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Metabolomics Workbench ST000670 - GNPS - Exposure to high fat diets and bisphenol

ABSTRACT: Wild type (a/a) agouti mouse dams were randomized to one of three diets (control, mediterranean, western) two weeks prior to pairing with an agouti (Avy/a) sire. Diet exposure continued through pregnancy and lactation. All pups were weaned onto the control diet and then followed for metabolic phenotyping measures to 10 months of age. Comprehensive phenotyping (body composition, CLAMS, blood draw) was completed at 2, 4, and 8 months, with an OGTT at 8 months. Weekly weights were also recorded. The study examines whether prenatal dietary exposure to high fat diets (HFD) and bisphenol a (BPA, those groups will not be tested in this pilot) impacts metabolic programming in offspring as measured by hepatic steatosis, serum hormone levels, and epigenetic changes in hepatic lipid metabolism genes.

INSTRUMENT(S): QTOF - NEGATIVE, QTOF - POSITIVE

ORGANISM(S): Mus Musculus

SUBMITTER: Maureen Kachman

PROVIDER: MSV000082731 | GNPS | Thu Aug 02 17:26:00 BST 2018

REPOSITORIES: GNPS

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Metabolomics Workbench ST000779 - GNPS - Lipidomics pilot project for mice exposure to bisphenol A and high fat diets

Project description:Wild type (a/a) agouti mouse dams were randomized to one of three diets (control, Mediterranean, western) two weeks prior to pairing with an agouti (Avy/a) sire. Diet exposure continued through pregnancy and lactation. All pups were weaned onto the control diet and then followed for metabolic phenotyping measures to 10 months of age. Comprehensive phenotyping (body composition, CLAMS, blood draw) was completed at 2, 4, and 8 months, with an OGTT at 8 months. Weekly weights were also recorded. The study examines whether prenatal dietary exposure to high fat diets (HFD) and bisphenol a (BPA, those groups will not be tested in this pilot) impacts metabolic programming in offspring as measured by hepatic steatosis, serum hormone levels, and epigenetic changes in hepatic lipid metabolism genes. Shotgun lipidomics will add insight into the potentially changing lipid composition of membranes in offspring following different prenatal diet exposures as a means of assessing risk of steatosis and metabolic changes.

2018-08-02 | MSV000082736 | GNPS

Exposure to high fat diets and bisphenol

Project description:Wild type (a/a) agouti mouse dams were randomized to one of three diets (control, mediterranean, western) two weeks prior to pairing with an agouti (Avy/a) sire. Diet exposure continued through pregnancy and lactation. All pups were weaned onto the control diet and then followed for metabolic phenotyping measures to 10 months of age. Comprehensive phenotyping (body composition, CLAMS, blood draw) was completed at 2, 4, and 8 months, with an OGTT at 8 months. Weekly weights were also recorded. The study examines whether prenatal dietary exposure to high fat diets (HFD) and bisphenol a (BPA, those groups will not be tested in this pilot) impacts metabolic programming in offspring as measured by hepatic steatosis, serum hormone levels, and epigenetic changes in hepatic lipid metabolism genes.

2017-06-05 | ST000670 | MetabolomicsWorkbench

Effect of lactational high fat diet on offspring liver RNA expression

Project description:The goal was to study the long term metabolic programming effects of exposure of offspring to a dam eating 60% high fat diet during the lactation period only. We previously showed that offspring from dams given lactational high fat diet (HFD) are predisposed to obesity, glucose intolerance and inflammation. The purpose of these studies was to understand the programming implications of lactational HFD on offspring metabolic liver disease risk. Dams were fed a 60% lard-based HFD from the day of delivery through the 21 day lactation period. Starting at weaning offspring were fed normal fat diet until 3 months of age at which point a subset were challenged with an additional HFD stressor. Lactational HFD fed male offspring developed hepatic insulin resistance. Postweaning HFD challenge led male offspring progressing to NAFLD with more severe outcomes in the lactational HFD challenged offspring.

2021-08-14 | GSE182071 | GEO

Lipidomics pilot project for mice exposure to bisphenol A and high fat diets

2017-06-05 | ST000779 | MetabolomicsWorkbench

Genome-wide expression profile of livers from mice fed HFD,SO-HFD or Viv chow [RNAseq]

Project description:Purpose: Aim of the study is to identify changes in hepatic gene expression induced by either a 40kcal% coconut oil rich high fat diet (HFD), a 40kcal% soybean oil plus coconut oil high fat diet (SO-HFD) or a low fat vivarium chow diet (Viv). Methods: Livers from mice that had been fed one of the above mentioned diets for 35 weeks, were used to make cDNA libraries that were then sent for deep sequencing, using the Illumina TruSeq RNA. Result: Many genes involved in metabolism, lipid binding, transport and storage and many Cyp genes are dysregulated in the two high fat diets as compared to Viv HFDs in SO-HFD mice. Comparing the two HFDs shows more metabolism and disease related genes dysregulated in SO-HFD vs HFD. Conclusion: A diet high in soybean oil may be more detrimental to metabolic health than a diet high in saturated fats. cDNA isolated from livers from mice fed HFD, SO-HFD or Viv for 35 weeks, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.

2015-08-28 | E-GEOD-68360 | biostudies-arrayexpress

Genome-wide expression profile of livers from mice fed HFD,SO-HFD or Viv chow [RNAseq]

2015-08-28 | GSE68360 | GEO

Effect of lactational high fat diet and metformin on mid-lactation murine mammary gland gene expression

Project description:Maternal health and diet can have important consequences for offspring nutrition and metabolic health. Signals are communicated from the mother to the infant during lactation through milk via macronutrients, hormones and bioactive molecules. In this study we designed experiments to probe the mother-milk-infant triad in the condition of normal maternal health and upon exposure to high fat diet (HFD) with or without concurrent metformin exposure. We examined maternal characteristics, milk composition and offspring metabolic parameters on postnatal day 16, prior to offspring beginning to wean. We found that lactational HFD increased maternal adipose tissue, mammary gland adipocytes, and altered milk lipid composition causing a higher amount of n-6 long chain fatty acids and lower n-3. Offspring of HFD dams were heavier with more body fat during suckling. Metformin exposure decreased maternal glucose and several amino acids. Offspring of met dams were smaller during suckling. Gene expression in the lactating mammary glands was impacted to a greater extent by metformin but both metformin and HFD altered genes related to muscle contraction, indicating that these genes may be more susceptible to lactational stressors. Our study demonstrates the impact of common maternal exposures during lactation on milk composition, mammary gland function and offspring growth with metformin having little capacity to recuse from the effects of a maternal HFD during lactation.

2021-06-04 | GSE176118 | GEO

Nicotinamide mononucleotide, a key NAD+ precursor, treats the pathophysiology of diet- and age-induced diabetes

Project description:Type 2 diabetes (T2D) has become an epidemic in our modern lifestyle, likely due to calorie-rich diets overwhelming our adaptive metabolic pathways. One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD+ biosynthesis, and the NAD+-dependent protein deacetylase SIRT1. Here we show that NAMPT-mediated NAD+ biosynthesis is severely compromised in metabolic organs by high-fat diet (HFD). Strikingly, nicotinamide mononucleotide (NMN), a product of the NAMPT reaction and a key NAD+ intermediate, ameliorates glucose intolerance by restoring NAD+ levels in HFD-induced T2D mice. NMN also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation. Furthermore, NAD+ and NAMPT levels show significant decreases in multiple organs during aging, and NMN improves glucose intolerance and lipid profiles in age-induced T2D mice. These findings provide critical insights into a novel intervention against diet- and age-induced T2D. 4 regular chow fed mice (RC1-4) vs 4 high-fat diet fed (HFD) (HFD1a-4a) mice were analyzed on one chip (Chip-A). 4 HFD mice (HFD1b-4b) vs 4 HFD-NMN treated mice (NMN1-4) were examined on the other chip (Chip-B).

2011-12-05 | E-GEOD-31647 | biostudies-arrayexpress

Proteomics reveals PFOS-induced alteration of lipid utilization and xenobiotic metabolism in a model of PFOS-augmented diet-induced fatty liver

Project description:Perfluorooctanesulfonic acid (PFOS) is a persistent, bio-accumulative pollutant that has been used for the last 60+ years in numerous industrial and commercial applications. In mice, PFOS administration is known to induce hepatomegaly and hepatic steatosis. The aim of the present study was to evaluate potential PFOS and diet interactions and explore the mechanism of PFOS induced liver lipid accumulation. Prior to PFOS administration, mice were fed either a standard chow diet (SD) or 60% kCal high fat diet (HFD) for 4 weeks to establish significant body weight increase. After 4 weeks of diet acclimation, the treatment groups received 0.0003% PFOS in diet for an additional 10 weeks. In addition, a subset of the mice fed HFD were switched to a SD (H-SD) to mimic weight-loss induced improvement of hepatic steatosis. A total of six treatment groups: i) SD, ii) HSD, iii) HFD (H), iv) SD +PFOS(SDP), v) H-SD +PFOS (HSDP), and vi) HFD +PFOS (HP) were included. PFOS and lipid concentrations were measured in both serum and liver. Relative liver mRNA expression was determined by targeted bead array and proteins were quantified using untargeted mass spectrometry. PFOS exposure increased liver weight, and in the HFD increased liver triglycerides and liver cholesterol content. Gene and protein expression in the liver demonstrated that PFOS exposure induced lipid utilization and xenobiotic metabolism pathways, and in a HFD, induced lipid synthesis. The data suggests that PFOS exposure acts on lipid utilization genes and exacerbates hepatic steatosis in mice fed a HFD.

2020-09-30 | PXD016161 | Pride

Interactive effects of arsenic and a high-fat diet on hepatic gene expression

Project description:Chronic exposure to inorganic arsenic (iAs) or a high-fat diet (HFD) can produce liver injury. However, the interactive molecular biological effects and mechanism of iAs and HFD are as of yet unclear. We used microarrays to detail the interactive effects of arsenic and a high-fat diet on hepatic gene expression. The C57BL/6 Mice fed low-fat diet (LFD) or HFD were exposed to 3 mg/L iAs or deionized water for 10 weeks. Then, hepatic RNA were extraction and hybridization on Affymetrix microarrays. Differentially expressed genes in LFD+As, HFD, and HFD+As groups compared to LFD group were identified, and interactive molecular biological effects and mechanism of iAs and HFD were discussed.

2013-11-30 | E-GEOD-52702 | biostudies-arrayexpress

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