Project description:Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause liver damage. Green tea is one of the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few study report on GTP relieving DEHP-induced liver damage.
Project description:This study considers the physiological modulation of liver proteins due to the supplementation with fish oils under two different dietary backgrounds: low- or high- fat and sucrose diets, and the effect of their combination with an antioxidant agent (grape polyphenols) which provides reducing power. For this scope, a quantitative proteomics approach based on the Isobaric Tag for relative and Absolute Quantitation methodology (iTRAQ)-coupled to nano-LC-MS/MS and complemented with 2D-DIGE analysis were used for determining the regulation of liver proteins exerted by the supplementation with fish oils, polyphenols or their combination of Wistar Kyoto rats in the two chosen dietary backgrounds. This experimental design was useful to investigate if the behavior of fish oils changes when the dietary background is modified and the possible synergy between fish oils and polyphenols. Results show that the capacity of fish oils, polyphenols or their combination for down or up-regulating liver proteins depends on the dietary context. In the background of low-fat low-sucrose healthy diets, 10 different proteins were altered by the sum of three supplements, in opposite to the 45 altered proteins found in the high-fat high-sucrose unhealthy diets. In both situations, fish oils seemed to be the main force for regulating liver proteins, although the addition of polyphenols was able to modulate some fish oils effects. Moreover, we provide evidence of the effect of fish oils and their combination with grape polyphenols for improving biochemical parameters and for reducing enzymes of hepatic lipogenesis and glycolysis, for enhancing fatty acid beta oxidation and insulin signaling and for the amelioration of endoplasmic reticule stress and protein oxidation when are included in an unhealthy diet.
Project description:This study considers the physiological modulation of liver proteins due to the supplementation with fish oils under two different dietary backgrounds: low- or high- fat and sucrose diets, and the effect of their combination with an antioxidant agent (grape polyphenols) which provides reducing power. For this scope, a quantitative proteomics approach based on the Isobaric Tag for relative and Absolute Quantitation methodology (iTRAQ)-coupled to nano-LC-MS/MS and complemented with 2D-DIGE analysis were used for determining the regulation of liver proteins exerted by the supplementation with fish oils, polyphenols or their combination of Wistar Kyoto rats in the two chosen dietary backgrounds. This experimental design was useful to investigate if the behavior of fish oils changes when the dietary background is modified and the possible synergy between fish oils and polyphenols. Results show that the capacity of fish oils, polyphenols or their combination for down or up-regulating liver proteins depends on the dietary context. In the background of low-fat low-sucrose healthy diets, 10 different proteins were altered by the sum of three supplements, in opposite to the 45 altered proteins found in the high-fat high-sucrose unhealthy diets. In both situations, fish oils seemed to be the main force for regulating liver proteins, although the addition of polyphenols was able to modulate some fish oils effects. Moreover, we provide evidence of the effect of fish oils and their combination with grape polyphenols for improving biochemical parameters and for reducing enzymes of hepatic lipogenesis and glycolysis, for enhancing fatty acid beta oxidation and insulin signaling and for the amelioration of endoplasmic reticule stress and protein oxidation when are included in an unhealthy diet.
Project description:This is a randomized, placebo controlled, multicentric trial to investigate the effect of diet supplementation with green tea extract containing 300mg epigallocatechin gallate (EGCG), the major polyphenol of green tea, on the recurrence of colon adenomas.
Project description:Folic acid (FA) supplementation may protect from obesity and insulin resistance, the effects and mechanism of FA on chronic high-fat-diet-induced obesity-related metabolic disorders are not well elucidated. We adopted a genome-wide approach to directly examine whether FA supplementation affects the DNA methylation profile of mouse adipose tissue and identify the functional consequences of these changes. Mice were fed a high-fat diet (HFD), normal diet (ND) or an HFD supplemented with folic acid (20 μg/ml in drinking water) for 10 weeks, epididymal fat was harvested, and genome-wide DNA methylation analyses were performed using methylated DNA immunoprecipitation sequencing (MeDIP-seq). Mice exposed to the HFD expanded their adipose mass, which was accompanied by a significant increase in circulating glucose and insulin levels. FA supplementation reduced the fat mass and serum glucose levels and improved insulin resistance in HFD-fed mice. MeDIP-seq revealed distribution of differentially methylated regions (DMRs) throughout the adipocyte genome, with more hypermethylated regions in HFD mice. Methylome profiling identified DMRs associated with 3787 annotated genes from HFD mice in response to FA supplementation. Pathway analyses showed novel DNA methylation changes in adipose genes associated with insulin secretion, pancreatic secretion and type 2 diabetes. The differential DNA methylation corresponded to changes in the adipose tissue gene expression of Adcy3 and Rapgef4 in mice exposed to a diet containing FA. FA supplementation improved insulin resistance, decreased the fat mass, and induced DNA methylation and gene expression changes in genes associated with obesity and insulin secretion in obese mice fed a HFD.
Project description:This study tested the anti-inflammatory potential of a green tea extract rich in polyphenols (GrTP) in the colon of the multi-drug resistance targeted mutation (Mdr1a-/-) mouse model of IBD. A colonic histological injury score was determined for each mouse to establish the effect of GrTP on inflammation. Insights into mechanisms responsible for changes in inflammation were gained using transcriptome (microarray) and proteome (2-D gel electrophoresis and LCMS protein identification) analyses. A total of 24 male Mdr1a-/- mice purchased from Taconic (Hudson, NY, USA) at 4-5 weeks of age were used for this study. 12 mice were randomly assigned to each of two different dietary groups: control (AIN-76A powdered diet), or GrTP (AIN-76A + 0.6% green tea polyphenol). At 21 and 24 weeks of age, mice were euthanized and colon samples taken for histological and microarray analyses. The total histology score (HIS) in the colon was determined according to previously described criteria. Total RNA was isolated using TRIzol reagent. Colon RNA from four Mdr1a-/- mice on the GrTP diet (with low HIS) was compared with colon RNA from four Mdr1a-/- mice on the AIN-76A diet (with high HIS). All individual RNA samples were hybridized against a common reference RNA on separate slides. The reference RNA was prepared using equimolar RNA extracts from small intestine, colon, kidney and liver of normal healthy growing Swiss mice plus RNA extracts from Swiss mouse fetuses.
Project description:Although aging is a physiological process to which all organisms are subject, the presence of obesity and type 2 diabetes accelerates biological aging. Recent studies have demonstrated the causal relationships between dietary interventions suppressing obesity and type 2 diabetes and delaying the onset of age-related endocrine changes. Curcumin, a natural antioxidant, has putative therapeutic properties such as reinstating insulin sensitivity in obese mice. However, how curcumin contributes to maintaining insulin homeostasis in aged organisms largely remains unclear. Thus, the objective of this study is to examine the pleiotropic effect of dietary curcumin on insulin homeostasis in a diet-induced obese (DIO) aged mouse model. Aged (18-20 months old) male mice given a high-fat high-sugar diet supplemented with curcumin displayed a different metabolic phenotype compared to mice given a high-fat high-sugar diet alone. Furthermore, curcumin supplementation altered hepatic gene expression profiling, especially insulin signaling and senescence pathways. We then mechanistically investigated how curcumin functions to fine-tune insulin sensitivity. We found that curcumin supplementation increased hepatic insulin degrading enzyme (IDE) expression levels and preserved islet integrity, both of which are beneficial during aging. Our findings suggest that the multifaceted therapeutic potential of curcumin can be used as a protective agent for age-induced metabolic diseases.