- C57BL/6J mice with mutations in leptin (B6-ob, Strain 000632) or its receptor (B6-db, Strain 000697) are hyperglycemic at young ages, but blood glucose levels decline over time due to pancreatic islet cell hypertrophy (Figure 1).
- C57BLKS/J mice with a leptin receptor mutation (BKS-db, Strain 000642) have persistent hyperglycemia and decline in body weight after 16 weeks of age (Figure 1).
- C57BL/6J male mice fed a high fat diet (DIO-B6, Strain 380050) are obese but not overtly diabetic (Figure 2, Figure 3).
- BTBR mice with a leptin mutation (BTBR-ob, Strain 004824) are obese, hyperglycemic, and dyslipidemic (Figure 2, Figure 3). They also develop diabetic nephropathy.
- Females and males with leptin pathway mutations often display similar metabolic phenotypes by strain, including changes in glucose, HbA1c, insulin, leptin, body weight, and body fat (Figure 1, Figure 2, Figure 3).
- Detailed phenotypes for each strain are available.
Figure 1 Weekly weights and blood glucose. Groups of 60-75 homozygous (ob/ob or db/db) females and males per strain were weighed weekly (left) or bled via the submental route to measure non-fasted glucose (right).
Figure 2 Clinical chemistry. All values were measured from serum collected from submental blood except HbA1c, which was measured from submental whole blood. Approximately 20 non-fasted mice per sex, strain, and age are represented. Values show mean and one standard deviation.
Figure 3 Body composition and weight. Mice were analyzed using a Lunar PIXImus DEXA scanner (Body Fat). Calculations of body composition exclude the head. Values show mean and one standard deviation of 5-10 homozygous mice per sex, strain, and age. The Body Weight graphs represent the weights of 60-75 mice per group.