Obesity and Diabetes Model

Biocytogen has developed a diverse range of obesity and diabetes mouse models to advance preclinical metabolic disease research. These include high-fat diet–induced obesity (DIO) models, as well as chemically induced and spontaneous diabetes models, which replicate key metabolic and endocrine dysfunctions observed in humans. Biocytogen's metabolic disease models provide reliable in vivo platforms for studying insulin resistance, glucose metabolism, and therapeutic efficacy in obesity and diabetes drug development.

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Obesity and Diabetes Model Introduction
Results

Obesity and Diabetes Model Introduction

Obesity and diabetes are among the most prevalent metabolic diseases and continue to pose major public health challenges worldwide. Both conditions are characterized by metabolic dysfunction, insulin resistance, and chronic low-grade inflammation, often leading to cardiovascular complications, nonalcoholic fatty liver disease, and metabolic syndrome. To support preclinical obesity and diabetes research, Biocytogen has developed a comprehensive portfolio of obesity models and diabetes mouse models that accurately mimic human metabolic disorders.

These include high-fat diet–induced obesity (DIO) mouse models, chemically induced diabetes models, and spontaneous diabetes mouse models, which reproduce critical features of metabolic dysfunction, such as glucose intolerance, insulin resistance, hyperglycemia, and weight gain observed in human obesity and diabetes. These disease models serve as valuable in vivo platforms for studying insulin signaling pathways, energy balance regulation, and therapeutic efficacy of anti-obesity and anti-diabetic drugs.

In addition, Biocytogen has created a series of humanized mouse models targeting key metabolic and hormonal pathways, including B-hGLP1R and B-hGCGR mice, to facilitate drug discovery, mechanistic studies, and in vivo pharmacodynamic evaluation for metabolic disease therapeutics. These obesity and diabetes mouse models provide reliable and reproducible systems for preclinical metabolic research, enabling researchers to test and validate potential treatments that address obesity, insulin resistance, and diabetes.

Results

High-Fat Diet-Induced Obese (DIO) Mouse Model

Obesity is a chronic disease that results from an imbalance of endogenous and environmental exposures, such as basal metabolic rate, energy expenditure, and food intake. Of note, excessive caloric intake and energy-dense meals are the leading causes of obesity. Surrogate animal models have been developed to study obesity-related complications. At Biocytogen, we have developed a high-fat diet-induced mouse model, which consists of 60 kcal%, to study pathophysiological changes associated with diabetes.

Characters of High-Fat Diet-Induced Obese (DIO) Mouse Model. A, Glucose tolerance ability after HFD induction. B, Area under curve of A. C-F, Blood biochemical analysis after HFD induction. Data are expressed as mean ± SEM. N = 10 mice per group. *p<0.05, **p<0.01,***p<0.001 ,****p<0.0001.

Efficacy study of semaglutide in HFD induced mouse model. A-C, Body weight change and terminal bodyweight after Semaglutide treatment. D, Accumulated food intake during treatment. DIO mice were grouped when body weight reached to about 40 g. N = 10 mice per group. *p<0.05, **p<0.01,***p<0.001 ,****p<0.0001.

Efficacy study of semaglutide in HFD induced mouse model. A-D, Adipose tissue weights after treatment. E-H, The percentage of adipose tissue weight to body weight after treatment. Data are expressed as mean ± SEM. N = 10 mice per group. *p<0.05, **p<0.01,***p<0.001 ,****p<0.0001.

Efficacy of GLP1R agonists and ActRII antibody on fat mass and lean mass

Efficacy of GLP1R agonists and ActRII Ab on fat mass and lean mass. A-B, Body weight change after treatment. C-F, Fat mass and lean mass change analyzed by in vivo Micro-CT scan on day14. N = 6-8 mice per group. *p<0.05, **p<0.01,***p<0.001 ,****p<0.0001.

Efficacy study of Semaglutide in HFD induced B-hGLP1R mice. A, Body weight change after HFD induction. B-D, Body weight change after Semaglutide treatment. E-F, Effect of semaglutide on food intake. Data are expressed as mean ± SEM. N = 8-10 mice per group. *p<0.05, **p<0.01,***p<0.001 ,****p<0.0001.

Efficacy study of Semaglutide in HFD induced mouse model. A, Blood glucose change after Semaglutide treatment. B, Glucose tolerance ability after treatment. C, Area under curve of B. D, Plasma insulin level. Data are expressed as mean ± SEM. N = 8-10 mice per group. *p<0.05, **p<0.01,***p<0.001 ,****p<0.0001.

Spontaneous Diabetes Mouse Model (B-ob/ob mice)

Leptin is a peptide hormone secreted by adipocytes and is mainly expressed by white adipose tissue. Additionally, leptin is also found to be expressed in the myocardium, skeletal muscle, placenta, lung, breast epithelium, and gastric mucosa. Functionally, leptin can inhibit appetite, increase energy expenditure, and inhibit fat synthesis to promote its decomposition. Insulin can promote the secretion of leptin, which in turn plays a negative feedback regulatory role in the synthesis and secretion of insulin.

Anti-obesity and hypoglycemic effect of Dulalgutide in B-ob/ob mice.

Spontaneous diabetes Mouse Model. A-B, Body weight and Blood glucose change of B-ob/ob mice from 4-21 weeks old age. C-F, Nine weeks old B-ob/ob mice were administrated 1mg/kg Dulaglutide (in house) twice per week for 4 weeks after grouping. Body weight and blood glucose were recorded at indicated time. Glucose tolerance test were performed the day after the last dose (n = 8 mice per group). G-J, Biochemical blood test showing the effect of Dulaglutide on B-ob/ob mice. Values are expressed as mean ± SEM. **p<0.01, ***p<0.001. (n = 8 mice per group).

Streptozotocin (STZ)-induced Diabetes Mouse Model

Streptozotocin (STZ) is an antibiotic that produces pancreatic islet β-cell destruction and is widely used experimentally to produce a model of type 1 diabetes mellitus (T1DM). STZ is a nitroso-containing compound that can specifically destroy islet B cells and increase the oxidative invasion of islet B cells by inducing the synthesis of nitric oxide (NO). It is generally believed that low-dose multiple injections of STZ can induce type 1 diabetes in experimental animals. The mechanism may be that after injection of low-dose STZ, a small number of islet cells are destroyed, and the dead islet cells release sensitizing proteins as antigens by macrophages. Phagocytosis, producing Th1-stimulating factor (IL-12), and inducing increased secretion of IL-2 and IFN-γ, forming inflammatory cell infiltration in the local islet, releasing cytokines such as IL-1β, TNF-α, IFN-γ and oxygen free radicals to kill a small number of cells. Dead cells use themselves as antigens, and after being processed by APC cells, release cytokines, amplify the cell damage effect, and eventually lead to type 1 diabetes.

STZ model establishment and in vivo efficacy of anti-GCCR in B-hGCGR diabetes Model

Included tests	Optional tests
Body weight	Insulin tolerance test
Blood glucose	Blood glucose
Glucose tolerance test	Food intake

STZ model establishment and in vivo efficacy of anti-GCCR in B-hGCGR diabetes Model 2

Hypoglycemic effect of GCGR antibody in STZ induced B-hGCGR mice. A-B, Body weight and Blood glucose change of 6 weeks old B-hGCGR mice after STZ (50mg/kg) induction (n = 8 mice per group). C-D, Three weeks after STZ induction, GCGR antibody (10mg/kg, made in house) was administrated once per week. Non-fasting blood glucose(C) and Fasting blood glucose(D) was measured. Values are expressed as mean ± SEM. *p<0.05, **p<0.01,***p<0.001.

Obesity and Diabetes Model

Publication

Obesity and Diabetes Model Introduction

Results