Simultaneous quantification of 8 key metabolic hormones and regulators — Insulin, Glucagon, Leptin, GLP-1, Ghrelin, GIP, Resistin, and PAI-1 — in a single well using Luminex xMAP technology. Designed for preclinical diabetes research, obesity and metabolic syndrome studies, and metabolic drug development in mouse models.
Metabolic diseases — type 2 diabetes, obesity, and metabolic syndrome — are among the most active areas of preclinical drug development, and the mouse is the dominant model organism for metabolic research. Mouse models including db/db, ob/ob, diet-induced obesity (DIO), and streptozotocin (STZ)-induced diabetes recapitulate key features of human metabolic disease. The metabolic state in these models is defined by an integrated hormonal network involving pancreatic islet hormones (Insulin, Glucagon), gut-derived incretins (GLP-1, GIP), adipokines (Leptin, Resistin), appetite regulators (Ghrelin), and metabolic stress markers (PAI-1) — all of which must be measured together to understand pathophysiology and therapeutic response.
Creative Proteomics offers the Mouse Metabolism 8-Plex Panel based on the Luminex xMAP platform for simultaneous quantification of eight key metabolic hormones and regulators in a single well. The panel covers glucose homeostasis (Insulin, Glucagon), appetite and energy balance (Leptin, Ghrelin), incretin signaling (GLP-1, GIP), and metabolic stress/inflammation (Resistin, PAI-1). Validated for serum and plasma from all standard mouse metabolic models, the panel is compatible with MAGPIX, Luminex 200, and FLEXMAP 3D systems, requiring only 25 μL of sample per well.
The panel is backed by validated performance data with intra-assay CV <10% and sensitive detection limits (Glucagon: 0.5 pg/mL LLOQ; GLP-1: 0.6 pg/mL; Insulin: 68 pg/mL; Leptin: 5 pg/mL), enabling accurate quantitation across the wide physiological and pathological concentration ranges encountered in metabolic disease models.
The Mouse Metabolism 8-Plex Panel covers the four functional axes of metabolic regulation: glucose homeostasis, appetite/energy balance, incretin signaling, and metabolic stress.
| Target | Alternative Name | Functional Axis | Biological Function in Metabolism |
|---|---|---|---|
| Insulin | — | Glucose Homeostasis | Pancreatic β-cell hormone; primary anabolic signal promoting glucose uptake, glycogenesis, and lipogenesis; the defining defect in type 1 (absolute deficiency) and type 2 (relative deficiency + resistance) diabetes |
| Glucagon | GCG | Glucose Homeostasis | Pancreatic α-cell counter-regulatory hormone; stimulates hepatic glycogenolysis and gluconeogenesis; opposes insulin action; dysregulated hyperglucagonemia contributes to diabetic hyperglycemia; LLOQ 0.5 pg/mL |
| Leptin | OB Protein | Appetite & Energy Balance | Adipocyte-derived satiety hormone; signals body fat stores to hypothalamic appetite centers; leptin deficiency (ob/ob mice) causes hyperphagia and severe obesity; leptin resistance in DIO mimics human obesity; LLOQ 5 pg/mL |
| Ghrelin | Appetite-Regulating Hormone | Appetite & Energy Balance | Stomach-derived orexigenic (appetite-stimulating) hormone; rises before meals, falls after eating; stimulates growth hormone release via GHS-R1a; implicated in meal initiation and hedonic feeding behavior |
| GLP-1 | Glucagon-Like Peptide-1 | Incretin Signaling | Gut L-cell-derived incretin hormone; potentiates glucose-stimulated insulin secretion; suppresses glucagon; delays gastric emptying; target of GLP-1 receptor agonists (semaglutide, liraglutide), now first-line diabetes/obesity therapy; LLOQ 0.6 pg/mL |
| GIP | Gastric Inhibitory Polypeptide, Glucose-Dependent Insulinotropic Peptide | Incretin Signaling | Gut K-cell-derived incretin; augments glucose-stimulated insulin secretion; promotes lipid storage in adipocytes; target of dual GIP/GLP-1 receptor agonists (tirzepatide); GIPR agonism adds metabolic benefit beyond GLP-1 alone |
| Resistin | ADSF, FIZZ3 | Metabolic Inflammation | Adipokine linking obesity to insulin resistance; promotes pro-inflammatory cytokine production from macrophages; elevated in DIO and ob/ob models; antagonizes insulin signaling in liver and skeletal muscle |
| PAI-1 | Serpin E1, Plasminogen Activator Inhibitor-1 | Metabolic Stress / Thrombosis | Elevated in obesity, insulin resistance, and metabolic syndrome; produced by visceral adipose tissue; impairs fibrinolysis, contributing to the pro-thrombotic state of obesity; independent cardiovascular risk factor |
Validated performance parameters for the Mouse Metabolism 8-Plex Panel.
Metabolic hormones are traditionally measured by individual ELISA or RIA. Luminex multiplex captures the full metabolic regulatory network from a single sample.
| Parameter | Luminex 8-Plex | Individual ELISA (8 assays) | RIA (per analyte) |
|---|---|---|---|
| Targets per Well | 8 | 1 | 1 |
| Sample Volume | 25 μL | 200–800 μL total | 100–200 μL per test |
| Radioactive? | No (fluorescent) | No (colorimetric/chemiluminescent) | Yes (I-125 labeled) |
| Assay Time | ~4 hours | 24–40 hours total | Overnight + counting |
| HOMA-IR Calculation | Yes (Insulin from panel + glucose from chemistry) | Yes (separate insulin ELISA + glucose) | Yes (separate insulin RIA + glucose) |
The Insulin/Glucagon ratio is a key metabolic parameter reflecting the β-cell/α-cell balance that is disrupted in diabetes. Simultaneous measurement from the same sample aliquot is required because insulin and glucagon have different stability profiles during storage and freeze-thaw. Separate ELISA measurements on different days introduce between-assay variability that can mask physiological changes in the ratio — particularly problematic in mouse studies where inter-animal variability is already substantial.
Metabolic hormones are sensitive to feeding state. Proper fasting protocols and sample handling are critical for reproducible results.
| Sample Type | Volume | Requirement |
|---|---|---|
| Serum (Fasting, Preferred) | 25 μL | Overnight fast (12–16 hr) or 5–6 hr fast. Collect via submandibular or retro-orbital bleed. Fed-state is appropriate for GLP-1/GIP measurement (incretins require nutrient stimulus). |
| EDTA Plasma | 25 μL | Add DPP-IV inhibitor (e.g., sitagliptin at 10 μL/mL blood) immediately upon collection if measuring GLP-1 — GLP-1 is rapidly degraded by DPP-IV (t½ <2 min in vivo) |
| Minimum Project Size | — | One 96-well plate; smaller batches accepted with surcharge |
| Fasting Protocol | — | Critical: record fasting duration (hours) and whether fast was overnight (dark cycle) or daytime. This affects insulin, glucagon, leptin, and ghrelin — fasting duration must be consistent across all animals within a study |
| Sample Storage | — | -80°C; GLP-1 and Glucagon are susceptible to degradation — avoid repeated freeze-thaw |
| Shipping | — | Dry ice; samples must remain frozen throughout transit |
Metabolic disease is defined by the integrated dysfunction of multiple hormonal axes. The 8-plex panel captures four dimensions of the metabolic state in a single assay.
Insulin, Glucagon — the pancreatic β-cell/α-cell axis. In db/db mice, insulin is massively elevated (insulin resistance) and glucagon is inappropriately normal or high despite hyperglycemia. HOMA-IR can be calculated from fasting insulin. 25 μL per well.
Leptin, Ghrelin — the adipose-gut-brain axis. ob/ob mice have undetectable leptin (genetic deficiency). DIO mice have elevated leptin (leptin resistance). Ghrelin rises with fasting, falls with feeding. 25 μL per well.
GLP-1, GIP, Resistin, PAI-1 — the gut-pancreas incretin axis (GLP-1/GIP) and the adipose-vascular stress axis (Resistin/PAI-1). GLP-1 measurement is critical for evaluating GLP-1 receptor agonist efficacy in preclinical models. 25 μL per well.
The Mouse Metabolism 8-Plex Panel supports preclinical research in diabetes, obesity, incretin biology, and metabolic drug development.
db/db (leptin receptor mutant) and DIO mice are the standard models of type 2 diabetes. The panel quantifies hyperinsulinemia (compensatory β-cell response), glucagon dysregulation, leptin resistance, and elevated resistin/PAI-1 — capturing the full metabolic syndrome profile from a single sample. HOMA-IR calculation from fasting insulin and glucose enables quantitative insulin resistance assessment.
GLP-1 receptor agonists (semaglutide, liraglutide, tirzepatide) are the most prescribed metabolic drugs. The panel quantifies the endogenous incretin axis (GLP-1, GIP) alongside the insulin/glucagon response to treatment. Rising endogenous GLP-1 during therapy distinguishes compounds that stimulate endogenous incretin secretion from those that only provide exogenous receptor agonism.
Diet-induced obesity (DIO) in C57BL/6 mice fed a 60% high-fat diet recapitulates human metabolic syndrome. The panel tracks the progression from normoglycemia to insulin resistance to frank hyperglycemia through serial hormone measurement: rising leptin (adiposity), rising insulin (β-cell compensation), rising resistin and PAI-1 (adipose inflammation), and eventual β-cell failure (declining insulin-to-glucose ratio).
Oral glucose tolerance test (OGTT) with timed GLP-1 and GIP measurement reveals the functional incretin response. The panel distinguishes impaired incretin secretion (low GLP-1/GIP response to oral glucose) from incretin resistance (normal GLP-1 but blunted insulin response) — two mechanistically distinct causes of postprandial hyperglycemia.
STZ-induced and NOD mouse models of type 1 diabetes are characterized by absolute insulin deficiency and glucagon dysregulation. The panel quantifies the progressive loss of insulin secretion, paradoxical hyperglucagonemia, and altered leptin/ghrelin signaling during disease development and following islet transplantation or β-cell regenerative therapy.
New-generation anti-obesity agents (GLP-1/GIP dual agonists, amylin analogues, MC4R agonists) require comprehensive metabolic phenotyping for efficacy assessment. The 8-plex panel provides simultaneous readout of appetite hormones (ghrelin, leptin), incretins (GLP-1, GIP), insulin sensitivity (insulin, resistin), and metabolic stress (PAI-1) — capturing the multi-dimensional metabolic response to therapy from a single 25 μL sample per time point.
Every Luminex mouse metabolism assay includes a comprehensive data package with full quality control documentation.
Explore other Luminex panels available for mouse metabolic and inflammatory disease research.
Common questions about our mouse metabolic hormone Luminex multiplex panel service.
Contact us to discuss your mouse metabolism study requirements, fasting/feeding protocols, DPP-IV inhibitor usage, and panel customization options. We respond within 24 hours.
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