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B6-DIO-induced obese mice

Jiangsu Aniphe BioLab offers you ready-to-use, mature and stable B6‑DIO obesity models! Backed by a standardized induction protocol and ample inventory, we ensure rapid response and swift shipping, helping you overcome the challenges of lengthy modeling cycles and poor model consistency, so your metabolic research projects can accelerate with ease.

Strain Introduction

B6-DIO (Diet-Induced Obesity) mice are an obesity and metabolic syndrome model induced by long-term feeding on a high-fat diet (HFD) in a C57BL/6J genetic background. They represent the most widely used preclinical platform for studying diet‑related obesity, type 2 diabetes, non‑alcoholic fatty liver disease (NAFLD), metabolic inflammation, and cardiovascular complications. Unlike single‑gene genetic obesity models such as ob/ob or db/db, this model is polygenic, chronic, and driven by environmental factors, thereby more accurately mimicking the progressive metabolic dysregulation observed in humans under the influence of a high‑calorie diet.

Typically, significant differences in body weight and insulin resistance emerge after 8–12 weeks of HFD feeding; by 16–24 weeks, hyperglycemia, hyperinsulinemia, hepatic steatosis, adipose tissue remodeling, and mild low-grade inflammation are observed.

Product Advantages

Closely mimicking the progression of human diseases, with high translational potential.

Obesity, insulin resistance, and fatty liver are progressively induced through a long-term high-fat diet, thereby mimicking diet‑related metabolic syndrome in humans. Unlike genetically engineered models, this approach does not produce dramatic mutant phenotypes, making it more clinically translatable.

Pure genetic background, well‑developed supporting resources.

Based on the C57BL/6J inbred strain, with a well-characterized genome and an abundant supply of reagents and genetically edited mouse lines, this model is well suited for mechanistic studies and target validation.

Phenotypic stability and excellent experimental reproducibility.

Obesity and insulin resistance develop in male rats fed a standard 60% high-fat diet between 8 and 12 weeks of age, with sustained hyperglycemia and steatosis emerging by 16 to 24 weeks. The model exhibits minimal batch-to-batch variability, making it well suited for long-term interventions and large-scale drug screening.

Standardization of the approach facilitates cross‑project comparisons of outcomes.

Induction diets, timing of model establishment, and methods for assessing metabolic function all have established standard protocols; these procedures are straightforward to implement, and the resulting experimental data are readily comparable across laboratories, thereby facilitating the publication of high‑impact research.

Data parameters

Strain Name

B6-DIO diet-induced obesity mouse model (C57BL/6J DIO)
Induction method

High-fat diet (HFD, typically 60 kcal% fat)
Types of gene editing

Wild type, without genetic modification or gene editing.
Genetic background

C57BL/6J, with a homogeneous genetic background, is well suited for multi-omics and immunological analyses.
Microbial Grade

SPF grade
Available by week of age

3 weeks of age and older

Validate data

Six-week-old male C57BL/6 mice were selected and divided into three groups: a normal chow diet group, a high-fat diet–induced model group, and a high-fat diet plus dulaglutide intervention group. The high-fat diet was administered for 12 weeks to establish the model; thereafter, the intervention group received dulaglutide (1 mg/kg, once every two weeks, for a total of eight doses). Following completion of the treatment regimen, a glucose tolerance test (GTT) was performed.

Body weight indicators (Figures B and C)

During the treatment period, body weight remained stable in the normal‑diet group, whereas it continued to increase in the high‑fat diet model group. Compared with the HFD group, dulaglutide treatment significantly inhibited weight gain in high‑fat–fed mice, resulting in a marked reduction in body weight; the relative weight‑change curve further confirmed the weight‑loss effect of dulaglutide.

Continuous glucose monitoring (Figure D)

In the high-fat diet–induced model group, blood glucose remained persistently elevated; following treatment with dulaglutide, blood glucose in the high-fat–fed mice decreased significantly and was maintained at a lower range, suggesting that dulaglutide can attenuate hyperglycemia induced by a high-fat diet.

Glucose Tolerance Test (Figures E and F)

Following glucose loading, the HFD group exhibited a higher peak plasma glucose level and a slower clearance rate, with a significantly larger area under the glucose‑time curve (AUC) compared to the normal control group, suggesting that a high‑fat diet induces glucose intolerance.

In the HFD + dulaglutide group, the peak blood glucose level was reduced, and glucose levels returned to baseline more rapidly; the glucose AUC was significantly lower than that of the HFD model group, indicating that dulaglutide effectively ameliorates impaired glucose tolerance induced by a high-fat diet.

Dulaglutide treatment effectively suppresses diet‑induced weight gain in mice, lowers fasting blood glucose levels, and improves glucose intolerance in high‑fat–fed mouse models.

 

Application areas

● Type 2 Diabetes and Insulin Resistance : Mechanistic studies and efficacy evaluations of insulin sensitizers/antidiabetic agents (such as GLP‑1 receptor agonists and SGLT2 inhibitors).
● Obesity and Regulation of Energy Metabolism: Evaluation of the effects of the feeding center, gut hormones, thermogenesis in brown adipose tissue (UCP1), and exercise/dietary interventions.
● Non-alcoholic fatty liver disease (NAFLD/NASH): Pathological studies on the progression from simple steatosis to steatohepatitis and fibrosis, as well as screening of anti‑NASH drugs (e.g., FXR agonists, THR‑β agonists).
● Adipose Tissue Inflammation and Immune Metabolism: Macrophage polarization, T cell/ILC function, and the adipokine network.
● Cardiovascular complications: Obesity‑related hypertension and susceptibility to atherosclerosis (which can be superimposed on an ApoE⁻⁻ or Ldlr⁻/⁻ genetic background).
● The Brain–Gut Axis and Cognitive Function: Obesity‑induced hypothalamic inflammation, blood–brain barrier disruption, and neurodegenerative associations.
● Drug Metabolism and Safety Evaluation: PK/PD changes under obese pathological conditions.

Breeding Techniques and Precautions

Strictly control inbreeding systems to mitigate genetic divergence.

High-fat diet

Use D12492 diet containing 60% fat; both imported and domestic formulations are suitable for model development. The diet must be stored at low temperature and replaced 1–2 times per week, with a pre‑warming period before feeding to enhance palatability. Provide an adequate amount of food in the cage to facilitate feeding in obese mice; scattered feed on the cage floor can interfere with accurate measurement of food intake, so prioritize ensuring ease of access to food.

 

 

Strictly control environmental stimuli to reduce experimental stress.

Water Management

High-fat–fed mice exhibit higher water intake than standard‑diet mice; consistently providing an adequate water supply promotes weight gain.

 

 

 

Standardize breeding management to improve the survival rate of pups.

Mouse Choice and Adaptation

Select mice that are 6 weeks old, weigh approximately 18 g, and exhibit uniform body weight. After transport, allow a 1–2 week acclimatization period; initiate formal model establishment only after their body weight has stabilized.

 

Monitor age-related spontaneous lesions and eliminate experimental confounding.

Housing environment

It is recommended to house mice in groups to prevent fighting when housed together, and to minimize human disturbance. The ideal housing temperature is around 26°C; monitor the mice closely to avoid excessive heat or cold, which can lead to increased energy expenditure and compromise model establishment.

 

 

 

Control male mouse fighting and standardize breeding practices.

Bedding Selection

Avoid using corn cob bedding (as mice tend to gnaw on it and it may reduce intake of high-fat diets); prioritize wood shavings as bedding, which can be supplemented with paper scraps to help maintain an appropriate ambient temperature.

 

 

 

Control male mouse fighting and standardize breeding practices.

Blood glucose testing

Blood samples are collected at a fixed time in the early morning to ensure data comparability; this value represents non-fasting blood glucose.

 

 

Literature support

Frequently Asked Questions

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Q1: Why was the C57BL/6J strain chosen for diet-induced obesity, rather than other inbred strains?

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Answer: C57BL/6J is one of the most sensitive strains to a high-fat diet, consistently developing obesity, insulin resistance, and steatosis when fed a diet with 60% of its energy from fat. Moreover, this strain boasts an exceptionally well-characterized genomic resource, a wide array of genetic modification tools, and extensive historical data, facilitating mechanistic studies and comparative analyses with gene-knockout or transgenic models. In contrast, other strains (such as BALB/c and FVB/N) exhibit weaker or atypical responses to HFD.

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Q2: At what gestational age should HFD be initiated? Why?

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A: We recommend starting at 6–8 weeks of age. At this stage, mice have completed their major growth and development and are transitioning into early adulthood, exhibiting the most consistent metabolic responses to a high-fat diet. Starting too early (<4 weeks) may interfere with normal development, while initiating the study too late (>12 weeks) can slow metabolic remodeling, reduce intergroup differences, and require a longer period to elicit significant phenotypes.

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Q3: How should I choose a high-fat diet? What is the difference between a 60% fat diet and a 45% fat diet?

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A: A 60 kcal% fat diet (e.g., D12492) is used to rapidly induce severe obesity, insulin resistance, and NASH phenotypes, making it suitable for high‑throughput drug screening. In contrast, a 45 kcal% fat diet (e.g., D12451) produces milder phenotypic progression and more closely mimics human dietary patterns, making it ideal for studying early metabolic disturbances or long‑term complications. Control diets must be matched in composition—such as sucrose and cellulose—at equivalent ratios (e.g., D12450J or D12450B) and should not be replaced arbitrarily with standard maintenance diets.

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Q4: How are the glucose tolerance test (GTT) and the insulin tolerance test (ITT) standardized?

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A: GTT recommends a 6-hour fast (overnight fasting is not advisable), with an intraperitoneal glucose dose of 2 g/kg body weight; ITT requires a 4–6-hour fast, and an intraperitoneal insulin dose of 0.75–1.0 U/kg. During the fast, mice should be transferred to clean, bedding-free cages and provided with ad libitum access to water. Calculate the injection volume precisely based on body weight, use an insulin syringe to ensure accurate dosing, and standardize blood sampling from the tail tip at the following time points for glucose monitoring: 0, 15, 30, 60, 90, and 120 minutes. Prior to the experiment, allow mice to acclimate to the experimental room for at least 30 minutes.

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