Protective effects of a unique combination of nutritionally active ingredients on risk factors and gene expression associated with atherosclerosis in C57BL/6J mice fed a high fat diet

Moss, Joe; Williams, Jessica O.; Al-Ahmadi, Wijdan; O'Morain, Victoria; Chan, Yee-Hung; Hughes, Timothy R.; Menendez-Gonzalez, Juan Bautista; Almotiri, Alhomidi; Plummer, Sue; Rodrigues, Neil P.; Michael, Daryn R.; Ramji, Dipak Purshottam

doi:10.1039/d0fo02867c

Cited by 12 publications

(23 citation statements)

References 65 publications

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“…The primary mechanism by which supplementation with 8% TKO prevents hyperlipidemia is the inhibition of liver fat deposition, which directly or indirectly results in systemically decreased serum TC and TG. Many studies have illustrated that active substance supplementation reduces NAFLD by modulating the composition of the intestinal microecology [ 34 , 35 ]. TKO is rich in nutrients with high contents of PUFAs and active substances such as phytosterols and tocopherols, which enhance the economic and nutritional value of TKO.…”

Section: Discussionmentioning

confidence: 99%

Effects of Torreya grandis Kernel Oil on Lipid Metabolism and Intestinal Flora in C57BL/6J Mice

Xiao

Huang

Huan

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Recent experimental studies have shown that vegetable oil supplementation ameliorates high-fat diet- (HFD-) induced hyperlipidemia and oxidative stress in mice via modulating hepatic lipid metabolism and the composition of the gut microbiota. The aim of this study was to investigate the efficacy of the Torreya grandis kernel oil (TKO) rich in unpolysaturated fatty acid against hyperlipidemia and gain a deep insight into its potential mechanisms. Methods. Normal mice were randomly divided into three groups: ND (normal diet), LO (normal diet supplement with 4% TKO), and HO (normal diet supplement with 8% TKO). Hyperlipidemia mice were randomly divided into two groups: HFN (normal diet) and HFO (normal diet supplement with 8% TKO). Blood biochemistry and histomorphology were observed; liver RNA-seq, metabolomics, and gut 16S rRNA were analyzed. Results. Continuous supplementation of TKO in normal mice significantly ameliorated serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and free fatty acid (FFA) accumulation, decreased blood glucose and malondialdehyde (MDA), and enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. According to GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, most differentially expressed genes (DEGs) were significantly enriched in the biosynthesis of unsaturated fatty acid pathways, and significantly changed metabolites (SCMs) might be involved in the metabolism of lipids. High-dose TKO improved gut alpha diversity and beta diversity showing that the microbial community compositions of the five groups were different. Conclusion. Supplementation of TKO functions in the prevention of hyperlipidemia via regulating hepatic lipid metabolism and enhancing microbiota richness in normal mice. Our study is the first to reveal the mechanism of TKO regulating blood lipid levels by using multiomics and promote further studies on TKO for their biological activity.

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Section: Discussionmentioning

confidence: 99%

Effects of Torreya grandis Kernel Oil on Lipid Metabolism and Intestinal Flora in C57BL/6J Mice

Xiao

Huang

Huan

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…[ 11 ] Human THP‐1 monocytes, which can be differentiated into macrophages using phorbol 12‐myristate 13‐acetate (PMA), were used as they demonstrate conservation of responses relevant to atherosclerosis seen in primary cultures and in vivo. [ 10 , 12 ] For monocytes, cells treated with either vehicle or probiotic CM were counted daily for 7 days and proliferation determined as the percentage change in cell number. Linear regression analysis showed significant reduction in monocyte proliferation over the 7‐day period when treated with CM from Lab4 ( p < 0.05) or CUL66 ( p < 0.001) ( Figure 7 A ).…”

Section: Resultsmentioning

confidence: 99%

“…Immunophenotyping of bone marrow cell populations was performed using marker antibodies and reagents (Table S1 and S2 , Supporting Information) as previously described. [ 12 ] Thus, 10 or 8 million cells, respectively, were used to analyze the signaling lymphocytic activation molecule (SLAM) and progenitor cell populations whereas 1 million cells were employed for lineage cell populations. Samples were analyzed on a BD LSR Fortessa 4 lasers flow cytometer and data analysis performed using FlowJo v.10 software.…”

Section: Methodsmentioning

confidence: 99%

“…Preparation of RNA, conversion to cDNA and either standard real‐time quantitative PCR (RT‐qPCR) using primers shown in Table S3 , Supporting Information or Atherosclerosis RT 2 Profiler PCR Arrays (Qiagen, Manchester, UK) was performed as previously described. [ 10 , 12 , 28 ] Gene transcript levels were calculated using the comparative Ct method.…”

Section: Methodsmentioning

confidence: 99%

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The Lab4P Consortium of Probiotics Attenuates Atherosclerosis in LDL Receptor Deficient Mice Fed a High Fat Diet and Causes Plaque Stabilization by Inhibiting Inflammation and Several Pro‐Atherogenic Processes

O'Morain

Chan

Williams

et al. 2021

Molecular Nutrition Food Res

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Scope: Previous studies show that Lab4 probiotic consortium plus Lactobacillus plantarum CUL66 (Lab4P) reduces diet-induced weight gain and plasma cholesterol levels in C57BL/6J mice fed a high fat diet (HFD). The effect of Lab4P on atherosclerosis is not known and is therefore investigated. Methods and Results: Atherosclerosis-associated parameters are analyzed in LDL receptor deficient mice fed HFD for 12 weeks alone or supplemented with Lab4P. Lab4P increases plasma HDL and triglyceride levels and decreases LDL/VLDL levels. Lab4P also reduces plaque burden and content of lipids and macrophages, indicative of dampened inflammation, and increases smooth muscle cell content, a marker of plaque stabilization. Atherosclerosis arrays show that Lab4P alters the liver expression of 19 key disease-associated genes. Lab4P also decreases the frequency of macrophages and T-cells in the bone marrow. In vitro assays using conditioned media from probiotic bacteria demonstrates attenuation of several atherosclerosis-associated processes in vitro such as chemokine-driven monocytic migration, proliferation of monocytes and macrophages, foam cell formation and associated changes in expression of key genes, and proliferation and migration of vascular smooth muscle cells. Conclusion: This study provides new insights into the anti-atherogenic actions of Lab4P together with the underlying mechanisms and supports further assessments in human trials.

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“…Nevertheless, as a sensitive cell group, the effect of comprehensive food intake on MDSC may change. In a recent experiment that examined atherosclerotic subjects, the number and proportion of MDSC in the bone marrow of high-fat diet mice were both decreased following co-administration with omega-3 polyunsaturated fatty acids, flavanols, and phytosterols ( Moss et al, 2021 ). However, the number and function of MDSC in the blood are not currently known under these feeding conditions.…”

Section: Mdsc Is a Candidate Target For The Treatment Of Diabetesmentioning

confidence: 99%

Emerging Roles of Myeloid-Derived Suppressor Cells in Diabetes

et al. 2021

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Diabetes is a syndrome characterized by hyperglycemia with or without insulin resistance. Its etiology is attributed to the combined action of genes, environment and immune cells. Myeloid-derived suppressor cell (MDSC) is a heterogeneous population of immature cells with immunosuppressive ability. In recent years, different studies have debated the quantity, activity changes and roles of MDSC in the diabetic microenvironment. However, the emerging roles of MDSC have not been fully documented with regard to their interactions with diabetes. Here, the manifestations of MDSC and their subsets are reviewed with regard to the incidence of diabetes and diabetic complications. The possible drugs targeting MDSC are discussed with regard to their potential of treating diabetes. We believe that understanding MDSC will offer opportunities to explain pathological characteristics of different diabetes. MDSC also will be used for personalized immunotherapy of diabetes.

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Protective effects of a unique combination of nutritionally active ingredients on risk factors and gene expression associated with atherosclerosis in C57BL/6J mice fed a high fat diet

Abstract: Atherosclerosis, an inflammatory disorder of the vasculature and the underlying cause of cardiovascular disease, is responsible for one in three global deaths. Consumption of active food ingredients such as omega-3...

Cited by 12 publications

References 65 publications

Effects of Torreya grandis Kernel Oil on Lipid Metabolism and Intestinal Flora in C57BL/6J Mice

Effects of Torreya grandis Kernel Oil on Lipid Metabolism and Intestinal Flora in C57BL/6J Mice

The Lab4P Consortium of Probiotics Attenuates Atherosclerosis in LDL Receptor Deficient Mice Fed a High Fat Diet and Causes Plaque Stabilization by Inhibiting Inflammation and Several Pro‐Atherogenic Processes

Emerging Roles of Myeloid-Derived Suppressor Cells in Diabetes

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