Leptin Knockout Rat — KiloRat™

TGRA3780

Animal Model
Leptin

Nomenclature
SD- Lep tm1sage

Zygosity Genotype
Cryopreserved as heterozygous embryos

Colony Size
Cryopreserved

Technical Information
Leptin is essential for energy intake and expenditure. It is one of the most important adipose-derived hormones, being primarily expressed in adipocytes of white adipose tissue. Loss of function of Leptin creates an uncontrolled appetite leading to severe obesity and abnormal metabolism, making this a useful model for the study of lifestyle diseases, such as obesity, diabetes, atherosclerosis, high cholesterol and high blood pressure.

Technical Data

Diet Value
LabDiet #5R24 (RMH2500)

Research Applications

Research Application
• Obesity
• Type II diabetes
• Atherogenesis
• Atherosclerosis
• HypertensionInsulin resistance
• Lipoprotein/Cholesterol transportation
• Metabolism (Triglyceride/Cholesterol)
Research Area
Cardiovascular

Characteristics

Characteristics
• This model possesses a 151 bp deletion within Exon 1 on chromosome 4
• Homozygous knockout rats display loss of Leptin protein via Western blot
• Homozygous knockout rats demonstrate significant weight gain compared to wild type littermates
• Homozygous knockout rats demonstrate insulin resistance
• Homozygous knockout rats show greatly elevated serum cholesterol levels
Background Strain: Sprague-Dawley
Figure 1
Leptin Knockout Rat — KiloRat™ - Figure 1
Figure 1: Homozygous knockout rats demonstrate significant weight gain compared to wild type
Leptin homozygous knockout rats demonstrate significant weight gain relative to their wild type and heterozygous littermates.
Figure 2
Leptin Knockout Rat — KiloRat™ - Figure 2
Figure 2. Homozygous knockout rats demonstrate insulin resistance
Insulin resistance was assessed in 5-week-old Leptin knockout rats by glucose tolerance test. Serum glucose levels remained elevated relative to wild type following IP injection of glucose at 2 g/kg body weight. Animals were fasted 16 hours prior to glucose challenge.
Protocols & Documents
Additional Information

Additional Information

Back to top