60% HFD Induced Obesity (DIO) models

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 MASH ModelsBKS-db MASH ModelsB6-Alms1-del MASH ModelsOther MASH 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

Study Outline


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Fig 1. HFD: 60% high-fat diet; HFHSD: 45% high-fat, high-sugar diet. Experimental period: 12-20 weeks

 

Data Validation

1. DIO mice show the higher body weight gain, higher body fat ratio and leptin resistance

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Fig 2. Body weight and body composition measurement of DIO mice at different weeks of age

Data were presented as Mean±SD. *, p<0.05; ****, p<0.0001 by unpaired t test.

 

2. DIO mice develop type2 diabetes

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Fig 3. Fasting blood glucose, insulin and glucose tolerance test in DIO mice


After 12 weeks of being fed a high-fat diet (60% fat), C57BL/6JGpt mice exhibited significantly elevated fasting blood glucose and insulin levels, along with markedly impaired glucose tolerance.


3. DIO mice develop dyslipidemia and fatty liver

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Fig 4. Plasma Cholesterol Levels, Liver Function, and Hepatic Pathology Evaluation in DIO Mice


16 weeks of HFD feeding increased plasma cholesterol level, impaired liver function and induced hepatic steatosis in C57BL/6J mice. Data were presented as Mean±SD. ***, p<0.001; ****, p<0.0001 by unpaired t test.

 

4. Semaglutide treatment decreased body weight, body fat ratio, food intake and improved leptin resistance in DIO mice

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Fig 5. Body weight, body composition, food intake, and plasma leptin levels of  DIO mice upon 4 weeks of treatment of semaglutide

Data were presented as Mean±SEM. n=8~10，*, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001 by one way ANOVA with Dunnett’s post-hoc test.

 

5. Semaglutide treatment improved hyperglycemia, hyperinsulinemia and glucose intolerance in dio mice

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Fig 6. Fasting blood glucose, insulin and gtt of DIO mice upon 4 weeks of treatment of semaglutide

Data were presented as Mean±SEM. n=8~10，***, p<0.001; ****, p<0.0001 by one way ANOVA with Dunnett’s post-hoc test.

 

6. Semaglutide treatment improved hypercholesterolemia in DIO mice

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Fig 7. Blood lipid levels of DIO mice upon 4 weeks of treatment of semaglutide

Data were presented as Mean±SEM. n=8~10，**, p<0.01; ***, p<0.001; ****, p<0.0001 by one way ANOVA with Dunnett’s post-hoc test. 

 

7. Semaglutide treatment improved fatty liver in DIO mice

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Fig 8. Assessment of liver function and hepatic pathology in DIO mice after 4 weeks of semaglutide treatment

Data were presented as Mean±SEM. n=8~10，**, p<0.01; ***, p<0.001; ****, p<0.0001 by one way ANOVA with Dunnett’s post-hoc test.

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