C57BL/6-Alms1-del

Obesity Models and Efficacy Services
60% HFD Induced Obesity (DIO) models45% HFHSD Induced Obesity(DIO) modelsC57BL/6-Alms1-delWild Mouse 750
Type II Diabetes Models and Efficacy Service
BKS-dbHFHSD+STZ Induced Diabetes Models
Liver Disease Models and Efficacy Services
CCl4-induced Liver Fibrosis ModelsHFD+CCl4-induced NASH ModelsBKS-db NASH ModelsB6-Alms1-del NASH ModelsOther NASH Models
Atherosclerosis Models and Efficacy Services
ApoE KO ModelsLdlr KO Models
Hyperlipidemia Models and Efficacy Services
hPCSK9-UTR ModelshPCSK9 Models
Gout/Hyperuricemia Models and Efficacy Services
Monosodium Urate (MSU)-induced Gouty Arthritis ModelsUrate Oxidase Knockout (Uox-KO) Gout Models

Data Validation

1. Body weight

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Figure 1. Body weight curves of C57BL/6-Alms1-del mice vs control mice. Data are presented as Mean±SEM.


2. Glucose tolerance test

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Figure 2. After ten weeks, studies on glucose tolerance were carried out on C57BL/6-Alms1-del mice. We measured blood glucose levels at 0, 15, 30, 60, 90, and 120 minutes. C57BL/6-Alms1-del mice have lower glucose tolerance, when compared to the control group. Data are presented as Mean±SD, with n=5. ****, p<0.0001; by unpaired two-tailed Student's t-test.


3. Serum insulin levels

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Figure 3. Insulin levels were significantly increased in C57BL/6-Alms1-del mices. Data are presented as Mean±SD, n=5. ****, p<0.0001; by unpaired two-tailed Student's t-test.


4. Blood lipid levels

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Figure 4. The hyperlipidemic phenotype of C57BL/6-Alms1-del mice became more severe with age. Data are presented as Mean±SD, n=5. **，p<0.05，**，p<0.01；***, p<0.001；****, p<0.0001; by unpaired two-tailed Student's t-test.


5. Liver enzymes

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Figure 5. After 16 weeks, C57BL/6-Alms1-del mice showed liver damage.Data are presented as Mean±SD, n=5. **，p<0.01；****, p<0.0001; by unpaired two-tailed Student's t-test.


6. Fatty liver phenotype

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Figure 6. After 21 weeks, C57BL/6-Alms1-del mice developed a severe fatty liver phenotype that included steatosis, inflammation, and cellular vacuolation lesions.


7. Expression of inflammation, fibrosis-related biomarkers

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Figure 7. Expression levels of inflammatory, fibrosis-related markers were significantly increased in C57BL/6-Alms1-del mice. Data are presented as Mean±SD, n=5. **，p<0.05，**，p<0.01；***, p<0.001; by unpaired two-tailed Student's t-test.


Efficacy data

1. Semaglutide reduced the body weight, food intake and fasting blood glucose

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Figure 8. Semaglutide significantly reduced body weight, food intake, and postpranpranal blood glucose levels in B6-AIms1-del mice. Data are presented as Mean±SD. *，p<0.05；**，p<0.01；***，p<0.001; by unpaired two-tailed Student's t-test.


2. Liver enzymes and blood lipid levels

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Figure 9. Semaglutide significantly improved liver function and dyslipidemia of the B6-Alms1-del model. Data are presented as Mean±SD.***, p<0.001;****, p<0.0001 by unpaired two-tailed Student's t-test.


3. Semaglutide improved liver function 

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Figure 10. Semaglutide significantly improved hepatic steatosis, inflammation, and ballooning in the B6-Alms1-del model. Data are presented as Mean±SD.*, p<0.05 by unpaired two-tailed Student's t-test.


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