ARKO mice even after testosterone supplementation. These results are consistent with an AR-dependent as well as an AR-independent component of testosterone atheroprotection in male mice.


2012 ◽  
Vol 60 (6) ◽  
pp. 508-512 ◽  
Author(s):  
Ayelet Raz-Pasteur ◽  
Aviva Gamliel-Lazarovich ◽  
Raymond Coleman ◽  
Shlomo Keidar

PLoS ONE ◽  
2017 ◽  
Vol 12 (7) ◽  
pp. e0181832 ◽  
Author(s):  
James Phie ◽  
Smriti M. Krishna ◽  
Joseph V. Moxon ◽  
Safraz M. Omer ◽  
Robert Kinobe ◽  
...  

2010 ◽  
Vol 212 (1) ◽  
pp. 107-115 ◽  
Author(s):  
Ramona L. Burris ◽  
Cheng-Hui Xie ◽  
Prajitha Thampi ◽  
Xianli Wu ◽  
Stepan B. Melnyk ◽  
...  

2004 ◽  
Vol 32 (1) ◽  
pp. 128-130 ◽  
Author(s):  
S.L. Parkin ◽  
J.P. Pritchett ◽  
D.C. Grimsditch ◽  
K.R. Bruckdorfer ◽  
P.K. Sahota ◽  
...  

We have investigated serum chemokines for their suitability as markers of atherosclerosis development in apoE (apolipoprotein E)-deficient (−/−) mice. Female C3H apoE−/− and C57BL apoE−/− mice were fed on either diet W (Western diet; 6 weeks) or normal rodent diet (12 weeks). Serum lipids (0, 6 and 12 weeks) and terminal chemokine levels were measured using commercially available assays, whereas the lesion area was determined using Oil-Red O-stained aortic sections. Serum lipids were higher in C3H apoE−/− mice for both diets throughout the study; however, lesions were significantly larger in C57BL apoE−/− mice fed on either diet. Chemokine levels were significantly lower in C3H apoE−/− mice fed on the normal diet, but no difference was observed between the two groups fed on diet W. We conclude that serum chemokine levels are potential markers for atherosclerosis susceptibility in C3H and C57BL apoE−/− mice fed on a normal rodent diet.


2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Rod Partow-Navid ◽  
Soban Umar ◽  
Humann Matori ◽  
Andrea Iorga ◽  
Alan M Fogelman ◽  
...  

Apolipoprotein E (ApoE) is a multifunctional protein and its deficiency leads to the development of atherosclerosis in mice. Patients with pulmonary hypertension (PH) have reduced expression of ApoE in lung tissue. ApoE is known to inhibit endothelial and smooth muscle cell proliferation and has anti-inflammatory and anti-platelet aggregation properties. Young ApoE deficient mice have been shown to develop high fat diet-induced PH in a gender specific manner. Estrous cyclicity peaks at 7–8 months and declines by 9 months of age in mice. Here we investigated the effects of monocrotaline (MCT) on young and middle-aged ApoE deficient mice.Middle-Aged (MA) (11–12 month old) male (n=4) and female (n=4) and young (7–8 month old) male (n=5) and female (n=5) ApoE deficient mice were injected with a single intraperitoneal dose of MCT (60 mg/kg). Mice were closely monitored for ∼4 weeks with serial echocardiography for cardiopulmonary hemodynamic assessment. Direct cardiac catheterisation was performed terminally to record peak systolic right ventricular pressure (RVP). RV, LV, IVS and lung tissue was dissected and weighed. Trichrome staining and histochemical analyses were performed. At ∼4 weeks after MCT, MA male and female and young male mice developed severe PH (RVP: MA male=64±5 mmHg, MA female=71±4 mmHg, young male=60±5 mmHg, p=n.s between all the groups) whereas young females developed significantly less severe PH (RVP: 37±5 mmHg, P<0.05 vs. MA male and female, and young male). MA male and female and young male mice developed severe RV dysfunction (RV ejection fraction (RVEF): MA male=31±2%, MA female=28±4%, young male=36±1%, p=n.s between all the groups) whereas young females showed significantly better RV function (RVEF: 43±2%, P<0.05 vs. MA male and female, and young male). MA male and female mice also developed more severe RV hypertrophy (RV/LV+Septum, MA male=0.49, MA female=0.53, young female=0.39). MA male and female mice also manifested increased peripheral pulmonary artery muscularization and pulmonary fibrosis. Interestingly, the gender differences witnessed between young ApoE deficient male and female mice in the development of severe PH and RV dysfunction are abolished as the mice increase in age.


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