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Related Experiment Videos

Glucokinase gene locus transgenic mice are resistant to the development of obesity-induced type 2 diabetes.

M Shiota1, C Postic, Y Fujimoto

  • 1Department of Molecular Physiology and Biophysics, School of Medicine, Vanderbilt University, Nashville, Tennessee 37232-0615, USA. masakazu.shiota@mcmail.vanderbilt.edu

Diabetes
|March 15, 2001
PubMed
Summary
This summary is machine-generated.

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Overexpressing the glucokinase (GK) gene in mice significantly reduced hyperglycemia and hyperinsulinemia. This suggests increased GK levels may prevent or diminish diet-induced diabetes.

Area of Science:

  • Metabolic disorders
  • Genetics
  • Animal models

Background:

  • Transgenic mice overexpressing glucokinase (GK) exhibit mild hypoglycemia and improved glucose tolerance.
  • Diet-induced obesity is a common model for studying type 2 diabetes.
  • The role of GK in preventing diet-induced diabetes remains unclear.

Purpose of the Study:

  • To investigate the effect of increased glucokinase (GK) levels on the development of diet-induced diabetes.
  • To determine if GK overexpression can prevent or diminish hyperglycemia and hyperinsulinemia in mice fed a high-fat diet.

Main Methods:

  • Feeding transgenic mice overexpressing the GK gene locus and control mice a high-fat, high-simple carbohydrate, low-fiber (HF) diet for 30 weeks.
  • Monitoring body mass index (BMI), blood glucose concentrations, plasma insulin, and plasma glucagon levels.

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Main Results:

  • Both normal and transgenic mice became obese with similar BMIs on the HF diet.
  • Control mice showed a linear increase in blood glucose, reaching 17.0 +/- 1.3 mmol/l by week 30.
  • GK transgenic mice exhibited significantly lower blood glucose levels (9.7 +/- 1.2 mmol/l at week 15, returning to 7.6 +/- 1.0 mmol/l by week 30) and lower plasma insulin concentrations (232 +/- 79 pmol/l vs. 595 +/- 77 pmol/l in controls).

Conclusions:

  • Increased GK levels dramatically reduce hyperglycemia and hyperinsulinemia in diet-induced obese mice.
  • GK overexpression may be a protective factor against the development of type 2 diabetes.
  • Targeting GK could be a potential therapeutic strategy for metabolic disorders.