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Metabolic Disease Models

Diabetes Mouse Models

Since 1998, ingenious targeting laboratory has supported diabetes researchers with custom mouse models contributing to peer reviewed publications in Diabetes, Cell Metabolism, Diabetologia, and leading metabolism journals worldwide.

Diabetes mouse models enable researchers to investigate the molecular mechanisms underlying glucose homeostasis, insulin secretion, and insulin action. From beta cell specific knockouts that isolate islet function to tissue specific deletions in liver, muscle, and adipose tissue that dissect peripheral insulin resistance.

2,500+
Projects Completed
800+
Publications
26+
Years Experience
100%
Success Rate

Type 1 Diabetes Models

Type 1 diabetes results from autoimmune destruction of pancreatic beta cells. Mouse models address both the immune and beta cell components of disease.

  • NOD background models: Spontaneous autoimmune diabetes with genetic modifications
  • Immune gene knockouts: Deletions affecting T cell, B cell, or innate immune function
  • Beta cell specific deletions: Study genes essential for cell survival under immune attack
  • Antigen presentation models: Modifications affecting MHC or antigen processing

Type 2 Diabetes Models

Type 2 diabetes involves both peripheral insulin resistance and eventual beta cell failure. Mouse models address these interconnected pathologies.

  • Liver specific knockouts: Study hepatic glucose production and insulin sensitivity
  • Adipose specific knockouts: Investigate adipokine signaling and lipid storage
  • Muscle specific knockouts: Analyze glucose uptake and insulin signaling
  • Beta cell specific knockouts: Study insulin secretion and beta cell compensation

Tissue Specific Approaches

Conditional knockouts enable dissection of gene function in specific metabolic tissues. A single floxed allele can be crossed to multiple Cre drivers to study gene function across metabolic tissues.

Cre DriverTarget TissueMetabolic Function
Albumin CreHepatocytesGluconeogenesis, lipid metabolism
Adiponectin CreAdipocytesLipid storage, adipokine secretion
Insulin Cre / Pdx1 CreBeta cellsInsulin secretion, beta cell mass
MCK Cre / MyoD CreSkeletal muscleGlucose uptake, insulin sensitivity
Nestin CreHypothalamusCentral metabolic regulation
Villin CreIntestinal epitheliumIncretin signaling, nutrient absorption

Strain Background Considerations

Strain background significantly impacts metabolic phenotypes. The Nnt mutation in C57BL/6J should be considered when studying beta cell function or insulin secretion.

StrainCharacteristicsConsiderations
C57BL/6JNnt mutation impairs insulin secretion; susceptible to diet induced obesityDocument Nnt status; consider for obesity studies
C57BL/6NIntact Nnt; more robust insulin secretionPreferred for beta cell function studies
NODSpontaneous autoimmune diabetesRequired background for T1D studies
BALB/cRelatively resistant to diet induced obesityLess commonly used for metabolic studies

Metabolic Phenotyping

Glucose Homeostasis

  • Fasting and fed blood glucose
  • Glucose tolerance testing (GTT)
  • Insulin tolerance testing (ITT)
  • Hyperinsulinemic euglycemic clamp

Insulin & Beta Cell

  • Fasting and stimulated insulin levels
  • HOMA IR and HOMA B calculations
  • Islet isolation and perifusion
  • Beta cell mass quantification

Body Composition

  • Body weight and food intake
  • Body composition (MRI, DEXA)
  • Indirect calorimetry
  • Activity monitoring

Selected Publications in Diabetes Research

Models generated by ingenious targeting laboratory have supported diabetes research:

What Researchers Say

I've been working with iTL over the past 5 years in the production of 3 different genetically altered mice. Not only did iTL help in the design of the mice, but the entire process was transparent with the opportunity at any time along the way to discuss my questions or concerns with scientists who had significant insight into the process. The mice were delivered on time, as billed!

Raghu Mirmira, MD, PhD

University of Chicago

✦ New for 2026

Breeding Scheme Architect

Plan complex multi-allele breeding strategies, calculate expected genotype ratios, and estimate time to experimental cohorts—all before starting your project.

Visualize multi-generation breeding paths
Calculate Mendelian ratios automatically
Estimate timeline to study-ready cohorts

Free Research Tool

No account required

Allele 1Gene-flox (conditional)
Allele 2Cre-driver (tissue-specific)
TargetHomozygous knockout

→ 3 generations to target genotype

Start Your Diabetes Model Project

Our scientific consultants are ready to discuss your diabetes research requirements and recommend the optimal model design for your program. Initial consultation is provided at no charge and includes target analysis, tissue specific Cre recommendations, and timeline estimates.

Frequently Asked Questions

Type 1 diabetes models involve beta cell destruction or dysfunction (e.g., beta cell specific knockouts, autoimmune models). Type 2 diabetes models involve insulin resistance and metabolic dysfunction (e.g., insulin signaling knockouts, obesity models). Both can be generated using conditional knockout approaches.

Common targets include beta cells (Insulin Cre), liver (Albumin Cre), muscle (MCK Cre), adipose tissue (Adiponectin Cre), and hypothalamus (Nestin Cre). Tissue selection depends on whether you're studying insulin secretion, insulin action, or central metabolic control.

Standard assays include glucose tolerance testing (GTT), insulin tolerance testing (ITT), fasting glucose and insulin, body composition analysis, and indirect calorimetry. More advanced studies include hyperinsulinemic euglycemic clamps and islet perifusion studies.

Yes. Multiple alleles can be combined through breeding to study gene interactions in metabolic pathways. For example, combining beta cell knockouts with insulin signaling knockouts enables study of how insulin secretion and action interact to control glucose homeostasis.

Phenotype timing depends on the gene and model type. Some models show glucose intolerance within weeks of gene deletion (inducible systems). Others require months of aging or high fat diet challenge. Beta cell specific knockouts may develop diabetes more rapidly than insulin resistance models.

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