Prebiotic prevents impaired kidney and renal Oat3 functions in obese rats

Keerati Wanchai1,2, Sakawdaurn Yasom3, Wannipa Tunapong1,4

  • 1Department of PhysiologyFaculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

Insights

Xylooligosaccharide (XOS) supplementation improved kidney function in obese rats by reducing oxidative stress and apoptosis. XOS also restored organic anion transporter 3 (Oat3) function, offering a potential therapeutic strategy for obesity-related kidney disease.

Area of Science:

  • Nephrology
  • Nutritional Science
  • Biochemistry

Background:

  • Obesity is a global health concern linked to kidney dysfunction.
  • Prebiotics, like xylooligosaccharide (XOS), offer potential health benefits.
  • Kidney dysfunction in obesity involves podocyte injury and impaired organic anion transporter 3 (Oat3) function.

Purpose of the Study:

  • To investigate the effects of xylooligosaccharide (XOS) on renal function and Oat3 in obese rats.
  • To elucidate the underlying mechanisms, including oxidative stress and apoptosis pathways.

Main Methods:

  • Male Wistar rats were fed a high-fat diet for 12 weeks, followed by XOS supplementation (1000 mg/day) for another 12 weeks.
  • Evaluated obesity, insulin resistance, renal function markers (microalbuminuria, creatinine clearance), and Oat3 function.
  • Assessed oxidative stress markers (MDA, AT1R, NOX4, 4-HNE, PKCα, ERK1/2), Nrf2-Keap1 pathway, antioxidant enzymes (SOD2, GCLC), and renal apoptosis.

Main Results:

  • High-fat diet induced obesity, insulin resistance, podocyte injury, and impaired Oat3 function.
  • XOS treatment significantly improved renal function, attenuated oxidative stress, and reduced renal apoptosis.
  • XOS modulated the AT1R-PKCα-NOXs pathway and improved the Nrf2-Keap1/SOD2/GCLC antioxidant defense system.

Conclusions:

  • Xylooligosaccharide (XOS) ameliorates kidney dysfunction in obese, insulin-resistant rats.
  • XOS restores renal and Oat3 function by reducing oxidative stress and apoptosis.
  • These protective effects are mediated through the modulation of the AT1R-PKCα-NOXs pathway and enhancement of antioxidant defenses.

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