Diabetes Models

Wild Mouse 750
Wild Mouse 750
Human Xenograft Models
Cell Derived Xenograft Models
Autoimmune Disease Models
Autoimmune Nephropathy modelsAcute Lung Injury ModelsIdiopathic Pulmonary Fibrosis ModelsSjögren’ s Syndrome ModelsSystemic Lupus Erythematosus (SLE) ModelsMultiple Sclerosis ModelsRheumatoid Arthritis ModelsPsoriasis ModelsInflammatory Bowel Disease ModelsAtopic Dermatitis Models Asthma Models
Metabolic Disease Mouse Models
Obesity ModelsDiabetes ModelsMASH ModelsHyperlipidemia ModelsOsteoporosis ModelsHyperuricemia Models
Humanized Immune System Models
huPBMC-NCGhuHSC-NCG-XhuHSC-NCG-hIL15huHSC-NCG
Organs or Tissue Humanized Mouse Models
Wild Mouse 765
Wild Mouse 765
Rare Disease Mouse Models
Progressive Muscular Dystrophy ModelsHemophilia A Models
Neurodegenerative Disease Mouse Models
Alzheimer’s Disease (AD) ModelsParkinson’s Disease (PD) ModelsHuntington's Disease (HD) ModelsAmyotrophic Lateral Sclerosis (ALS) ModelsTransthyretin Amyloidosis (ATTR) Models
Immuno-Oncology Mouse Models
Human Xenograft ModelsHumanized Immune Checkpoint ModelsHumanized Immune System ModelsSpontaneous Tumor Models

Diabetes is a group of metabolic diseases caused by genetic, environmental, or immunologic factors that lead to hypoglycemia and insulin resistance, which in turn leads to more complicated metabolic dysfunctions. Diabetes is subdivided into type I diabetes, type II diabetes, and other unique forms, with type II diabetes accounting for around 90% of people with diabetes. GemPharmatech has developed a series of diabetes models for pathogenesis study and drug evaluation through gene editing and diet treatment.

Strain No.
 Strain Name Strain Type Description
T002407 BKS-db KO C57BLKS/JGpt mice lacking the Lepr gene develop severe morbid obesity, significant and persistent increase in blood glucose, islet damage and atrophy, severe insulin resistance, severe diabetic nephropathy, and diabetic retinopathy. These mice are ideal models for studying Type II diabetes and related complications.
T017633 B6-Alms1-del(c.3802-3812) KO(TM) An 11-bp base deletion in exon 8 of the Alms1 gene in C57BL/6JGpt mice led to early termination of translation of the Alms1 gene, leading to a combined phenotype of obesity, early diabetes and metabolic dysfunction-associated steatotic liver disease. These mice are ideal models for studies on obesity and fatty liver.