Linda Dunder1, Margareta Halin Lejonklou2, Lars Lind3, Ulf Risérus4, P Monica Lind5. 1. Department of Medical Sciences, Occupational and Environmental Medicine, Uppsala University, Sweden. Electronic address: linda.dunder@medsci.uu.se. 2. Department of Medical Sciences, Occupational and Environmental Medicine, Uppsala University, Sweden. Electronic address: margareta.halin@medsci.uu.se. 3. Department of Medical Sciences, Cardiovascular Epidemiology, Uppsala University, Sweden. Electronic address: lars.lind@medsci.uu.se. 4. Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University, Sweden. Electronic address: ulf.riserus@pubcare.uu.se. 5. Department of Medical Sciences, Occupational and Environmental Medicine, Uppsala University, Sweden. Electronic address: monica.lind@medsci.uu.se.
Abstract
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 µg/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.
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 µg/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 FAlinoleic 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.
Authors: Marcello Dallio; Nadia Diano; Mario Masarone; Antonietta Gerarda Gravina; Vittorio Patanè; Mario Romeo; Rosa Di Sarno; Sonia Errico; Carla Nicolucci; Ludovico Abenavoli; Emidio Scarpellini; Luigi Boccuto; Marcello Persico; Carmelina Loguercio; Alessandro Federico Journal: Int J Environ Res Public Health Date: 2019-08-28 Impact factor: 3.390
Authors: Christopher J Martyniuk; Rubén Martínez; Laia Navarro-Martín; Jorke H Kamstra; Adam Schwendt; Stéphane Reynaud; Lorraine Chalifour Journal: Environ Res Date: 2021-08-19 Impact factor: 6.498