Diabetic Research Models | Type 1 and Type 2 | Charles River

db/db model 

The metabolic abnormalities demonstrated by the db/db mouse are due to a defect in leptin signaling resulting from a point mutation in the gene for the leptin receptor.  The leptin receptor is highly expressed in the hypothalamus and mice with a defect in this protein are unable to regulate their energy stores appropriately.  Plasma insulin levels become elevated very early in life (10-14 days of age), and the affected animals are obese by the time they are 3-4 weeks old.  Blood glucose levels begin rising at this time.  The animals are insulin resistant, hypertriglyceridemic, and have impaired glucose tolerance. 

DataEffect of Standard Agents on Plasma Insulin in db-db Mice

 

 

Effect of Standard Agents on Plasma TG in db/db Mice

 

  

 

Effect of Standard Agents on Plasma TG in db-db Mice


 

Non-Fasting Blood Glucose in db/db Mice

 

 

 

 

Non-Fasting Blood Glucose in db-db Mice

 

Effects of Standard Therapies on Non-Fasting Blood Glucose of db/db Mice 

 

 

OGTT Net AUC for db-db Mice Treated for 28 Days

 
OGTT Net AUC for db/db Mice Treated for 28 Days

 

 

 

 

For more information about our db/db models, please contact us at 1.877.CRIVER.1 or askcharlesriver@crl.com.

 

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1.877.CRIVER.1 (1.877.274.8371)
askcharlesriver@crl.com

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