Proteome from patients with metabolic syndrome is regulated by quantity and quality of dietary lipids.
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ABSTRACT:
SUBMITTER: Rangel-Zuniga OA
PROVIDER: S-EPMC4493955 | biostudies-literature | 2015 Jul
REPOSITORIES: biostudies-literature
Publications
Proteome from patients with metabolic syndrome is regulated by quantity and quality of dietary lipids.
Rangel-Zúñiga Oriol Alberto OA Camargo Antonio A Marin Carmen C Peña-Orihuela Patricia P Pérez-Martínez Pablo P Delgado-Lista Javier J González-Guardia Lorena L Yubero-Serrano Elena M EM Tinahones Francisco J FJ Malagón María M MM Pérez-Jiménez Francisco F Roche Helen M HM López-Miranda José J
BMC genomics 20150708
<h4>Background</h4>Metabolic syndrome is a multi-component disorder associated to a high risk of cardiovascular disease. Its etiology is the result of a complex interaction between genetic and environmental factors, including dietary habits. We aimed to identify the target proteins modulated by the long-term consumption of four diets differing in the quality and quantity of lipids in the whole proteome of peripheral blood mononuclear cells (PBMC).<h4>Results</h4>A randomized, controlled trial co ...[more]
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2014-05-09 | GSE57484 | GEO
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Project description:Purpose: Dietary fat-driven hyperphagia increase intestinal growth and permeability and create microbial imbalance in the gut. Over-nutrition coupled with increase in intestinal nutrient absorbance capacity then lead to nutrient overload in the liver, visceral adipose tissue followed by ectopic fat deposition with consequential lipotoxicity and inflammation. We investigated how protein quantity (10-30%) and quality (casein and whey) interact with dietary fat (20-55%) to affect these outcomes in adult mice. High (30%) protein groups showed differential response to high fat diets (40 and 55% fat) and these groups were selected for RNA-seq experiments. RNA-seq was performed on RNA extracted from the jejunum, liver and hypothalami of mice exposed to the different diets. Methods: C57BL/6J male mice used in this work. All mice were fed a 20% kcal casein, 10% kcal fat and 70% kcal carbohydrate diet (Research Diets; USA; D12450Bi), until they were aged 20 weeks. Following 15 weeks of intake of the latter diet (at age 20 weeks), all animals were weight matched and randomly allocated to different groups and switched to experimental diets for 12 weeks. After 12 weeks of dietary interventions all animals were sacrificed and dissected. Methods: The dietary treatments consisted of 3 different levels of dietary fat (20, 40 and 55%) combined with 3 different levels of protein (10, 20 and 30%), each replicated with the protein coming from either casein (CAS) (diet codes: D17052701- D17052709) or whey protein isolate (WPI) (diet codes: D17052710- D17052718). The levels of cellulose and sucrose were fixed at 5% by weight and energy respectively. The carbohydrate (starch) amount was reduced in parallel with increase of dietary protein and fat. All these diets can be ordered direct from research diets (www.researchdiets.com) using the diet codes provided. The 18 different treatments with 12 mice per group, where mice were housed in cages of 3 animals. Methods: The hypothalamus, liver, and jejunum of all animals from 30% protein groups (6 diets [D17052703, D17052706, D17052709, D17052712, D17052715, D17052718], 71 animals) were collected. Total RNA was extracted from hypothalamic blocks using Tri-reagent (Sigma) and from liver and jejunum using the RNeasy Mini Kit (QIAGEN, 74104) according to manufacture instructions. Hypothalamic RNA was paired-end (PE) sequenced by PE100 on BGISEQ-500 platform at Beijing Genomic Institute (PE 2 x 75 bp, 150 bp per fragment, 20M read-pairs per sample). Sequencing of liver and jejunal RNA was performed using the NovaSeq 6000 platform (chemistry V4.0 Illumina) at Macrogen Inc Seoul, South Korea (PE 2 x 75 bp, 150 bp per fragment, 25M read-pairs per sample). Raw sequence reads were obtained in FASTQ format and these sequence reads were quality assessed using the software FastQC (v 0.111.58; http://www.bioinformatics.babraham.ac.uk/projects/fastqc/). Sequences from all samples were quality trimmed, and cleaned of adaptor sequences using BBDuk java package to trim Illumina adapter sequences. On average 0.1% of the bases were trimmed per sample. Trimmed reads were aligned to the Mus musculus reference genome assembly GRCm38 (ftp://ftp.ensembl.org/pub/release-96/fasta/mus_musculus/dna/) using STAR RNA-seq aligner v2.5.2, and uniquely mapped read counts per Ensembl annotated gene/ transcript were estimated using the STAR -- quantMode option. Genes with zero read counts across all samples as well as non-protein coding genes were removed prior to subsequent analysis. Differential gene expression analysis and data transformations and visualization were carried out using DeSeq2 v1.18.1 in R 3.5.2. Sample clustering was carried out on variance stabilizing transformed data and visualised using PCA. Differentially expressed genes lists were generated using a negative binomial generalized linear model and pairwise comparisons using each combination of fat and protein content in each tissue. P values were adjusted for multiple comparisons using a Benjamini and Hochberg (B-H) method. DE genes with an adjusted P value < 0.05 were used for further DE gene data exploration and pathway analysis. The fold changes and p values were loaded into the Ingenuity Pathway Analysis (IPA) program (Ingenuity Systems; http://www.ingenuity.com/) for core analysis. IPA Knowledge Database was used to analyse the dietary impacts on canonical pathways and upstream regulators available in IPA. Results: Differential gene expression and IPA results revealed that jejunal immunity of the high (30%) CAS fed groups at 40 and 55% fat was oriented toward pro-inflammatory responses, whereas the corresponding WPI fed groups showed a reduction of inflammation. The liver transcriptome reveals genes involved in FA/lipid uptake and synthesis to be upregulated and genes involved in FA/lipid degradation were downregulated following a proportional increase of dietary fat (20 to 55%) in 30% CAS fed animals and these effects were not seen in WPI fed animals. In the hypothalamus, the intake of 40 and 55% fat significantly increased the number of differentially expressed genes compared to 20% fat. The effect of protein quality on hypothalamic gene expression (CAS vs WPI) was only seen at the highest fat content (55%), where several changes in signalling pathways were seen in WPI relative to CAS. These include a decreased reactive oxygen species production, reduction interleukin and chemokine inflammatory pathways and increased oxidative phosphorylation compared with mice fed CAS and 55% fat. Conclusions: Analysis of jejunal, liver and hypothalamic transcriptomic revealed that the intake of high WPI impeded the negative effects of high fat feeding (increased lipogenesis in the liver, inflammation, activation of disease-related pathways etc.), whereas the intake of high CAS exacerbated these effects. The data highlight the importance of selecting proteins rich in essential amino acids, for improving the metabolic outcomes of high fat diet.
2021-04-01 | GSE167498 | GEO
Project description:Dietary restriction (DR) reduces adiposity and improves metabolism in patients with one or more symptoms of metabolic syndrome. Nonetheless, it remains elusive whether the benefits of DR in humans are mediated by calorie or nutrient restriction. This study was conducted to determine whether isocaloric dietary protein restriction is sufficient to confer the beneficial effects of dietary restriction in patients with metabolic syndrome. We performed a prospective, randomized controlled dietary intervention under constant nutritional and medical supervision. Twenty-one individuals diagnosed with metabolic syndrome were randomly assigned for caloric restriction (CR; n = 11, diet of 5941 ± 686 KJ per day) or isocaloric dietary protein restriction (PR; n = 10, diet of 8409 ± 2360 KJ per day) and followed for 27 days. Like CR, PR promoted weight loss due to a reduction in adiposity, which was associated with reductions in blood glucose, lipid levels, and blood pressure. More strikingly, both CR and PR improved insulin sensitivity by 62.3% and 93.2%, respectively, after treatment. Fecal microbiome diversity was not affected by the interventions. Adipose tissue bulk RNA-Seq data revealed minor changes elicited by the interventions. After PR, terms related to leukocyte proliferation were enriched among the upregulated genes. Protein restriction is sufficient to confer almost the same clinical outcomes as calorie restriction without the need for a reduction in calorie intake. The isocaloric characteristic of the PR intervention makes this approach a more attractive and less drastic dietary strategy in clinical settings and has more significant potential to be used as adjuvant therapy for people with metabolic syndrome.
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