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Neonatal exposure to parathion alters lipid metabolism in adulthood: Interactions with dietary fat intake and implications for neurodevelopmental deficits.

Publication ,  Journal Article
Lassiter, TL; Ryde, IT; Levin, ED; Seidler, FJ; Slotkin, TA
Published in: Brain Res Bull
January 15, 2010

Organophosphates are developmental neurotoxicants but recent evidence also points to metabolic dysfunction. We determined whether neonatal parathion exposure in rats has long-term effects on regulation of adipokines and lipid peroxidation. We also assessed the interaction of these effects with increased fat intake. Rats were given parathion on postnatal days 1-4 using doses (0.1 or 0.2mg/kg/day) that straddle the threshold for barely detectable cholinesterase inhibition and the first signs of systemic toxicity. In adulthood, animals were either maintained on standard chow or switched to a high-fat diet for 7 weeks. We assessed serum leptin and adiponectin, tumor necrosis factor-alpha (TNFalpha) in adipose tissues, and thiobarbituric acid reactive species (TBARS) in peripheral tissues and brain regions. Neonatal parathion exposure uncoupled serum leptin levels from their dependence on body weight, suppressed adiponectin and elevated TNFalpha in white adipose tissue. Some of the effects were offset by a high-fat diet. Parathion reduced TBARS in the adipose tissues, skeletal muscle and temporal/occipital cortex but not in heart, liver, kidney or frontal/parietal cortex; it elevated TBARS in the cerebellum; the high-fat diet again reversed many of the effects. Neonatal parathion exposure disrupts the regulation of adipokines that communicate metabolic status between adipose tissues and the brain, while also evoking an inflammatory adipose response. Our results are consistent with impaired fat utilization and prediabetes, as well as exposing a potential relationship between effects on fat metabolism and on synaptic function in the brain.

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Published In

Brain Res Bull

DOI

EISSN

1873-2747

Publication Date

January 15, 2010

Volume

81

Issue

1

Start / End Page

85 / 91

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Thiobarbituric Acid Reactive Substances
  • Rats, Sprague-Dawley
  • Rats
  • Random Allocation
  • Parathion
  • Neurology & Neurosurgery
  • Male
  • Lipid Metabolism
  • Leptin
 

Citation

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Lassiter, T. L., Ryde, I. T., Levin, E. D., Seidler, F. J., & Slotkin, T. A. (2010). Neonatal exposure to parathion alters lipid metabolism in adulthood: Interactions with dietary fat intake and implications for neurodevelopmental deficits. Brain Res Bull, 81(1), 85–91. https://doi.org/10.1016/j.brainresbull.2009.07.002
Lassiter, T Leon, Ian T. Ryde, Edward D. Levin, Frederic J. Seidler, and Theodore A. Slotkin. “Neonatal exposure to parathion alters lipid metabolism in adulthood: Interactions with dietary fat intake and implications for neurodevelopmental deficits.Brain Res Bull 81, no. 1 (January 15, 2010): 85–91. https://doi.org/10.1016/j.brainresbull.2009.07.002.
Lassiter, T. Leon, et al. “Neonatal exposure to parathion alters lipid metabolism in adulthood: Interactions with dietary fat intake and implications for neurodevelopmental deficits.Brain Res Bull, vol. 81, no. 1, Jan. 2010, pp. 85–91. Pubmed, doi:10.1016/j.brainresbull.2009.07.002.
Journal cover image

Published In

Brain Res Bull

DOI

EISSN

1873-2747

Publication Date

January 15, 2010

Volume

81

Issue

1

Start / End Page

85 / 91

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Thiobarbituric Acid Reactive Substances
  • Rats, Sprague-Dawley
  • Rats
  • Random Allocation
  • Parathion
  • Neurology & Neurosurgery
  • Male
  • Lipid Metabolism
  • Leptin