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Obese animal model


Obese animal model

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Simple Obesity/Metabolic Syndrome
Endocrine and Immune system models

Simple Obesity/Metabolic Syndrome

Introduction to Obesity Animal Models

Obesity has emerged as a rapidly escalating global epidemic, serving as an independent risk factor for cardiovascular and cerebrovascular diseases, hepatobiliary disorders, hypertension, diabetes, and hyperlipidemia, thereby posing a serious threat to human health. Animal models of obesity are predominantly established using mice and rats, with high‑fat diets as the primary induction method. Long-term feeding on such diets leads to excessive caloric intake, resulting in progressive weight gain, increased body fat percentage, adipose tissue accumulation, and disturbances in glucose and lipid metabolism—features that closely mimic human simple obesity. Moreover, these models can further progress to insulin resistance, fatty liver, and other metabolism‑related pathologies, making them well suited for research on obesity and related metabolic disorders.

Advantages of Aniphe Biolaboratory's Obesity Animal Model Platform Services

This platform boasts mature technologies for establishing obese animal models and a comprehensive, well‑established assay system, enabling efficient execution of relevant experiments and research and development.

 Comprehensive model coverage

There are various methods for model creation.

Primarily induced by a high-fat diet, this model can employ different strains of mice and rats as needed, with a typical phenotypic profile.

 Standardization of the modeling process

The indicators are stable and under control.

The animals are maintained under standardized housing conditions, with inter‑batch body weight variation within 10%. Following model establishment, body weight, body fat percentage, and glucose‑lipid metabolism parameters remain stable, ensuring adequate statistical power.

 Multidimensional Evaluation System

Multi-dimensional detection

It can perform a wide range of assessments, including body composition analysis, blood glucose and lipid profiling, histopathological examination, and molecular testing.

 Adapted for multi-cycle studies

Flexible Customization Solutions

It can be flexibly discontinued within 8 to 20 weeks according to customer needs, offering animal models with varying degrees of obesity.

 Standardization of Data Delivery

One-stop, end-to-end service

The entire process—from model establishment and observation to testing—is performed independently, ensuring high efficiency. To date, more than 200 DIO mouse models have been successfully generated, with a success rate exceeding 95%. We support both basic research and preclinical regulatory submissions.

Modeling cycle

Around 12 weeks

1  Laboratory animals

C57BL/6J male mice

1  Positive drug

There is no single first-line pharmacologic agent; orlistat, a gastrointestinal lipase inhibitor, may be selected to reduce caloric intake by blocking the absorption of dietary fats, thereby effectively controlling body weight and improving lipid profiles. Alternatively, semaglutide, a GLP‑1 receptor agonist, can be used to regulate blood glucose and appetite, delay gastric emptying, and enhance satiety, thus reducing caloric intake.

1  Application areas

Obesity, metabolic syndrome, insulin resistance, prediabetes (type 2), non-alcoholic fatty liver disease (NAFLD), and other conditions, as well as the screening of weight-loss and glucose-lowering drugs.

Experimental results

Construction of an Obesity Animal Model

DIO diet-induced obese mice: These mice are fed a high-fat diet long-term, with a hypercaloric regimen that progressively induces weight gain, leading to simple obesity and metabolic abnormalities, thereby mimicking diet‑induced obesity.

References: Delhanty, Patric J D, and Jenny A Visser. “Navigating the Strengths and Constraints of Mouse Models in Obesity Research.” Endocrinology vol. 166,9 (2025): bqaf123.

 

 

Schematic diagram of model construction

Weight monitoring curve

Mouse body weight was measured and recorded weekly, and body‑weight change curves were plotted. In the DIO model mice, body weight increased significantly over time compared with age‑matched control mice, with the difference becoming more pronounced as time progressed.

 

 

Blood glucose monitoring curve

Mouse blood glucose levels were measured and recorded weekly, and blood glucose profiles were plotted. In DIO model mice, the increase in blood glucose is less pronounced than in diabetic model mice; therefore, this measurement may be included or omitted depending on the specific research objectives.

 

 

Biochemical marker testing

Compared with the control group, mice in the DIO model exhibited significant increases in all lipid‑related and liver‑function biochemical parameters, indicating that obesity impairs lipid metabolism and, over time, causes marked hepatic damage.

 

 

Levels of TG, TC, LDL‑c, HDL‑c, ALT, and AST in the serum of mice from the DIO model group and the control group. Data are presented as Mean ± SD (n = 3). p* < 0.05, p** < 0.01, p*** < 0.001, p**** < 0.0001.

Pathological analysis: Oil Red O staining, H&E staining

Oil Red O staining and liver H&E staining were performed on abdominal brown adipose tissue (BAT), inguinal white adipose tissue (iWAT), and liver tissues. The results showed that in the control group, the hepatic architecture was intact, with no obvious steatosis in hepatocytes; in the model group, hepatocytes exhibited extensive lipid vacuolization accompanied by inflammatory cell infiltration, Oil Red O staining revealed extensive red lipid droplet deposition, and iWAT adipocytes displayed a marked increase in size, consistent with the features of obesity-associated fatty liver.