Ftalater i plast, övervikt och fettinlagring

[King Grub]

Di-(2-ethylhexyl)-phthalate (DEHP), an ubiquitous environmental contaminant, has been shown to cause adverse effects on glucose homeostasis and insulin sensitivity in epidemiological studies, but the underlying mechanisms are still unknown. We therefore tested the hypothesis that chronic DEHP exposure causes impaired insulin sensitivity, affects body weight, adipose tissue (AT) function and circulating metabolic parameters of obesity resistant 129S6 mice in vivo. An obesity-resistant mouse model was chosen to reduce a potential obesity bias of DEHP effects on metabolic parameters and AT function. The metabolic effects of 10-weeks exposure to DEHP were tested by insulin tolerance tests and quantitative assessment of 183 metabolites in mice. Furthermore, 3T3-L1 cells were cultured with DEHP for two days, differentiated into mature adipocytes in which the effects on insulin stimulated glucose and palmitate uptake, lipid content as well as on mRNA/protein expression of key adipocyte genes were investigated. We observed in female mice that DEHP treatment causes enhanced weight gain, fat mass, impaired insulin tolerance, changes in circulating adiponectin and adipose tissue Pparg, adiponectin and estrogen expression. Serum metabolomics indicated a general increase in phospholipid and carnitine concentrations. In vitro, DEHP treatment increases the proliferation rate and alters glucose uptake in adipocytes. Taken together, DEHP has significant effects on adipose tissue (AT) function and alters specific serum metabolites. Although, DEHP treatment led to significantly impaired insulin tolerance, it did not affect glucose tolerance, HOMA-IR, fasting glucose, insulin or triglyceride serum concentrations. This may suggest that DEHP treatment does not cause impaired glucose metabolism at the whole body level.

Di-(2-Ethylhexyl)-Phthalate (DEHP) Causes Impaired Adipocyte Function and Alters Serum Metabolites. PLOS One December 2, 2015.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0143190

[King Grub]

Förkrympta könsorgan.

Prior studies report that penile size and male anogenital distance (AGD), sensitive markers of androgen action in utero, may be shortened by prenatal exposure to certain phthalates, including diethylhexyl phthalate (DEHP), but no human study has investigated the importance of exposure timing in these associations. The aim of this study was to examine the significance of exposure timing on the action of prenatal phthalates in particular DEHP, on male infant penile size and AGD. In The Infant Development and the Environment Study (TIDES) we measured penile width (PW) as well as anoscrotal distance (AGDAS) and anopenile distance (AGPAP) in newborn males. We modeled these endpoints in relation to phthalate metabolite concentrations in maternal urine samples collected in each trimester (T1, T2, and T3) in a subset of TIDES mothers (N = 168). PW was inversely associated with T2 oxidized DEHP metabolites, mono-2-ethyl-5-oxohexyl (MEOHP, β=−0.48; 95% confidence interval, −0.93, −0.02), MEHHP (−0.48; −0.92, −0.05), mono-2-ethyl-5-carboxypentyl (MECPP, −0.51; −1.01, −0.004), although no appreciable associations were seen between PW and T1 and T3 DEHP metabolite concentrations in this subset. Concentrations of DEHP metabolites in T1 urine samples were inversely related to male AGD. For example, in T1 samples in this subset of women mono-2-ethyl-5-hydroxyhexyl (MEHHP) was inversely associated with male AGDAP (β = −1.73; 95% confidence interval, −3.45, 0.0004). However, no appreciable associations were seen between AGD measures and any DEHP metabolite in T2 and T3 samples. These data suggest that DEHP exposure is inversely associated with AGD and PW, with PW primarily associated with T2 exposure and AGD associations seen only for T1 exposure, but no associations were found between T3 DEHP metabolites and any of these genital endpoints. These findings are consistent with data on critical windows in rodent studies, supporting the biological plausibility of these associations in humans.

Timing of prenatal phthalate exposure in relation to genital endpoints in male newborns. Andrology 7 APR 2016.

[caelus]

Kanske är dags att köpa en sån där matlåda i glas istället för plast...

[King Grub]

Background:

Phthalates and bisphenol A (BPA) are widely used industrial chemicals that may adversely impact human health. Human exposure is ubiquitous and can occur through diet, including consumption of processed or packaged food.

Objective:

To examine associations between recent fast food intake and BPA and urinary metabolites of di(2-ethylhexyl) phthalate (ΣDEHPm) and diisononyl phthalate (DiNPm) among the US population.

Methods:

We combined data on 8877 participants from the National Health and Nutrition Examination Survey (NHANES 2003-2010). Using 24-hour dietary recall data, we quantified: 1) fast food intake (percent of total energy intake (TEI) from fast food); 2) fast food-derived fat intake (percent of TEI from fat in fast food); and 3) fast food intake by food group (dairy, eggs, grains, meat, and other). We examined associations between dietary exposures and urinary chemical concentrations using multivariate linear regression.

Results:

We observed evidence of a positive, dose-response relationship between fast food intake and exposure to phthalates (p-trend<0.0001) but not BPA; participants with high consumption (≥34.9% TEI from fast food) had 23.8% (95% CI: 11.9%, 36.9%) and 39.0% (95% CI: 21.9%, 58.5%) higher levels of ΣDEHPm and DiNPm, respectively, than non-consumers. Fast food-derived fat intake was also positively associated with ΣDEHPm and DiNPm (p-trend <0.0001). After adjusting for other food groups, ΣDEHPm was associated with grain and other intake, and DiNPm was associated with meat and grain intake.

Conclusion:

Fast food may be a source of exposure to DEHP and DiNP. These results, if confirmed, could inform individual and regulatory exposure reduction strategies.


Recent Fast Food Consumption and Bisphenol A and Phthalates Exposures among the U.S. Population in NHANES, 2003–2010. Environ Health Perspect 13 April 2016.

[BobaFett]

hur fan undviker man plast? Det går inte. Allt är gjort i plast idag. Tänker förpackningar för mat främst men även annat.

[Wzup2u]

På livsmedelsverket finns lite info om plast generellt för den som är intresserad.
Mkt bra läsning. http://www.livsmedelsverket.se/livsmedel-och-innehall/tillagning-hygien-forpackningar/forpackningar/plast/

[Termy]

Hur bör man tänka där kring flaskan man dricker från på gymmet? Får man i sig någon dos av ftalater där? Är det klokt att t.ex. byta ut den med visst intervall, eller har det ingen betydelse hur mycket man har "slitit" på flaskan? Har det någon betydelse hur ofta man diskar den?

[caelus]

Hur bör man tänka där kring flaskan man dricker från på gymmet? Får man i sig någon dos av ftalater där? Är det klokt att t.ex. byta ut den med visst intervall, eller har det ingen betydelse hur mycket man har "slitit" på flaskan? Har det någon betydelse hur ofta man diskar den?

En del plastflaskor jag använt har haft en tendens att ge ifrån sig en bismak av plast oavsett hur noggrannt eller hur många gånger man diskat flaskan. Vet dock inte hur vanligt det är med Bisfenol A och liknande substanser i plastflaskor nuförtiden. Vill man vara på den säkra sidan kan man ju alltid införskaffa en flaska i rostfri stål.

[demode85]

Jag tror det är värre när man värmer plasten i micron t.ex.- En vattenflaska hade jag inte varit orolig för men jag är inte beläst.

[olle lindblad]

Om jag inte minns fel så urlakas ftalater när man diskar matlådor etc i varmt vatten.

[Luca Brasi]

Jag tror människor tenderar att bara tänka på det de stoppar i munnen och inte på att gifter kommer in kroppen på mer indirekta sätt.

https://i1.wp.com/branchbasics.com/wp-content/uploads/2015/06/Phthalates-Branch-Basics.jpg?w=680

Släng ut all inredning och allt ni äger?

[exevision]

Många av kung markattas konserver är fria från bisfenol A.
http://www.kungmarkatta.se/nyheter-och-press/posts/2014/december/nu-blir-kung-markattas-konservburkar-bisfenolfria/

[King Grub]

Benzyl butyl phthalate (BBP) has been known to induce developmental and reproductive toxicity. However, its association with dysregulation of adipogenesis has been poorly investigated. The present study aimed to examine the effect of BBP on the adipogenesis, and to elucidate the underlying mechanisms using the 3T3-L1 cells. The capacity of BBP to promote adipogenesis was evaluated by multiple staining approaches combined with a High Content Cellomics analysis. The dynamic changes of adipogenic regulatory genes and proteins were examined, and the metabolite profile was identified using GC/MC based metabolomic analysis. The High Content analysis showed BBP in contrast with Bisphenol A (BPA), a known environmental obesogen, increased lipid droplet accumulation in a similar dose-dependent manner. However, the size of the lipid droplets in BBP-treated cells was significantly larger than those in cells treated with BPA. BBP significantly induced mRNA expression of transcriptional factors C/EBPα and PPARγ, their downstream genes, and numerous adipogenic proteins in a dose and time-dependent manner. Furthermore, GC/MC metabolomic analysis revealed that BBP exposure perturbed the metabolic profiles that are associated with glyceroneogenesis and fatty acid synthesis. Altogether, our current study clearly demonstrates that BBP promoted the differentiation of 3T3-L1 through the activation of the adipogenic pathway and metabolic disturbance.

Toxicol In Vitro. 2016 Apr;32:297-309. Benzyl butyl phthalate promotes adipogenesis in 3T3-L1 preadipocytes: A High Content Cellomics and metabolomic analysis.