Summary of Study ST000598

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR000436. The data can be accessed directly via it's Project DOI: 10.21228/M8PW36 This work is supported by NIH grant, U2C- DK119886.


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Study IDST000598
Study TitleDysfunctional lipid metabolism underlies the effect of the perinatal DDT exposure on the development of metabolic syndrome (part II)
Study SummaryThis study aims to identify changes in lipid mediators in the hypothalamus with triphenyl phosphate (TPP) exposure. UC Davis type 2 diabetes mellitus (UCD-T2DM) rats were treated with TPP (n=8 per group) or not treated (n=8 per group). Each group was analyzed for oxylipin, nitro lipids, endocannabinoid, and endocannabinoid-like monoacylglycerol and N-acylethanolamide changes to investigate alterations in lipid mediator signaling due to TPP exposure. Targeted metabolomic analysis of lipid mediators in rat hypothalamus samples was performed by the Newman lab.
University of California, Davis
DepartmentUSDA Western Human Nutrition Research Center
LaboratoryNewman Lab
Last NameNewman
First NameJohn
Address430 W. Health Sciences Dr., Davis, CA 95616
Submit Date2017-04-19
Raw Data AvailableYes
Raw Data File Type(s)wiff
Analysis Type DetailLC-MS
Release Date2017-07-10
Release Version1
John Newman John Newman application/zip

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Treatment ID:TR000635
Treatment Summary:"Adult non-pregnant female UCD-T2DM rats (n = 16; 3 months old) were paired with males (n = 10; 3–4 months old) for a 24 h period at which point males were removed. This was defined as gestational day zero (G0) if a sperm plug was observed or if the female rats gained at least 30 g of body weight over the next 7 days. The day of birth was designated postnatal day zero (P0). Pregnant dams were randomly assigned to an exposure group (n = 8 per group), and received daily oral TPhP or ethanol vehicle exposure from G8 through weaning (P21) as described in Section 2.2 below. Gestational length and litter size were recorded on P0 and the sex of pups was determined and recorded on P4. Body weights of all pups in each litter were obtained periodically from P4–21. On P4 the litters were culled to 8 pups ensuring up to 4males and 2 females in each litter by random selection (Fig. 1A & B). This was done to ensure consistent exposure of pups between litters [13,23]. The time ittakes to develop T2DM is accelerated among UCD-T2DM rats with higher body weights on P21. Hence at weaning the largest pups were housed in same sex littermate groups of two females and up to four males as available (Fig. 1A & B). Urine was collected from the dams using an adapted plastic wrap method outlined by Kurien [24], 60 mins after final dose. Dams were placed in clean cages without bedding for at least 20 min then using a pipette up to 500 L of urine was collected in ethanol rinsed glass vials and placed on ice. At weaning all dams and remaining weanlings were sacrificed (90–330 min post-exposure) by CO2 asphyxiation and rapid decapitation. Two male rats weighing between 350–400 g on P61, from the TPhP group and the vehicle group were weight-matched across treatments for the diabetes study to eliminate confounding effects of body mass on the association between TPhP and T2DM onset (Fig. 1B). This weight range was selected because male UCD-T2DM rats that are between 350 and 400 g at 8 weeks of age develop T2DM at approximately 23 weeks of age [18]. Weight-matched rats were followed until 26 weeks or until they developed T2DM, which was defined as two consecutive weekly non-fasting glucose measurements of ≥200 mg/dL [18] in accordance with the American Diabetes Association (ADA) guideline of diagnosing diabetes with a random plasma glucose of 200 mg/dL or higher [19]. The remaining rats were not weight-matched and followed for the 3.5 month obesity study (Fig. 1A).
Treatment Protocol Filename:Green_et_al_2017-TPP_Exposure_Accelerat_T2DM_Rats.pdf