All

All
Insight
Research Services
Preclinical CRO
Animal Resource Bank

中文 English

Type 2 Diabetes Mellitus (T2DM) Animal Model

Explore more

On this page

Model Introduction

Platform Service Advantages

Modeling method

Publish an article

2026-10-29

Naming Genetically Engineered Mice (Part II): From Being Understandable to Being Written Correctly

2026-10-29

How should a multi-disease composite mouse model be constructed? Let’s take a look at the CKM approach.

2026-08-12

2026 CKM Guidelines Released: Chronic Diseases Enter the Era of Integrated Cardiorenal-Metabolic Management—It’s Time to Rethink Animal Models

2026-08-12

A Guide to Safe Mouse Handling | Manual on Mouse Transport Protocols and Troubleshooting

2026-08-08

Standardized Modeling Platform for Endometriosis: Recreating Inflammatory Pathology to Accelerate the Validation of New Gynecological Therapeutics

2026-07-31

In vivo CRISPR library screening: How to pinpoint true signals amid vast numbers of cells and complex tissues?

Type 2 diabetes

Introduction to T2DM Animal Models

Type 2 diabetes mellitus (T2DM) is the most common form of diabetes; because it typically develops in adulthood, it is also referred to as adult‑onset diabetes. The disease results from multiple etiologies that lead to insufficient insulin secretion or impaired insulin action, causing persistently elevated blood glucose levels. In this hyperglycemic milieu, large vessels, microvessels, and nerves are subject to pathological changes, which can subsequently damage organs such as the heart, kidneys, and eyes. In basic research, a variety of animal models of type 2 DCM are employed, with induced and spontaneous models being the most widely used.

Service Advantages of Aniphe BioLab’s T2DM Animal Model Platform

This platform boasts a well-established system for establishing and evaluating type 2 diabetes mellitus (T2DM) models, with robust technical expertise and comprehensive services, capable of meeting the diverse needs of scientific research and new drug development.

	A wide variety of models are available. It encompasses multiple modeling approaches, including high-fat diet combined with STZ and spontaneous diabetes, with phenotypes that closely resemble human type 2 diabetes.
	High modeling success rate The protocol is standardized, with stable glycemic and body weight parameters, minimal inter-individual variability, and excellent reproducibility.
	Comprehensive standardized quality control Animals are housed under SPF conditions, with regular monitoring of blood glucose, lipid profiles, and other relevant parameters; experimental data are complete and fully traceable.
	Comprehensive testing items It enables multi-dimensional assays, including assessments of carbohydrate and lipid metabolism, insulin resistance, pathology, and molecular biology.
	Supports customized solutions The modeling cycle, drug dosage, and observation duration can be flexibly adjusted to accommodate various experimental protocols.
	One-stop service End-to-end closed-loop delivery spanning model building, observation, and testing, with a short project cycle that meets regulatory reporting requirements.

Modeling cycle	The duration varies depending on the modeling method.
Laboratory animals	Select different animal strains based on the specific modeling method.
Positive drug	Metformin, glimepiride, liraglutide, and other agents are commonly used as positive control drugs; they can regulate blood glucose, improve insulin resistance, and ameliorate disturbances in carbohydrate and lipid metabolism.
Application areas	It is primarily used to investigate the pathogenic mechanisms underlying insulin resistance, pancreatic β-cell dysfunction, and diabetic complications involving the liver, kidneys, and vasculature. It also supports the screening of candidate drugs for glycemic control, metabolic improvement, and the prevention and treatment of diabetic complications, as well as the evaluation of their pharmacodynamics and safety. Furthermore, it can be employed for validating drug targets and developing bioactive compounds, thereby fully meeting the preclinical research needs of basic science, new‑drug development, and IND submissions.

Different modeling methods for T2DM animal models

Induced model

At present, intraperitoneal injection of streptozotocin (STZ) following feeding with a high‑sugar, high‑fat diet is a widely used and well‑established method for establishing animal models of type 2 diabetes, offering advantages such as simplicity of procedure, short experimental duration, and high cost‑effectiveness.

Modeling principle: First, animals are fed a high-sugar, high-fat diet to induce insulin resistance; subsequently, a low dose of streptozotocin (STZ) is administered intraperitoneally to cause mild damage to pancreatic β cells, leading to impaired compensatory insulin secretion and resulting in hyperglycemia.

Modeling method:

Six-week-old C57 mice were fed a high-sugar, high-fat diet for 4–8 weeks.

Comparison of the external physical characteristics between mice fed a standard diet (A) and those fed a high-sugar, high-fat diet (B); image source: Aniphe BioLab. After 4–8 weeks, the mice exhibited a significant increase in body weight, followed by intraperitoneal injection of STZ at low doses for five consecutive days.

Effects of different doses of STZ injection on the modeling rate (A) and mortality rate (B) in T2D mice.

After injection, monitor blood glucose every 3 days; a fasting blood glucose level of ≥11 mmol/L indicates successful model establishment. (If the fasting blood glucose does not reach this threshold, continue administering low-dose STZ injections.)

Image source: Aniphe BioLab

H&E staining of adipose tissue and liver tissue in mice

Precautions: Repeated low-dose injections of STZ are safer than a single high-dose injection, with lower mortality and a higher success rate in establishing the model.

Spontaneous model

There are numerous mouse models of type 2 diabetes (T2D), yet no single model fully captures all the hallmarks or complications of human diabetes. The homozygous Lep^ob mutant mice (ob/ob) and Lepr^db mutant mice (db/db) were among the earliest diabetic mouse models and remain popular choices in diabetes research today.

db/db mice:

db/db mice carry a mutation in the Leptin gene, resulting in symptoms of type 2 diabetes. Obesity becomes readily apparent by approximately 3–4 weeks of age; plasma insulin levels begin to rise at 10–14 days, and blood glucose levels increase by 4–8 weeks. Affected mice typically exhibit polyphagia, polydipsia, and polyuria. Two common genetic backgrounds are available for db/db mice: C57BL/6J (referred to as B6) and C57BLKS/J (referred to as BKS). Mice from both backgrounds develop hyperglycemia and hyperinsulinemia starting at about 4 weeks of age. However, db/db mice on the B6 background subsequently undergo compensatory β-cell hyperplasia and maintain sustained hyperinsulinemia throughout their lifespan of 18–20 months, accompanied by delayed wound healing and increased metabolic efficiency. In contrast, db/db mice on the BKS background do not recover their hyperglycemic phenotype; therefore, the BKS‑background db/db strain is more suitable for evaluating antihyperglycemic agents.

Renal histopathological changes in 8-week-old db/db mice and db/m mice

ob/ob mice:

The ob/ob mouse is a strain carrying a homozygous mutation in the leptin (Lep) gene, exhibiting obesity and hyperglycemia; it is referred to as the ob mouse due to its obese phenotype. From an early age, these mice spontaneously develop hyperglycemia, glucosuria, and hyperinsulinemia, with fasting blood glucose levels averaging 16.67 mmol/L. By approximately four weeks of age, they begin to show mild obesity, accompanied by hyperinsulinemia and impaired glucose tolerance. After four weeks, body weight increases rapidly, reaching up to three times that of wild-type mice. In addition to obesity, the mutant mice display a range of features, including excessive appetite, a diabetes‑like syndrome characterized by hyperglycemia, glucose intolerance, elevated plasma insulin levels, reduced fertility, impaired wound healing, and increased hormone secretion from the pituitary and adrenal glands. Blood glucose levels are slightly elevated compared with controls before 12 weeks of age but return to normal thereafter, making this model suitable for studying early‑onset hyperglycemia.

Although the pathogenic mechanisms in both mouse models are associated with leptin, their key phenotypes differ substantially.

Image source: Aniphe BioLab

ZDF rat:

It is a widely recognized animal model of congenital, hereditary type 2 diabetes and obesity, derived from Zucker fatty rats (ZF). ZDF rats do not exhibit the obesity seen in ZF rats, but they display more severe insulin resistance and β-cell apoptosis.

Drawback: The monogenic obesity model exhibits defects in leptin signaling, as leptin normally induces satiety. Consequently, the absence of functional leptin in these animals leads to excessive food intake and obesity.

OLETF rats:

Mild obesity, hyperinsulinemia, and hypertriglyceridemia. By 14 weeks, rats already exhibit insulin resistance, with increased body and intra-abdominal fat mass, accompanied by elevated triglyceride and cholesterol levels. By 24 weeks, the incidence can reach 100%.