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Genetic Obese Animals

Creative Animodel offers comprehensive services for investigating the mechanism of obesity and anti-obesity drug development based on genetic obese animal models. Our extensive experienced scientific team will work closely with you on each step of your obesity study.

The incidence of obesity continues to climb worldwide, making it imperative that animal models sharing characteristics of human obesity and its co-morbidities be developed in the quest for novel preventions and/or treatments. In obesity study, genetically-obese rats and mice have been well-characterized and widely-used. There are many genetic models of obesity in both rats and mice, including the Zucker rats and ob/ob and db/db mice, in which obesity develops spontaneously. Animals are weighed daily to track weight change and their blood glucose levels can also be monitored. After animals are sacrificed, serum chemistry can be performed and samples of skin with adjacent subcutaneous fat can be harvested.

Genetic Obese Animals

ob/ob mice (Lepob/Lepob mouse, the ‘obese’ mouse)

The Lepob mutation was discovered in 1949 in an outbred mouse stock and was subsequently transferred to a C57BL/6 background. This model has since been well characterized as a model of obesity, exhibiting commonly published metabolic symptoms including hyperinsulinemia and hyperphagia.

✓ Coat color: Black
✓ Adipocyte hyperplasia
✓ Defective body temperature regulation
✓ Hyperinsulinemia
✓ Hyperlipemia
✓ Hyperphagia
✓ Insulin-resistant
✓ Lepob autosomal-recessive mutation on chromosome 6
✓ Leptin protein deficient
✓ Moderate transient hyperglycemia
✓ Obesity expressed at 4 to 5 weeks of age
✓ Sterile homozygous females

db/db mice (the ‘diabetic’ mouse)

The Leprdb mutation was discovered in 1966 in the inbred BKS mouse strain. This model has since been well characterized as a model of Type 2 diabetes mellitus, obesity, exhibiting commonly published metabolic symptoms including hyperglycemia and hyperinsulinemia.

✓ Coat color: Black or misty
✓ Elevation of plasma insulin demonstrated at 10-14 days
✓ Glycosuria
✓ Hyperglycemia develops at 4-8 weeks of age
✓ Hyperinsulinemia despite severe depletion of pancreatic islet insulin-producing B-cells
✓ Leprdb is an autosomal-recessive mutation on chromosome 4
✓ Leptin receptor deficient
✓ Obesity expressed at 4-5 weeks of age
✓ Polyphagia
✓ Polyuria/Polydipsia
✓ Proteinuria

Zucker obese rats

The fa mutation of Zucker fatty rats is associated with a processing defect of the leptin receptor, the receptor is generated but retained intracellularly, leading to reduced numbers of leptin receptors on the cell surface. This is associated with decreased leptin binding and signal transduction.

✓ Adipocyte hypertrophy and hyperplasia
✓ Animals have not been selectively bred to induce hyperglycemia
✓ Coat color: black, brown, brown/white, black/white
✓ Exhibit obesity at 4 to 5 weeks of age
fa is an autosomal-recessive mutation on chromosome 5
✓ Hypercholesterolemia
✓ Hyperinsulinemia
✓ Hyperphagia
✓ Leprfa/Lepr+ heterozygotes do not show partial expression of fa phenotype
✓ Muscle atrophy

Other genetic models include, but not limited to:

✓ s/s mice
✓ WDF rats
✓ POMC knockout mice
✓ POMC/AgRP knockout mice
✓ MC3R knockout mice
✓ MC4R knockout models
✓ MC4/MC3 receptor knockout mice
✓ New Zealand obese mouse

* For research use only. Not intended for any clinical use.

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