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Acetaminophen attenuates obesity-related renal injury through ER-mediated stress mechanisms

Cuifen Wang1, Miaozong Wu, Ravikumar Arvapalli

  • 1Center for Diagnostic Nanosystems, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|April 16, 2014
PubMed
Abstract

Insights

Obesity contributes to kidney damage by increasing endoplasmic reticulum (ER) stress. Low-dose acetaminophen treatment in obese rats reduced this ER stress, protecting against renal cell injury and albuminuria.

Area of Science:

  • Nephrology
  • Metabolic Disorders
  • Pharmacology

Background:

  • Obesity is a significant independent risk factor for developing kidney disease.
  • Understanding the mechanisms of obesity-induced renal damage is crucial for developing effective interventions.

Purpose of the Study:

  • To investigate how obesity contributes to renal damage in the obese Zucker rat model.
  • To determine if acetaminophen can mitigate obesity-associated renal cell injury.

Main Methods:

  • Obese Zucker rats were treated with acetaminophen (30 mg/kg/day) for 26 weeks.
  • Control groups included obese vehicle and lean Zucker rats.
  • Evaluated renal lipid deposition, endoplasmic reticulum (ER) stress markers, apoptosis, and urinary albumin excretion.

Main Results:

  • Obese rats exhibited increased renal lipid deposition and ER stress (GRP78, eIF2α-ATF4-CHOP, caspase 12, JNK-MAPK pathways) compared to lean rats.
  • These changes correlated with elevated renal cell apoptosis and albuminuria.
  • Acetaminophen treatment significantly reduced these markers of renal injury.

Conclusions:

  • Low-dose acetaminophen demonstrates protective effects against obesity-induced renal injury in Zucker rats.
  • These protective effects are, at least partly, mediated by the attenuation of endoplasmic reticulum (ER) stress.

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