Black rice and its pigment fraction may have antiatherogenic activity, but the exact component contributing to the beneficial effect remains unclear. The aim of the present study was to investigate the influence of the anthocyanin-rich extract from black rice on the vulnerability of advanced plaques in apolipoprotein (apo) E-deficient mice. Using LC-MS, the anthocyanin-rich extract from black rice was identified as containing cyanidin-3-glucoside and peonidin-3-glucoside. ApoE-deficient mice (n = 30; 30 wk old) were randomly divided into 3 groups: a control group (fed the AIN-93G diet), the simvastin group [simva; fed the AIN-93G diet containing simvastatin, 50 mg/(kg.d)], or the anthocyanin-rich extract group [antho; fed the AIN-93G diet supplemented with anthocyanin-rich extract from black rice, 300 mg/(kg.d)]. After 20 wk of intervention, the plaque area that developed in the brachiocephalic artery of mice in the antho group was smaller than that of the control mice. Both the antho and simva groups had lower frequencies of the large necrotic core and thin fibrous cap in plaques than the control group. Collagen I was increased and matrix metalloproteinase-1 contents were reduced in the brachiocephalic lesion of both the antho and simva groups compared with the control group. Furthermore, mRNA levels of tissue factor and inducible nitric oxide synthase in aortae were decreased in the antho and simva groups. Supplementation of anthocyanin-rich extract improved the lipid profile by decreasing serum triglyceride, total cholesterol, and non-HDL cholesterol. These results suggest that chronic diet intake of anthocyanin-rich extract from black rice may enhance plaque stabilization in old apoE-deficient mice. The underlying mechanism is related mainly to inhibiting proinflammatory factors and improving the serum lipid profile.
The influence of white, red and black rice consumption on atherosclerotic plaque formation induced by hypercholesterolemia was investigated in rabbits. Male rabbits (n = 36) were divided into five groups. They were fed a normal laboratory purified diet (normal group, n = 6), a high cholesterol (0.5 g/100 g) diet (HC group, n = 6), a high cholesterol diet with 30 g/100 g white rice (WR group, n = 8), 30 g/100 g red rice (RR group, n = 8), or 30 g/100 g black rice (BR group, n = 8) for 10 wk. Blood samples were collected for lipid measurements and aorta were removed for assessment of atherosclerotic plaques at the end of the protocol. The oxidant and antioxidant status of blood, erythrocytes, liver and aorta was evaluated. The area of atherosclerotic plaque was 50% lower in rabbits fed the red or black rice diets than in those fed the white rice diet. Compared with the HC and WR groups, serum HDL cholesterol and apolipoprotein (apo) A-I concentration were greater (P < 0.05) in the RR and BR groups. Liver reactive oxygen species (ROS) and aortic malondialdehyde (MDA) were significantly lower, and the liver total antioxidative capacity (TAC) and erythrocyte superoxide dismutase (SOD) activity were significantly higher in the RR and BR groups compared with the HC and WR groups. Red or black rice consumption reduced or retarded the progression of atherosclerotic plaque development induced by dietary cholesterol. The enhanced serum HDL cholesterol and apo A-I concentrations, and the increased antioxidant and decreased oxidative status may be mechanisms of the antiatherogenic effect of red or black rice.
Apolipoprotein (apo)E-deficient mice were used to study the antiatherogenic effect of black rice pigment fraction (BRF) and the possible mechanisms by which it inhibits atherogenesis. The apoE-deficient mice (n = 45) were randomly divided into three groups and received AIN-93G diet (positive group), AIN-93G with 5 g of black rice pigment fraction/100 g (BRF group) and AIN-93G with 5 g of white rice outer layer fraction/100 g (WRF group) for 16 wk. C57BL/6J mice (n = 15) received AIN-93G and were used as a control group. Blood samples were collected for measurement of lipid concentration, antioxidized LDL antibody and nitric oxide concentration. Livers were extracted for determination of cholesterol concentrations, and aortas were used to determine cholesterol concentrations and inducible nitric oxide synthase protein and mRNA expression. Hearts were used to assess atherosclerotic plaque formation. The apoE-deficient mice fed the black rice pigment fraction diet had 48% (P < 0.01) less atherosclerotic lesion area compared with apoE-deficient mice fed only the AIN-93G diet and 46% (P < 0.01) less lesion area compared with mice fed the white rice outer layer fraction diet. This observation corresponded with significantly (P < 0.05) lower total serum cholesterol, lower liver and aorta cholesterol (P < 0.01) and higher HDL cholesterol (P < 0.05) concentrations and lower (P < 0.05) antioxidized LDL antibody titer in apoE-deficient mice fed the black rice pigment fraction diet compared with positive and WRF groups. Notwithstanding this, mice fed the black rice pigment fraction diet also had lower CD4(+) T lymphocyte expression (P < 0.05) and weaker inducible nitric oxide synthase expression (P < 0.05) compared with mice fed the AIN-93G diet and the white rice outer layer fraction diet, respectively. We concluded that the inhibition of atherosclerotic lesions of the black rice pigment fraction is attributed to the improvement in cholesterol accumulation and reduction in oxidative stress and inflammation.
BackgroundCopy number variation (CNV) is a major source of structural variants and has been commonly identified in mammalian genome. It is associated with gene expression and may present a major genetic component of phenotypic diversity. Unlike many other mammalian genomes where CNVs have been well annotated, studies of porcine CNV in diverse breeds are still limited.ResultHere we used Porcine SNP60 BeadChip and PennCNV algorithm to identify 1,315 putative CNVs belonging to 565 CNV regions (CNVRs) in 1,693 pigs from 18 diverse populations. Total 538 out of 683 CNVs identified in a White Duroc × Erhualian F2 population fit Mendelian transmission and 6 out of 7 randomly selected CNVRs were confirmed by quantitative real time PCR. CNVRs were non-randomly distributed in the pig genome. Several CNV hotspots were found on pig chromosomes 6, 11, 13, 14 and 17. CNV numbers differ greatly among different pig populations. The Duroc pigs were identified to have the most number of CNVs per individual. Among 1,765 transcripts located within the CNVRs, 634 genes have been reported to be copy number variable genes in the human genome. By integrating analysis of QTL mapping, CNVRs and the description of phenotypes in knockout mice, we identified 7 copy number variable genes as candidate genes for phenotypes related to carcass length, backfat thickness, abdominal fat weight, length of scapular, intermuscle fat content of logissimus muscle, body weight at 240 day, glycolytic potential of logissimus muscle, mean corpuscular hemoglobin, mean corpuscular volume and humerus diameter.ConclusionWe revealed the distribution of the unprecedented number of 565 CNVRs in pig genome and investigated copy number variable genes as the possible candidate genes for phenotypic traits. These findings give novel insights into porcine CNVs and provide resources to facilitate the identification of trait-related CNVs.
Glycolytic potential (GP) in skeletal muscle is economically important in the pig industry because of its effect on pork processing yield. We have previously mapped a major quantitative trait loci (QTL) for GP on chromosome 3 in a White Duroc × Erhualian F2 intercross. We herein performed a systems genetic analysis to identify the causal variant underlying the phenotype QTL (pQTL). We first conducted genome-wide association analyses in the F2 intercross and an F19 Sutai pig population. The QTL was then refined to an 180-kb interval based on the 2-LOD drop method. We then performed expression QTL (eQTL) mapping using muscle transcriptome data from 497 F2 animals. Within the QTL interval, only one gene (PHKG1) has a cis-eQTL that was colocolizated with pQTL peaked at the same SNP. The PHKG1 gene encodes a catalytic subunit of the phosphorylase kinase (PhK), which functions in the cascade activation of glycogen breakdown. Deep sequencing of PHKG1 revealed a point mutation (C>A) in a splice acceptor site of intron 9, resulting in a 32-bp deletion in the open reading frame and generating a premature stop codon. The aberrant transcript induces nonsense-mediated decay, leading to lower protein level and weaker enzymatic activity in affected animals. The mutation causes an increase of 43% in GP and a decrease of>20% in water-holding capacity of pork. These effects were consistent across the F2 and Sutai populations, as well as Duroc × (Landrace × Yorkshire) hybrid pigs. The unfavorable allele exists predominantly in Duroc-derived pigs. The findings provide new insights into understanding risk factors affecting glucose metabolism, and would greatly contribute to the genetic improvement of meat quality in Duroc related pigs.
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