GemPharmatech has generated a series of metabolic disease mouse models targeting key genes that function in metabolic regulation. These mouse models are valuable tools for the study of molecular genetic mechanisms of these genes and related gene networks in metabolism and the pathophysiological aberrations that lead to various metabolic diseases.
Metabolic syndrome has become a serious global epidemic that has increased in prevalence over the past several decades. By 2016, over 2.2 billion people were overweight, with over 774 million of those being obese. Type 2 diabetes, which is often exacerbated by obesity, was estimated to afflict 463 million people worldwide in 2019. Comorbidities in the cardiovascular system, the liver, the kidney, the bone and the joints, the GI tract and the immune system have shown clearly that metabolic dysfunction is a multi-system and multi-organ disease. Many studies have shown that both genetic and non-genetic factors (such as lifestyle, nutrition choice and social influence) contribute to the onset of metabolic dysfunction. Developing therapies to combat these metabolic diseases is in urgent need, as is the need for animal models to test the efficacy of such therapies.
 
 

Disease 

Model 

Genetic Background 

Genetic Mutation 

Induction Method 

Availability Status 

Obesity 

DIO (B6J) 

C57BL/6J 

n.a. 

HFD 

Yes 

B6-ob 

C57BL/6J 

Lep PM 

n.a. 

Yes 

B6-Alms1 mutant 

C57BL/6J 

Alms1 mutation 

n.a. 

Yes 

B6-hMC4R 

C57BL/6J 

hMC4R knockin 

n.a. 

2022 Q3 

B6-hGPR75 

C57BL/6J 

hGPR75 knockin 

n.a. 

2022 Q3 

T2DM 

HFHSD+STZ 

C57BL/6J 

n.a. 

HFHSD+STZ 

Yes 

BKS-db 

BKS 

Lepr PM 

n.a. 

Yes 

B6-hGLP-1R 

C57BL/6J 

hGLP-1R knockin 

n.a. 

2022 Q3 

B6-hGCGR 

C57BL/6J 

hGCGR knockin 

n.a. 

2022 Q3 

B6-hGIPR 

C57BL/6J 

hGIPR knockin 

n.a. 

2022 Q3 

B6-Alms1 mutant 

C57BL/6J 

Alms1 mutation 

n.a. 

Yes 

Dyslipidemia 

WD Induced (B6J) 

C57BL/6J 

n.a. 

WD 

Yes 

ApoE KO 

C57BL/6J 

Apoe knockout 

n.a. 

Yes 

LDLR KO 

C57BL/6J 

Ldlr knockout 

n.a. 

Yes 

B6-hPCSK9 

C57BL/6J 

hPCSK9 knockin 

n.a. 

Yes 

B6-hANGPTL2 

C57BL/6J 

hANGPTL2 knockin 

n.a. 

2022 Q3 

B6-hANGPTL3 

C57BL/6J 

hANGPTL3 knockin 

n.a. 

2022 Q3 

B6-hANGPTL4 

C57BL/6J 

hANGPTL4 knockin 

n.a. 

2022 Q3 

B6-hLPA-tg 

C57BL/6J 

hLPA random transgene 

n.a. 

2022 Q4 

B6-hApoC3-tg 

C57BL/6J 

hAPOC3 randome transgene 

n.a. 

2022 Q4 

B6-hApoA1-tg 

C57BL/6J 

hAPOA1 random transgene 

n.a. 

2022 Q4 

B6-hApoB-tg 

C57BL/6J 

hAPOB random transngene 

n.a. 

2022 Q4 

NASH 

HFD+CCl4 

C57BL/6J 

n.a. 

HFD+CCl4 

Yes 

BKS-db+WD 

BKS 

Lepr PM 

WD 

Yes 

B6-Alms1 mutant+WD 

C57BL/6J 

Alms1 mutation 

WD 

Yes 

WD Induced NASH (B6J)  

C57BL/6J 

n.a. 

WD 

Yes 

B6-hHSD17B13 

C57BL/6J 

hHSD17B13 knockin 

n.a. 

2022 Q3 

B6-hPNPLA3 

C57BL/6J 

hPNPLA3 knockin 

n.a. 

2022 Q3 

Diabetic Nephropathy 

BKS-db; eNOS-/- 

BKS 

Lepr and Nos3 double knockout 

n.a. 

2022 Q4 

Hyperuricemia 

Uox-KO 

C57BL/6J 

Uox knockout 

n.a. 

2022 Q4 

Hepatic Fibrosis 

CCl4 

Any 

n.a. 

CCl4 

Yes 

Arthritis 

CIA (DBA/1J) 

DBA/1J 

n.a. 

Collagen II 

Yes 

CIA (DBA-hIl17a) 

DBA/1J 

hIl17a knockin 

Collagen II 

Yes 

Hemophilia 

F8 KO 

C57BL/6J 

F8 knockout 

n.a. 

Yes 

Osteoporosis 

B6-hRANKL-OPG KO 

C57BL/6J 

hRANKL knockin and Tnfrsf11b knockout 

n.a. 

Yes 

Psoriasis 

IMQ Induced (BALB/c) 

BALB/c 

n.a. 

Imiquimod (5%) 

Yes 

IMQ Induced (BALB/c-hIl17a) 

BALB/c 

hIl17a knockin 

Imiquimod (5%) 

Yes