Metabolic Disease Model Evaluation: Comprehensive Preclinical Assessment Services

Metabolic disease model evaluation provides systematic, multi-dimensional assessment of preclinical models for diabetes, obesity, NAFLD/NASH, hyperlipidemia, and related metabolic disorders. By integrating physiological testing, clinical biochemistry, histopathology, and molecular analysis, our platform delivers reliable efficacy data to accelerate drug development and mechanistic research.

Technical Overview

Metabolic diseases—including type 2 diabetes mellitus (T2DM), obesity, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), hyperlipidemia, atherosclerosis, hyperuricemia, and metabolic syndrome—represent one of the fastest-growing global health burdens. Preclinical evaluation of metabolism-related disease models is therefore a cornerstone of translational research, enabling investigators to dissect disease pathogenesis, validate therapeutic targets, and assess the efficacy and safety of drug candidates prior to clinical trials.

Our metabolic disease model evaluation platform provides end-to-end services covering model establishment, systematic phenotyping, dynamic monitoring of metabolic parameters, and terminal endpoint analysis. By combining in vivo physiological tests, clinical biochemistry, immunoassays, histopathology, and molecular biology, we deliver reproducible, publication-quality data packages that support IND-enabling studies, pharmacodynamic evaluation, and biomarker discovery.

Testing Samples

Animal Models

• Genetically modified models: db/db mice, ob/ob mice, db/db rats, Zucker fatty rats, KK-Ay mice, ApoE-/- mice, and LDLR-/- mice
• Diet-induced models: high-fat diet (HFD)-induced obesity (DIO), HFD-induced insulin resistance, western diet-induced NAFLD/NASH, high-cholesterol and high-fructose models
• Chemically induced models: streptozotocin (STZ)-induced type 1 diabetes, low-dose STZ combined with HFD for T2DM, and alloxan-induced diabetes
• Combined and specialized models: HFD plus CCl4 or choline-deficient diet for advanced NASH and fibrosis

Biological Specimens

• Blood specimens: serum, plasma, and whole blood for biochemical and immunoassay analysis
• Tissue specimens: liver, pancreas, epididymal and inguinal adipose tissue, skeletal muscle, kidney, aorta, intestine, and hypothalamus
• Excreta specimens: urine and feces for metabolic, renal, and microbiota-related analysis
• In vitro samples: primary hepatocytes, adipocytes, and differentiated cell models for mechanistic confirmation

Testing Items

Glucose Metabolism Indicators

• Fasting blood glucose (FBG), random blood glucose, and 24-hour glucose profiles
• Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) with area-under-curve (AUC) calculation
• Fasting insulin, C-peptide, glucagon, and HbA1c
• Homeostasis model assessment of insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI)

Lipid Metabolism Indicators

• Total cholesterol (TC), triglycerides (TG), LDL-C, HDL-C, and VLDL-C
• Free fatty acids (NEFA), apolipoproteins (ApoA1, ApoB), and ketone bodies (β-hydroxybutyrate)
• Liver and skeletal muscle triglyceride content

Liver, Kidney, and Pancreatic Function

• ALT, AST, ALP, GGT, total bilirubin, albumin, and liver coefficient
• Serum creatinine, blood urea nitrogen (BUN), and uric acid
• Islet morphology, beta-cell mass, and insulin secretion capacity

Adipokines, Inflammation, and Oxidative Stress

• Leptin, adiponectin, resistin, and FGF21
• TNF-α, IL-6, IL-1β, MCP-1, and high-sensitivity CRP
• SOD, GSH-Px, catalase (CAT), and MDA levels in serum and tissues

Testing Methods

In Vivo Physiological Testing

• OGTT, intraperitoneal glucose tolerance test (IPGTT), and ITT under standardized fasting conditions
• Hyperinsulinemic-euglycemic clamp as the gold standard for insulin sensitivity
• Body composition analysis by DEXA or MRI-based quantitative magnetic resonance for fat and lean mass
• Comprehensive laboratory animal monitoring system (metabolic cages) for energy expenditure, respiratory exchange ratio, food intake, and locomotor activity
• Non-invasive blood pressure measurement and body weight/food intake tracking

Clinical Biochemistry and Immunoassays

• Automated chemistry analyzer-based enzymatic and colorimetric assays for glucose, lipids, and organ function panels
• ELISA and multiplex bead-based assays for hormones, adipokines, and inflammatory cytokines
• HbA1c quantification by ion-exchange chromatography or turbidimetric inhibition immunoassay

Histopathology and Molecular Analysis

• Hematoxylin and eosin (H&E) staining for general morphology and NAFLD activity score (NAS) assessment
• Oil Red O staining for hepatic lipid deposition and adipocyte sizing
• Masson's trichrome and Sirius Red staining for fibrosis evaluation
• Immunohistochemistry and immunofluorescence for insulin, glucagon, F4/80, and collagen markers
• qRT-PCR and Western blot for insulin signaling (IRS-1/PI3K/AKT), AMPK, SREBP-1c, PPARα, and related pathways

Applications

• Efficacy evaluation of hypoglycemic agents, including GLP-1 receptor agonists, SGLT2 inhibitors, DPP-4 inhibitors, and insulin sensitizers
• Preclinical development of anti-obesity drugs and body-weight-management interventions
• Efficacy and mechanism studies for NAFLD/NASH therapeutics targeting steatosis, inflammation, and fibrosis
• Assessment of lipid-lowering and anti-atherosclerotic compounds in dyslipidemia and vascular injury models
• Evaluation of functional foods, nutraceuticals, and probiotics for metabolic health claims
• Biomarker discovery and target validation for insulin resistance, adipose tissue dysfunction, and metabolic inflammation

FAQ

Q: How long does it take to establish a stable metabolic disease model?

A: Model timelines vary by type. Genetically diabetic models such as db/db mice develop hyperglycemia spontaneously by 4–8 weeks of age. Diet-induced obesity and insulin resistance models typically require 8–16 weeks of high-fat feeding, while STZ-induced hyperglycemia is established within 3–7 days after injection. Full NASH models with fibrosis may require 16–24 weeks depending on the induction protocol.

Q: What criteria are used to confirm successful model establishment?

A: Standard validation criteria include fasting blood glucose above the defined threshold (for example, FBG ≥ 11.1 mmol/L in diabetic models), significantly elevated body weight or liver coefficient, impaired glucose tolerance with increased AUC, abnormal lipid profiles, and histopathological confirmation of steatosis, inflammation, or fibrosis as appropriate to the model.

Q: Which species are available for metabolic disease evaluation?

A: C57BL/6 mice, Sprague-Dawley and Wistar rats, golden Syrian hamsters (preferred for dyslipidemia and atherosclerosis studies), and New Zealand rabbits for atherosclerosis research. Humanized and transgenic lines can be arranged upon request.

Q: Can the testing panel be customized for a specific compound or mechanism?

A: Yes. Our standard panels can be flexibly combined or expanded with mechanism-specific endpoints such as gut microbiota sequencing, bile acid profiling, mitochondrial respiration assays, and single-cell or spatial transcriptomics to match your research objectives.

Q: What group sizes and statistical designs are recommended?

A: A typical efficacy study uses 8–12 animals per group with randomization and blinded endpoint assessment. Power analysis is performed during protocol design to ensure statistically robust conclusions while complying with the 3R principles of animal welfare.