Trigonelline reduced diabetic nephropathy and insulin resistance in type 2 diabetic rats through peroxisome

Yinyan Li1, Qaobei Li1, Chunyan Wang1

  • 1Department of Ultrasonic Diagnosis, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

Insights

Trigonelline supplementation improved kidney function and reduced blood glucose in type 2 diabetes mellitus (T2DM) rats. It mitigated inflammation, oxidative stress, and apoptosis by activating peroxisome proliferator-activated receptor gamma (PPAR-γ).

Area of Science:

  • Biochemistry
  • Endocrinology
  • Nephrology

Background:

  • Trigonelline is known for its roles in cell cycle control, stress response, and DNA methylation.
  • Type 2 diabetes mellitus (T2DM) often leads to complications like diabetic nephropathy.
  • Understanding natural compounds' effects on T2DM complications is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the protective effects of trigonelline on T2DM-induced renal dysfunction in rats.
  • To elucidate the underlying molecular mechanisms of trigonelline's action in T2DM.

Main Methods:

  • Rats were induced with T2DM using a high-fat diet and streptozotocin.
  • Trigonelline treatment was administered to T2DM rats.
  • Kidney function markers, inflammation, oxidative stress, apoptosis, and key protein expressions (PPAR-γ, GLUT4, TNF-α, leptin) were assessed.

Main Results:

  • Trigonelline improved body weight, reduced kidney weight/body weight ratio, and lowered blood glucose levels.
  • It decreased blood urea nitrogen, creatinine, and albumin levels, indicating improved kidney function.
  • Trigonelline attenuated inflammation, oxidative stress, and kidney cell apoptosis, while modulating PPAR-γ, GLUT4, TNF-α, and leptin expression.

Conclusions:

  • Trigonelline demonstrates significant renoprotective effects in a T2DM rat model.
  • The mechanism involves the activation of peroxisome proliferator-activated receptor gamma (PPAR-γ), leading to reduced diabetic nephropathy and insulin resistance.

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