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  3. Lower-dose Vs High-dose Oral Bisphenol S Action Of Lipid Metabolism In Liver Of Male Sd Rat Via Mediating Different Srebp Isoforms.
  1. Home
  3. Lower-dose Vs High-dose Oral Bisphenol S Action Of Lipid Metabolism In Liver Of Male Sd Rat Via Mediating Different Srebp Isoforms.

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Lower-dose vs high-dose oral bisphenol S action of lipid metabolism in liver of male SD rat via mediating different

Jiali Li1, Hongyuan Peng1, Shaoguo Ru1

  • 1College of Marine Life Sciences, Ocean University of China, Qingdao, 266003, China.

Environmental Pollution (Barking, Essex : 1987)
|October 25, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Bisphenol S (BPS) exposure causes liver lipid accumulation in rats. Lower doses promote triglyceride synthesis, while higher doses lead to cholesterol buildup, disrupting liver function.

Keywords:
Bisphenol SCholesterolLiverRatsTriglyceride

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Area of Science:

  • Environmental toxicology
  • Biochemistry
  • Hepatology

Background:

  • Bisphenol S (BPS) is widely used in industrial products like thermal paper and plastics.
  • Previous studies suggest BPS exposure can cause triglyceride (TAG) and/or cholesterol (CHO) accumulation in the liver.
  • The precise mechanisms behind differential lipid accumulation following BPS exposure remain unclear.

Purpose of the Study:

  • To investigate the effects of low-dose (10 mg/kg/day) and high-dose (50 mg/kg/day) BPS exposure on lipid accumulation in male Sprague-Dawley rat livers.
  • To elucidate the underlying molecular mechanisms responsible for BPS-induced hepatic lipid changes.

Main Methods:

  • Male Sprague-Dawley rats were administered low and high doses of BPS daily.
  • Hepatic levels of acetyl-CoA, glycogen, TAG, and CHO were quantified.
  • mRNA and protein expression of key lipogenic genes, including sterol regulatory element-binding protein 1 (srebp1), srebp2, hmgcr, and hmgcs, were analyzed.

    • Main Results:

    • BPS exposure increased hepatic acetyl-CoA and glycogen levels.
    • Low-dose BPS upregulated srebp1, enhancing de novo synthesis of diacylglyceride and TAG.
    • High-dose BPS induced CHO accumulation while downregulating genes involved in CHO synthesis (srebp2, hmgcr, hmgcs).

    Conclusions:

    • BPS exposure differentially affects hepatic lipid metabolism based on dose.
    • Low-dose BPS promotes triglyceride synthesis, whereas high-dose BPS leads to cholesterol accumulation through distinct mechanisms.
    • Excessive lipid accumulation induced by BPS disrupts liver structure and function, highlighting potential health risks.