Hypoglycemic and hypotriglyceridemic effects of tolbutamide in triphenyltin chloride-induced diabetic rabbits

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Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test
06:59

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Published on: November 13, 2016

Masatomo Watanabe1, Keita Watanabe, Hisao Matsui

  • 1Department of Hygiene, Dokkyo University School of Medicine, Mibu-machi, Tochigi, Japan.

Veterinary and Human Toxicology
|June 6, 2002
PubMed

Insights

Triphenyltin (TPT) disrupts insulin release, causing diabetes. However, tolbutamide stimulated insulin secretion in TPT-treated rabbits, lowering glucose and triglycerides, suggesting KATP channel involvement.

Area of Science:

  • Endocrinology
  • Toxicology
  • Cell Signaling

Background:

  • Triphenyltin (TPT) exposure causes transient hyperglycemia and hypertriglyceridemia.
  • TPT-induced diabetes involves impaired insulin release, potentially at the signal transduction level before Ca2+ channels.
  • The ATP-sensitive K+ channel (KATP channel) is upstream of voltage-dependent Ca2+ channels in insulin secretion signaling.

Purpose of the Study:

  • To investigate if KATP channel-mediated insulin secretion is inhibited in vivo by TPT.
  • To examine the effect of tolbutamide, a sulfonylurea drug, on plasma glucose, triglyceride, and insulin levels in TPT-diabetic rabbits.

Main Methods:

  • TPT-diabetic rabbits were prepared using oral administration of TPT-chloride.
  • The effects of tolbutamide (sulfonylurea) administration were studied on plasma glucose, triglyceride, and insulin levels.
  • Insulin secretion was measured after tolbutamide injection in TPT-diabetic and normal rabbits.

Main Results:

  • In TPT-diabetic rabbits, plasma glucose decreased by approximately 50%, and plasma triglyceride levels also decreased after tolbutamide administration.
  • Insulin release was detected following tolbutamide injection, with significantly higher secretion observed in TPT-diabetic rabbits compared to normal rabbits.
  • These results indicate that tolbutamide-stimulated insulin release effectively lowered plasma glucose and triglyceride levels in TPT-diabetic rabbits.

Conclusions:

  • The findings suggest that tolbutamide can stimulate insulin release in TPT-diabetic rabbits, leading to reduced hyperglycemia and hypertriglyceridemia.
  • A potential mechanism involves tolbutamide binding to its receptor, leading to KATP channel-mediated membrane depolarization and subsequent insulin release.
  • TPT may inhibit insulin secretion by disrupting glucose metabolism in beta cells, affecting KATP channel function upstream of membrane depolarization.

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