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Low-dose developmental bisphenol A exposure alters fatty acid metabolism in Fischer 344 rat offspring
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Arbets- och miljömedicin.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Arbets- och miljömedicin.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.ORCID-id: 0000-0003-2335-8542
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.ORCID-id: 0000-0002-8620-4586
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2018 (engelsk)Inngår i: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 166, s. 117-129Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background. Bisphenol A (BPA) is an endocrine disruptor and also a suggested obesogen and metabolism-disrupting chemical. Accumulating data indicates that the fatty acid (FA) profile and their ratios in plasma and other metabolic tissues are associated with metabolic disorders. Stearoyl-CoA desaturase 1 (SCD-1) is a key regulator of lipid metabolism and its activity can be estimated by dividing the FA product by its precursor measured in blood or other tissues. Objective: The primary aim of this study was to investigate the effect of low-dose developmental BPA exposure on tissue-specific FA composition including estimated SCD-1 activity, studied in 5- and 52-week (wk)-old Fischer 344 (F344) rat offspring. Methods: Pregnant F344 rats were exposed to BPA via their drinking water corresponding to 0: [CTRL], 0.5: [BPA0.5], or 50 mu g/kg BW/day: [BPA50], from gestational day 3.5 until postnatal day 22. Results: BPA0.5 increased SCD-16 (estimated as the 16:1n-7/16:0 ratio) and SCD-18 (estimated as the 18:1n-9/ 18:0 ratio) indices in inguinal white adipose tissue triglycerides (iWAT-TG) and in plasma cholesterol esters (PL-CE), respectively, in 5-wk-old male offspring. In addition, BPA0.5 altered the FA composition in male offspring, e.g. by decreasing levels of the essential polyunsaturated FA linoleic acid (18:2n-6) in iWAT-and liver-TG. No differences were observed regarding the studied FAs in 52-wk-old offspring, although a slightly increased BW was observed in 52-wk-old female offspring. Conclusions: Low-dose developmental BPA exposure increased SCD-16 in iWAT-TG and SCD-18 in PL-CE of male offspring, which may reflect higher SCD-1 activity in these tissues. Altered desaturation activity and signs of altered FA composition are novel findings that may indicate insulin resistance in the rat offspring. These aforementioned results, together with the observed increased BW, adds to previously published data demonstrating that BPA can act as a metabolism disrupting chemical.

sted, utgiver, år, opplag, sider
Elsevier, 2018. Vol. 166, s. 117-129
Emneord [en]
BPA, Bisphenol A, Metabolism disrupting chemical, Low-dose exposure, FA, Fatty acid, SCD-1, Stearoyl-CoA desaturase 1, Adipose tissue
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Identifikatorer
URN: urn:nbn:se:uu:diva-363414DOI: 10.1016/j.envres.2018.05.023ISI: 000445318200016PubMedID: 29885613OAI: oai:DiVA.org:uu-363414DiVA, id: diva2:1257023
Forskningsfinansiär
Swedish Research Council Formas, 216-2012-475Tilgjengelig fra: 2018-10-18 Laget: 2018-10-18 Sist oppdatert: 2018-10-18bibliografisk kontrollert

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