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.
Effect of Standard Agents on Plasma TG 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
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