How to Jointly Analyze Metabolic Syndrome Biomarkers: Detection Strategies for Insulin Resistance, Adipokine Networks, and Chronic Inflammation
How to Jointly Analyze Metabolic Syndrome Biomarkers: Detection Strategies for Insulin Resistance, Adipokine Networks, and Chronic Inflammation
Metabolic syndrome is not a single abnormality in blood glucose or blood lipids, but the combined result of insulin resistance, adipose tissue endocrine dysfunction, chronic low-grade inflammation, hepatic lipid metabolism disorder, and cardiometabolic risk. Detection strategies should place blood glucose and lipid indicators, insulin, HOMA-IR, adiponectin, leptin, resistin, TNF-α, IL-6, CRP, and related markers within the same analytical framework to determine whether metabolic abnormalities are in an early compensatory stage, inflammation-driven stage, aggravated lipotoxicity stage, or glucose-lipid metabolic decompensation stage.
Keywords: metabolic syndrome; insulin resistance; adipokines; chronic inflammation; HOMA-IR; adipose tissue inflammation; hepatic lipid metabolism
1 Overall Logic of Metabolic Syndrome Biomarker Analysis
1.1 Multilevel features of metabolic syndrome
(1) Glucose metabolism abnormalities
Glucose metabolism abnormality is one of the core detection layers in metabolic syndrome. Fasting blood glucose, postprandial blood glucose, OGTT, HbA1c, fasting insulin, and C-peptide respectively reflect immediate glycemic status, long-term glycemic exposure, glucose clearance ability, and compensatory capacity of pancreatic β cells. In early metabolic syndrome, fasting blood glucose may not be significantly elevated, but fasting insulin and HOMA-IR may already be abnormal, indicating that insulin resistance is already present.
(2) Lipid metabolism abnormalities
Lipid metabolism abnormalities mainly include elevated triglycerides, decreased HDL-C, increased LDL-C or non-HDL-C, increased free fatty acids, and hepatic lipid deposition. Dyslipidemia not only indicates atherosclerotic risk but also reflects changes in hepatic VLDL output, adipose tissue lipolysis, and peripheral fatty acid utilization.
(3) Imbalance in the adipokine network
Adipose tissue is an important endocrine organ that secretes adipokines such as adiponectin, leptin, resistin, visfatin, and PAI-1. Decreased adiponectin usually indicates weakened protective secretory function of adipose tissue. Elevated leptin is mostly associated with increased fat mass and leptin resistance. Resistin is related to inflammation, macrophage activation, and insulin resistance. Compared with BMI or fat mass alone, the adipokine network better reflects the functional quality of adipose tissue.
(4) Chronic low-grade inflammation
Metabolic syndrome is often accompanied by chronic low-grade inflammation rather than typical acute infectious inflammation. CRP, IL-6, TNF-α, MCP-1, IL-1β, and related markers can reflect systemic inflammation, immune cell recruitment in adipose tissue, and inflammatory insulin resistance. Combined analysis of inflammatory cytokines with adipokines, FFA, and insulin markers can more clearly determine whether metabolic abnormalities are jointly driven by adipose tissue inflammation and lipotoxicity.
1.2 Why joint detection is necessary
(1) A single marker can miss early abnormalities
Normal fasting blood glucose does not mean normal metabolic function. During early insulin resistance, the body can maintain stable blood glucose by increasing insulin secretion. Therefore, blood glucose may remain normal, while insulin, HOMA-IR, TG, adiponectin, and inflammatory cytokines have already changed. If only blood glucose is detected, compensatory hyperinsulinemia can easily be missed.
(2) Dyslipidemia cannot explain the inflammatory source
Elevated TG, decreased HDL-C, and increased FFA can indicate lipid metabolism disorder, but they do not directly show whether inflammation is involved. If CRP, IL-6, TNF-α, and MCP-1 are detected at the same time, it is possible to further determine whether chronic low-grade inflammation, adipose tissue macrophage recruitment, or inflammatory insulin resistance is present.
(3) Adipokines supplement functional information on adipose tissue
Body weight, BMI, and fat mass only reflect adipose tissue size and cannot reflect adipose tissue endocrine function. Decreased adiponectin, increased leptin, increased resistin, and elevated MCP-1 suggest that adipose tissue may have shifted from an energy-storage tissue to a metabolically active tissue that promotes inflammation and insulin resistance.
Table 1 Joint Analysis Framework for Metabolic Syndrome Biomarkers
Analysis Level | Core Markers | Main Information Reflected | Recommended Methods | Interpretation Focus |
Glucose metabolism | Fasting blood glucose, OGTT, HbA1c | Glucose homeostasis and long-term glycemic exposure | Biochemical method, HPLC, enzymatic method | Normal blood glucose cannot exclude early insulin resistance |
Insulin resistance | Insulin, C-peptide, HOMA-IR | β-cell compensation and insulin sensitivity | ELISA, chemiluminescence, computational models | Interpret compensation or decompensation together with blood glucose |
Lipid profile | TG, TC, HDL-C, LDL-C, non-HDL-C | Lipoprotein metabolism and cardiovascular risk | Biochemical analysis, enzymatic method | TG/HDL-C and non-HDL-C supplement conventional lipid interpretation |
Fatty acid metabolism | FFA, glycerol, hepatic TG | Lipolysis, lipotoxicity, and hepatic lipid deposition | Colorimetric method, enzymatic method, tissue staining | FFA connects adipose tissue lipolysis with insulin resistance |
Adipokines | Adiponectin, leptin, resistin | Adipose tissue endocrine function | ELISA, multiplex detection, qPCR | An increased leptin/adiponectin ratio helps assess adipose tissue functional imbalance and a pro-insulin-resistance tendency |
Chronic inflammation | CRP, IL-6, TNF-α, MCP-1 | Systemic inflammation and adipose tissue inflammation | ELISA, multiplex detection, qPCR | Acute infection and acute inflammation must be excluded |
Hepatic lipid metabolism | ALT, AST, hepatic TG, SREBP1, PPARα | Hepatic lipid deposition and fatty acid oxidation | Biochemical method, WB, qPCR, Oil Red O | Analyze together with FFA, TG, and inflammatory cytokines |
Cardiometabolic risk | ApoB, ApoA1, oxLDL, PAI-1 | Atherogenic and vascular risk | ELISA, immunoassay | Suitable for metabolic syndrome risk stratification |
2 Insulin Resistance-Related Markers
2.1 Blood glucose markers
(1) Fasting blood glucose
Fasting blood glucose reflects hepatic glucose output, peripheral glucose utilization, and insulin regulation under basal conditions. Elevated fasting blood glucose often indicates impaired glucose homeostasis, but normal fasting blood glucose does not mean normal insulin sensitivity. In early metabolic syndrome, pancreatic β cells can maintain blood glucose by increasing insulin secretion, making glucose abnormalities lag behind insulin abnormalities.
(2) OGTT
OGTT evaluates the body’s ability to clear glucose after a glucose load and is suitable for identifying impaired glucose tolerance. If fasting blood glucose is normal but the OGTT curve declines slowly, this suggests that postprandial glucose regulation has already declined. In animal experiments, fasting duration, glucose dose, blood collection time points, and stress conditions should be standardized.
(3) HbA1c
HbA1c reflects average glycemic exposure over a relatively long period and is more suitable for long-term clinical samples or chronic animal models. Short-term pharmacodynamic studies, acute interventions, or cell experiments should not rely on HbA1c alone. Anemia, altered red blood cell lifespan, or bleeding can affect HbA1c interpretation.
2.2 Insulin and C-peptide
(1) Fasting insulin
Fasting insulin is an important marker for determining compensatory hyperinsulinemia. If blood glucose is normal but insulin is elevated, this indicates that the body already requires a higher insulin level to maintain glucose homeostasis. This condition is common in early metabolic syndrome, obesity, high-fat diet models, and mild-to-moderate insulin resistance.
(2) C-peptide
C-peptide is related to endogenous insulin secretion and is not directly affected by exogenous insulin, making it suitable for evaluating pancreatic β-cell secretory capacity. When blood glucose is elevated but insulin and C-peptide are insufficient, this suggests decreased β-cell compensatory capacity or progression of glucose metabolism abnormalities into a decompensated stage.
(3) Insulin release curve
The insulin release curve reflects the β-cell response after glucose stimulation. Early insulin resistance may show increased insulin secretion or delayed peak secretion, while later β-cell functional decline may show insufficient peak secretion. This marker is suitable for combined use with OGTT.
2.3 HOMA-IR and result interpretation
(1) Uses of HOMA-IR
HOMA-IR is commonly used to estimate insulin resistance and is suitable for preliminary stratification in clinical cohorts, animal experiments, and large-sample studies. Its calculation is usually based on fasting blood glucose and fasting insulin. Therefore, samples must be collected under stable fasting conditions, and glucose and insulin units must be consistent.
(2) Limitations of HOMA-IR
HOMA-IR cannot replace the hyperinsulinemic-euglycemic clamp test and cannot directly localize insulin resistance to the liver, skeletal muscle, or adipose tissue. In mechanistic studies, p-AKT, IRS1, GLUT4, hepatic gluconeogenic genes, adipose tissue lipolysis, and inflammatory cytokines should be combined.
(3) Joint interpretation
Elevated HOMA-IR together with elevated TG, decreased HDL-C, decreased adiponectin, and increased CRP/IL-6 more strongly supports metabolic syndrome-related insulin resistance. If HOMA-IR is elevated but inflammatory cytokines are unchanged, the process may be more related to lipid load or energy excess. If inflammatory cytokines are clearly elevated, inflammatory insulin resistance should be considered.
Table 2 Insulin Resistance-Related Marker Combinations and Interpretation
Marker Combination | Possible Indication | Recommended Additional Tests | Interpretation Focus |
Normal blood glucose, elevated insulin | Early insulin resistance or compensatory stage | HOMA-IR, OGTT, adiponectin, TG | Normal blood glucose cannot exclude metabolic risk |
Elevated blood glucose, elevated insulin | Obvious insulin resistance with β-cell compensation | C-peptide, OGTT, p-AKT, FFA | Determine compensatory capacity and peripheral insulin sensitivity |
Elevated blood glucose, decreased insulin | β-cell insufficiency or decompensation | C-peptide, pancreatic islet staining, HbA1c | Focus on risk of diabetes progression |
Elevated HOMA-IR, decreased adiponectin | Insulin resistance with weakened protective adipose function | Leptin, resistin, FFA | Supports adipose tissue functional imbalance |
Elevated HOMA-IR, elevated CRP/IL-6 | Inflammation involved in insulin resistance | TNF-α, MCP-1, CD68 | Inflammatory source should be localized |
Delayed decline in OGTT curve | Impaired glucose tolerance | Insulin release curve, HOMA-IR | Suitable for early identification of glucose metabolism abnormalities |
Elevated HbA1c | Increased long-term glycemic exposure | Fasting glucose, postprandial glucose, insulin | Suitable for long-term models and clinical samples |
3 Adipokine Network
3.1 Adiponectin
(1) Protective adipokine
Adiponectin is mainly secreted by adipocytes and has insulin-sensitizing, fatty acid oxidation-promoting, anti-inflammatory, and vascular protective effects. In obesity and metabolic syndrome, increased fat mass does not necessarily lead to increased adiponectin. Instead, adiponectin often decreases, indicating reduced functional quality of adipose tissue.
(2) Relationship with insulin resistance
Decreased adiponectin is commonly associated with increased HOMA-IR, elevated fasting insulin, elevated TG, increased FFA, and decreased HDL-C. If decreased adiponectin is accompanied by weakened p-AKT, reduced GLUT4 translocation, or enhanced hepatic gluconeogenesis, this more strongly supports the involvement of adiponectin insufficiency in insulin resistance.
(3) High-molecular-weight adiponectin
High-molecular-weight adiponectin is more closely associated with insulin sensitivity. If total adiponectin does not change significantly but high-molecular-weight adiponectin decreases, adiponectin function may still be impaired. In mechanistic studies, total adiponectin and high-molecular-weight adiponectin can be measured together.
3.2 Leptin
(1) Fat mass and energy homeostasis
Leptin is secreted by adipose tissue and is usually associated with fat mass. In obesity and metabolic syndrome, leptin is often elevated, but this does not indicate enhanced metabolic protection. Instead, it usually suggests leptin resistance. Elevated leptin combined with abnormal appetite control, weight gain, and increased inflammatory cytokines more strongly supports reduced leptin signaling efficiency.
(2) Leptin/adiponectin ratio
The leptin/adiponectin ratio can reflect the balance of adipose tissue endocrine function. An increased ratio usually indicates an enhanced pro-inflammatory and pro-insulin-resistance state with relative deficiency of protective adiponectin. This marker is more suitable for metabolic risk stratification than leptin or adiponectin alone.
(3) Relationship with inflammatory cytokines
Leptin can participate in immune regulation and is associated with inflammatory markers such as IL-6, TNF-α, and CRP. The simultaneous presence of elevated leptin and inflammatory cytokines in obesity suggests that adipose tissue expansion may be accompanied by immunometabolic activation.
3.3 Resistin
(1) Adipokine related to inflammation and insulin resistance
Resistin is closely associated with inflammation and insulin resistance, but its source differs across species. In mice, resistin is more closely related to adipocytes, whereas in humans it is more strongly associated with monocytes and macrophages. When detecting resistin, interpretation should consider the research species and sample source.
(2) Linkage with TNF-α and IL-6
Elevated resistin often occurs together with increased inflammatory markers such as TNF-α, IL-6, and MCP-1, suggesting immunometabolic activation. If elevated resistin is accompanied by increased HOMA-IR and decreased adiponectin, this more strongly supports a shift of the adipokine network toward a pro-inflammatory and pro-insulin-resistance direction.
(3) Cardiometabolic risk
Resistin is associated with endothelial dysfunction, inflammation, and atherosclerotic risk. If elevated resistin is accompanied by increased CRP, oxLDL, ApoB, or PAI-1, extended evaluation of cardiometabolic risk should be considered.
Table 3 Adipokine Network and Metabolic Significance
Adipokine | Main Function | Common Change in Metabolic Syndrome | Recommended Combined Markers | Interpretation Focus |
Adiponectin | Insulin sensitization, anti-inflammation, promotion of fatty acid oxidation | Often decreased | Insulin, HOMA-IR, FFA, TG | Decrease indicates weakened protective adipose function |
High-molecular-weight adiponectin | More closely related to insulin sensitivity | Often decreased | HOMA-IR, OGTT, TG | More suitable for refined stratification than total adiponectin |
Leptin | Fat mass, energy homeostasis, immune regulation | Often increased | Fat mass, adiponectin, CRP | Increase usually suggests leptin resistance |
Leptin/adiponectin ratio | Balance of adipose tissue function | Often increased | HOMA-IR, TG, inflammatory cytokines | Used to evaluate adipose tissue endocrine imbalance |
Resistin | Related to inflammation and insulin resistance | May increase | TNF-α, IL-6, MCP-1 | Species differences must be considered |
Visfatin/NAMPT | Related to immunometabolism and adipose tissue function | May increase | Inflammatory cytokines, insulin | Suitable for expanded adipokine analysis |
PAI-1 | Fibrinolysis inhibition and vascular risk | May increase | CRP, ApoB, oxLDL | Reflects cardiometabolic risk |
RBP4 | Liver- and adipose-related insulin resistance | May increase | Hepatic TG, insulin, FFA | Suitable for fatty liver-related studies |
4 Chronic Inflammation and Adipose Tissue Inflammation
4.1 Systemic chronic inflammation
(1) CRP
CRP is a commonly used marker of systemic inflammatory burden, and hs-CRP is more suitable for detecting low-grade inflammation in metabolic syndrome. Elevated CRP can be seen in obesity, insulin resistance, fatty liver, and increased cardiovascular risk, but it is also easily affected by infection, trauma, immune diseases, and acute inflammation.
(2) IL-6
IL-6 can be produced by adipose tissue, liver, immune cells, and skeletal muscle. In metabolic syndrome, elevated IL-6 can connect adipose tissue inflammation with hepatic acute-phase responses and promote CRP production. If IL-6 and CRP are both elevated, the inflammatory signal usually has systemic characteristics.
(3) TNF-α
TNF-α is an important marker of inflammatory insulin resistance and can interfere with insulin signaling nodes such as IRS1, AKT, and GLUT4. Blood TNF-α levels may be low and fluctuate substantially. In mechanistic studies, TNF-α mRNA and protein expression in adipose tissue, liver, or muscle are often required.
4.2 Adipose tissue inflammation
(1) MCP-1 and monocyte recruitment
MCP-1/CCL2 promotes monocyte recruitment into adipose tissue and is an important chemokine in adipose tissue inflammation. In high-fat diet, obesity, and adipocyte hypertrophy, increased MCP-1 is often accompanied by increased macrophage markers such as CD68, F4/80, and CD11c.
(2) Macrophage infiltration
In obese adipose tissue, adipocyte hypertrophy, hypoxia, cell death, and fatty acid release can promote macrophage infiltration. Increased CD68, F4/80, CD11c, TNF-α, and MCP-1 suggest formation of a pro-inflammatory adipose tissue microenvironment. CD206, Arg1, and related markers can be used to evaluate repair-associated or anti-inflammatory phenotypes.
(3) Adipose tissue inflammation and adipokine imbalance
Adipose tissue inflammation can suppress adiponectin secretion and promote increases in leptin, resistin, IL-6, TNF-α, and MCP-1. When decreased adiponectin occurs together with increased MCP-1 and TNF-α, this suggests that adipose tissue has shifted from a protective endocrine state to a pro-inflammatory metabolic state.
4.3 Inflammatory insulin resistance
(1) TNF-α and inhibition of insulin signaling
TNF-α can promote abnormal insulin signaling and affect the IRS1, PI3K-AKT, and GLUT4 pathways. If elevated TNF-α is accompanied by reduced insulin-stimulated p-AKT, decreased GLUT4 membrane translocation, and increased HOMA-IR, inflammatory insulin resistance is more strongly supported.
(2) IL-6 and hepatic metabolism
IL-6 can affect hepatic acute-phase responses, glucose-lipid metabolism, and inflammatory signaling. Increased IL-6 together with CRP, ALT/AST, hepatic TG, and fatty liver pathology suggests that hepatic inflammation and lipid metabolism abnormalities may contribute to systemic metabolic risk.
(3) MCP-1 and localization of adipose tissue origin
The value of MCP-1 lies in indicating the direction of immune cell recruitment. If MCP-1, CD68, F4/80, and TNF-α are simultaneously elevated in adipose tissue while circulating inflammatory cytokines are only mildly elevated, local adipose tissue inflammation may precede overt systemic inflammation.
Table 4 Chronic Inflammation and Adipose Tissue Inflammation Markers
Marker | Main Significance | Common Samples | Recommended Combined Markers | Interpretation Focus |
CRP/hs-CRP | Systemic low-grade inflammation | Serum, plasma | IL-6, adiponectin, blood lipids | Acute infection interference must be excluded |
IL-6 | Inflammation and acute-phase response | Serum, adipose tissue, liver tissue | CRP, TNF-α, liver function | Can connect adipose inflammation with hepatic response |
TNF-α | Inflammatory insulin resistance | Serum, adipose tissue, muscle | p-AKT, IRS1, HOMA-IR | Tissue levels often have stronger interpretive value |
MCP-1/CCL2 | Monocyte recruitment | Serum, adipose tissue | CD68, F4/80, CD11c | Suitable for localizing adipose tissue inflammation |
IL-1β | Inflammasome activation and metabolic injury | Adipose tissue, liver tissue, pancreatic islets | NLRP3, Caspase-1 | Suitable for lipotoxicity and inflammasome studies |
CD68 | Macrophage infiltration | Adipose tissue, liver tissue | MCP-1, TNF-α | Reflects immune cell infiltration extent |
F4/80 | Mouse macrophage marker | Mouse adipose tissue | CD11c, CD206 | Suitable for high-fat diet animal models |
CD11c | Pro-inflammatory macrophage phenotype | Adipose tissue | TNF-α, IL-6 | Used for inflammatory phenotype classification |
CD206/Arg1 | Repair- or anti-inflammatory phenotype | Adipose tissue | IL-10, CD11c | Used to assess inflammatory balance |
5 Joint Detection Schemes and Result Classification
5.1 Basic screening scheme
(1) Recommended markers
Basic screening can include fasting blood glucose, fasting insulin, HOMA-IR, TG, TC, HDL-C, LDL-C, adiponectin, leptin, and CRP. This combination simultaneously covers glucose metabolism, lipid metabolism, adipokines, and systemic low-grade inflammation.
(2) Applicable scenarios
It is suitable for preliminary screening of clinical samples, animal model phenotype confirmation, and initial evaluation of intervention experiments. If basic screening shows increased insulin, elevated TG, decreased adiponectin, and increased CRP, inflammatory cytokines, FFA, and hepatic lipid metabolism markers can be added.
(3) Limitations
The basic scheme cannot fully localize the inflammatory source and cannot directly determine hepatic lipid deposition, adipose tissue macrophage infiltration, or insulin signaling pathway changes. Mechanistic studies require tissue-level detection.
5.2 Result classification
(1) Insulin resistance-dominant type
This type is characterized by elevated fasting insulin and increased HOMA-IR, while blood glucose may be normal or mildly elevated. It is often accompanied by elevated TG, decreased HDL-C, and decreased adiponectin. This type suggests that metabolic abnormality may still be in a compensatory stage, and intervention should focus on whether insulin, OGTT, and adiponectin recover.
(2) Adipokine imbalance type
This type is characterized by decreased adiponectin, increased leptin, increased resistin, or increased leptin/adiponectin ratio. If accompanied by increased FFA and elevated TG, this suggests that adipose tissue endocrine dysfunction has already affected glucose-lipid metabolism.
(3) Chronic inflammation-driven type
This type is characterized by increased CRP, IL-6, TNF-α, and MCP-1 and may be accompanied by decreased adiponectin and increased HOMA-IR. This type suggests that inflammatory cytokines participate in insulin resistance and adipose tissue functional injury, and tissue inflammatory markers should be added to confirm the source.
(4) Lipotoxicity and fatty liver type
This type is characterized by increased FFA, TG, hepatic TG, ALT/AST, and lipid droplets and may be accompanied by decreased PPARα/CPT1A or increased SREBP1/FASN. This type suggests that hepatic lipid metabolism disorder and increased fatty acid burden are the main features.
(5) Cardiometabolic risk type
This type is characterized by increased non-HDL-C, ApoB, oxLDL, PAI-1, and hs-CRP and may be accompanied by decreased HDL-C and decreased adiponectin. This type emphasizes lipoprotein particle burden, oxidative modification, and vascular inflammatory risk.
Table 5 Result Classification of Metabolic Syndrome and Recommended Marker Combinations
Classification | Core Features | Required Markers | Extended Markers | Interpretation Focus |
Insulin resistance-dominant type | Elevated insulin, increased HOMA-IR | Glucose, insulin, HOMA-IR, OGTT | C-peptide, p-AKT, GLUT4 | Determine compensatory hyperinsulinemia |
Adipokine imbalance type | Decreased adiponectin, increased leptin/adiponectin ratio | Adiponectin, leptin, resistin | FFA, PAI-1, RBP4 | Assess adipose tissue endocrine function |
Chronic inflammation-driven type | Increased CRP, IL-6, TNF-α, MCP-1 | CRP, IL-6, TNF-α, MCP-1 | CD68, F4/80, CD11c | Determine systemic inflammation and adipose tissue inflammation |
Lipotoxicity and fatty liver type | Increased FFA, hepatic TG, lipid droplets | FFA, TG, ALT/AST, hepatic TG | SREBP1, FASN, PPARα, CPT1A | Determine hepatic lipid deposition and fatty acid oxidation |
Cardiometabolic risk type | Increased ApoB, oxLDL, PAI-1 | Non-HDL-C, ApoB, hs-CRP | ApoA1, oxLDL, PAI-1 | Determine lipoprotein particle and vascular inflammatory risk |
Decompensated glucose metabolism type | Hyperglycemia with insufficient insulin compensation | Glucose, insulin, C-peptide, HbA1c | Pancreatic islet staining, β-cell markers | Determine β-cell functional decline |
6 Reagent and Material Selection for Metabolic Syndrome Biomarker Detection
Table 6 Products Related to Glucose Metabolism and Insulin Resistance Detection
Application Module | Cat. No. | Product Name | Grade/Specification | System Positioning |
Glucose detection | Glucose (Glu) Content Assay Kit (GOD-POD, Colorimetric Method) | BioReagent | Used to detect glucose content in serum, plasma, tissue homogenate, or cell supernatant; suitable for fasting glucose, glucose consumption, and basic glucose metabolism phenotype analysis | |
Glucose detection | Glucose Assay Kit (GOD-POD Microplate Method) | BioReagent, Colorimetric, Suitable for Analysis | Used for microplate glucose detection; suitable for metabolic experiments with many samples | |
Blood glucose detection | Blood Glucose Content Assay Kit (GOD-POD, Micro Method) | BioReagent | Used for micro-scale blood glucose detection; suitable for animal models or small-volume samples | |
Blood glucose detection | Blood Glucose Content Assay Kit (GOD-POD, Colorimetric Method) | BioReagent | Used for colorimetric blood glucose detection; suitable for basic metabolic syndrome screening | |
Glucose detection | Glucose Content Assay Kit (Folin-Wu, Micro Method) | BioReagent | Used for micro-scale glucose detection; can supplement different methodological systems | |
Glucose detection | Glucose Content Assay Kit (Folin-Wu, Colorimetric Method) | BioReagent | Used for colorimetric glucose detection; suitable for glucose metabolism phenotype analysis | |
Glucose detection | Glucose Content Assay Kit (o-Toluidine, Micro Method) | BioReagent | Used for micro-scale glucose detection; suitable for small-volume samples | |
Glucose detection | Glucose Content Assay Kit (o-Toluidine, Colorimetric Method) | BioReagent | Used for colorimetric glucose detection; can supplement the GOD-POD method | |
Glucose metabolism intermediate | Glucose-6-Phosphate (G6P) Content Assay Kit (Micro Method) | BioReagent | Used to detect G6P content; suitable for glycolysis, gluconeogenesis, and glucose metabolism intermediate analysis | |
Glucose metabolism intermediate | Glucose-6-Phosphate (G6P) Content Assay Kit (Colorimetric Method) | BioReagent | Used for colorimetric G6P detection; can assist in evaluating glucose metabolic flux changes | |
Gluconeogenesis/glucose output-related enzyme | Glucose-6-Phosphatase (G6P) Activity Assay Kit (UV Micro Method) | BioReagent | Used to detect G6Pase activity; suitable for hepatic glucose output and hepatic insulin resistance studies | |
Gluconeogenesis/glucose output-related enzyme | Glucose-6-Phosphatase (G6P) Activity Assay Kit (UV Colorimetric Method) | BioReagent | Used for colorimetric G6Pase activity detection; can assist in analyzing hepatic gluconeogenic status | |
Pentose phosphate pathway | Glucose-6-Phosphate Dehydrogenase (G6PDH) Activity Assay Kit (UV Micro Method) | BioReagent | Used to detect G6PDH activity; suitable for oxidative-reductive metabolism and NADPH production analysis | |
Pentose phosphate pathway | Glucose-6-Phosphate Dehydrogenase (G6PDH) Activity Assay Kit (UV Colorimetric Method) | BioReagent | Used for G6PDH activity detection; can assist in evaluating metabolic reprogramming under high-glucose or high-fat conditions | |
Insulin detection | Human Insulin (INS) ELISA Kit | BioReagent | Used for quantitative detection of insulin in human samples; suitable for HOMA-IR calculation and insulin resistance analysis | |
Insulin detection | Human Insulin ELISA Kit | BioReagent | Used to detect human insulin levels; can be interpreted with glucose, HbA1c, and adipokines | |
Proinsulin detection | Human Proinsulin ELISA Kit | BioReagent | Used to evaluate pancreatic β-cell precursor secretion levels; suitable for glucose metabolism decompensation or β-cell stress analysis | |
Proinsulin detection | Human Proinsulin (PI) ELISA Kit | BioReagent | Used to detect proinsulin and assist in evaluating β-cell processing and secretory burden | |
Insulin receptor detection | Human Insulin Receptor (INSR) ELISA Kit | BioReagent | Used to detect insulin receptor levels; suitable for insulin signaling pathway research | |
Insulin detection | Rat Fasting Insulin(FINS) ELISA Kit | BioReagent | Used to detect fasting insulin in rats; suitable for high-fat diet, fatty liver, and insulin resistance models | |
Insulin detection | Rat Insulin (INS) ELISA Kit | BioReagent | Used to detect rat insulin levels; can be analyzed with glucose, OGTT, and HOMA-IR | |
Insulin receptor detection | Rat Insulin Receptor (INSR) ELISA Kit | BioReagent | Used for rat INSR detection; suitable for insulin signaling mechanism studies | |
Insulin detection | Mouse Fasting insulin (FINS) ELISA Kit | BioReagent | Used to detect fasting insulin in mice; suitable for high-fat diet, ob/ob, db/db, and related models | |
Insulin detection | Mouse Insulin (INS) ELISA Kit | BioReagent | Used for mouse insulin quantification; suitable for HOMA-IR and glucose metabolism classification | |
Proinsulin detection | Mouse Proinsulin (PI) ELISA Kit | BioReagent | Used for mouse proinsulin detection and auxiliary evaluation of β-cell secretory stress | |
High-sensitivity insulin detection | Mouse Hypersensitive Insulin (hs-INS) ELISA Kit | BioReagent | Used for low-level insulin detection; suitable for low-concentration samples or refined stratification experiments | |
Insulin detection | Monkey Insulin (INS) ELISA Kit | BioReagent | Used to detect insulin in monkey samples; suitable for nonhuman primate metabolic studies | |
C-peptide detection | Human C-Peptide (C-P) ELISA Kit | BioReagent | Used to evaluate endogenous insulin secretion and β-cell function in human samples | |
C-peptide detection | Rat C-Peptide (C-P) ELISA Kit | BioReagent | Used for rat C-peptide detection; suitable for distinguishing insulin resistance from insufficient β-cell secretion | |
C-peptide detection | Mouse C-Peptide (C-P) ELISA Kit | BioReagent | Used for mouse C-peptide detection; suitable for glucose metabolism decompensation classification | |
HbA1c detection | Rat Glycated Hemoglobin A1C (GHbA1c) ELISA Kit | BioReagent | Used for evaluating long-term glycemic exposure in rats | |
HbA1c detection | Mouse Glycated Hemoglobin A1c(GHbA1c) ELISA Kit | BioReagent | Used for evaluating long-term glycemic exposure in mice |
Table 7 Products Related to Adiponectin, AdipoR1/AdipoR2, and Protective Adipose Tissue Secretory Function
Application Module | Cat. No. | Product Name | Grade/Specification | System Positioning |
Adiponectin detection | Human Adiponectin ELISA Kit | Bioactive, for ELISA, for enzyme immunoassay(ELISA) | Used for adiponectin quantification in human serum, plasma, or supernatant to evaluate protective secretory function of adipose tissue | |
Adiponectin detection | Mouse Adiponectin ELISA Kit | Bioactive, for enzyme immunoassay(ELISA), for ELISA | Used for mouse adiponectin detection; suitable for high-fat diet and obesity models | |
Adiponectin detection | Rat Adiponectin ELISA Kit | Bioactive, for enzyme immunoassay(ELISA), for ELISA | Used for rat adiponectin detection; suitable for metabolic syndrome animal models | |
Adiponectin detection | Human Adiponectin (ADPN) ELISA Kit | BioReagent | Used for adiponectin detection in human samples; suitable for insulin resistance, obesity, and adipokine network analysis | |
Adiponectin detection | Human Adiponectin/Acrp30 ELISA Kit | BioReagent | Used to detect human adiponectin levels; can be interpreted with insulin, leptin, and CRP | |
High-molecular-weight adiponectin detection | Human High Molecular Weight Adiponectin (HMW ADNP) ELISA Kit | BioReagent | Used to detect HMW adiponectin; suitable for refined insulin sensitivity stratification | |
Adiponectin detection | Rat Adiponectin (ADPN) ELISA Kit | BioReagent | Used for rat adiponectin detection | |
Adiponectin detection | Mouse Adiponectin (ADPN) ELISA Kit | BioReagent | Used for mouse adiponectin detection | |
High-molecular-weight adiponectin detection | Mouse High Molecular Weight Adiponectin (HMWAdiponectin) ELISA Kit | BioReagent | Used for mouse HMW adiponectin detection; suitable for refined analysis of high-fat diet models | |
Adiponectin detection | Monkey Adiponectin (ADPN) ELISA Kit | BioReagent | Used for adiponectin detection in monkey samples | |
Adiponectin antibody | Adiponectin Mouse mAb | Carrier Free, ExactAb™, Validated, High Performance, See COA | Used for adiponectin protein detection; suitable for WB, IF/IHC, or adipose tissue expression analysis | |
Adiponectin antibody | ADIPOQ Mouse mAb | Carrier Free, ExactAb™, Validated, High Performance, See COA | Used for ADIPOQ/adiponectin protein detection | |
Adiponectin antibody | Recombinant ADPN/Adiponectin Antibody | ≥90%(SDS-PAGE), See COA | Used for adiponectin protein detection and methodological validation | |
ADIPOQ intervention | ADIPOQ Human Pre-designed siRNA Set A |
| Used to knock down ADIPOQ and validate the role of adiponectin in insulin resistance and inflammatory regulation | |
ADIPOQ KO control | pLenti-ADIPOQ-sgRNA |
| Used for ADIPOQ antibody specificity validation and KO control | |
ADIPOQ KO control | pLenti-ADIPOQ-sgRNA |
| Used for ADIPOQ transcription-level KO control | |
Recombinant adiponectin | Recombinant Human Adiponectin/Acrp30 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,Azide Free,His Tag,≥95%(SDS-PAGE) | Used for human adiponectin stimulation, receptor signaling activation, and functional validation | |
Recombinant adiponectin | Recombinant Mouse Adiponectin/Acrp30 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,Azide Free,His Tag,≥95%(SDS-PAGE) | Used for adiponectin stimulation experiments in mouse systems | |
Recombinant adiponectin | Recombinant Rat Adiponectin Protein | ≥90%(SDS-PAGE) | Used for adiponectin functional research in rat systems | |
Adiponectin molecular form | adiponectin | Moligand™ | Used for adiponectin-related models or mechanistic experiments | |
Globular adiponectin | globular adiponectin | Moligand™ | Used for AdipoR receptor activation and adiponectin signaling mechanism research | |
AdipoR1 detection | Human Adiponectin Receptor 1 (ADIPOR1) ELISA Kit | BioReagent | Used for AdipoR1 detection in human samples; suitable for receptor-level analysis of adiponectin signaling | |
AdipoR2 detection | Human Adiponectin Receptor 2 (AdipoR2) ELISA Kit | BioReagent | Used for AdipoR2 detection in human samples; suitable for hepatic lipid metabolism-related research | |
AdipoR1 detection | Mouse Adiponectin Receptor 1 (ADIPOR1) ELISA Kit | BioReagent | Used for mouse AdipoR1 detection; suitable for adiponectin signaling analysis in skeletal muscle and adipose tissue | |
AdipoR2 detection | Mouse Adiponectin Receptor 2 (AdipoR2) ELISA Kit | BioReagent | Used for mouse AdipoR2 detection; suitable for hepatic lipid metabolism and fatty acid oxidation mechanism studies | |
AdipoR1 antibody | Recombinant Adiponectin receptor 1 Antibody | KD Validation | Used for AdipoR1 protein detection and knockdown validation | |
AdipoR2 antibody | Anti-Adiponectin Receptor 2/ADIPOR2 antibody | ExactAb™, Validated, 1.0 mg/mL | Used for AdipoR2 protein detection |
Table 8 Products Related to Chronic Inflammation, TNF-α, IL-6, and CRP Detection
Application Module | Cat. No. | Product Name | Grade/Specification | System Positioning |
TNF-α detection | Human TNF-α ELISA Kit | BioReagent | Used to detect TNF-α in human samples and evaluate inflammatory insulin resistance | |
TNF-α detection | Human Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit | BioReagent | Used for human TNF-α quantification; suitable for metabolic inflammation and adipose tissue inflammation analysis | |
TNF-α detection | Rat TNF-α ELISA Kit | BioReagent | Used for rat TNF-α detection | |
TNF-α detection | Rat Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit | BioReagent | Used for TNF-α quantification in rat metabolic inflammation models | |
TNF-α detection | Mouse TNF-α ELISA Kit | BioReagent | Used for mouse TNF-α detection | |
TNF-α detection | Mouse Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit | BioReagent | Used for mouse TNF-α quantification; suitable for high-fat diet and adipose tissue inflammation models | |
TNF-α detection | Mouse Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit | BioReagent | Used for mouse TNF-α detection | |
TNF-α detection | Monkey Tumor Necrosis Factor Alpha (TNF-α) ELISA Kit | BioReagent | Used for TNF-α detection in monkey samples | |
TNF-α reporter system | Lenti-TNF-α-promoter-Luc-EF1α-mCherry-T2A-Puro | 10^7TU/ml | Used for TNF-α promoter activity analysis; suitable for inflammatory signaling transcriptional regulation studies | |
Recombinant TNF-α | Recombinant Human TNF-α Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,≥95%(SDS-PAGE),expressed in E. coli; See COA | Used to establish inflammatory insulin resistance or adipose tissue inflammation models | |
Recombinant TNF-α | Recombinant Human TNF-α Protein | Carrier Free,Bioactive,ActiBioPure™,High Performance,PBS Only,≥95%(SDS-PAGE) | Used for cellular inflammatory stimulation and functional validation | |
Recombinant TNF-α | Recombinant Mouse TNF-α Protein | Carrier Free,Bioactive,ActiBioPure™,High Performance,≥95%(SDS-PAGE),See COA | Used for inflammatory stimulation experiments in mouse systems | |
TNF-α inhibition | TNF-α-IN-1 | ≥99% | Used to inhibit TNF-α-related signaling and validate mechanisms of inflammatory insulin resistance | |
TNF-α inhibition | TNF-α-IN-1 | 10mM in DMSO | Used for cellular-level TNF-α signaling intervention | |
TNF-α/IL-1β inhibition | TNF-α/IL-1β-IN-1 |
| Used for combined inflammatory cytokine intervention studies | |
IL-6 detection | Human Interleukin 6 (IL-6) ELISA Kit | BioReagent | Used for IL-6 detection in human samples and evaluation of chronic low-grade inflammation | |
IL-6 detection | Human IL-6 ELISA Kit | BioReagent | Used for human IL-6 quantification; can be interpreted with CRP and TNF-α | |
IL-6R detection | Human Interleukin 6 Receptor (IL-6R) ELISA Kit | BioReagent | Used to detect IL-6R; suitable for IL-6 signaling pathway analysis | |
IL-6 detection | Rat Interleukin 6 (IL-6) ELISA Kit | BioReagent | Used for rat IL-6 detection | |
IL-6 detection | Rat IL-6 ELISA Kit | BioReagent | Used for rat IL-6 quantification | |
IL-6R detection | Rat Interleukin 6 Receptor (IL-6R) ELISA Kit | BioReagent | Used for rat IL-6R detection | |
IL-6 detection | Mouse Interleukin 6 (IL-6) ELISA Kit | BioReagent | Used for mouse IL-6 detection | |
IL-6 detection | Mouse Interleukin 6 (IL-6) ELISA Kit | BioReagent | Used for mouse IL-6 quantification; suitable for high-fat diet and adipose tissue inflammation models | |
IL-6 detection | Mouse IL-6 ELISA Kit | BioReagent | Used for mouse IL-6 detection | |
IL-6R detection | Mouse Interleukin 6 Receptor (IL-6R) ELISA Kit | BioReagent | Used for mouse IL-6R detection | |
IL-6 antibody | IL-6 Antibody | ExactAb™, Validated, 1.0 mg/mL | Used for IL-6 protein detection | |
IL-6 antibody | IL-6 Mouse mAb | Carrier Free,ExactAb™,Azide Free,Validated,High Performance,PBS Only,≥95%(SDS-PAGE),1.0 mg/mL | Used for IL-6 protein detection | |
IL-6 reporter system | Lenti-IL-6 promoter-Luc-EF1α-mCherry-T2A-Puro | 10^8TU/ml | Used for IL-6 promoter activity detection; suitable for inflammatory signaling transcriptional regulation studies | |
Recombinant IL-6 | Recombinant Human IL-6 Protein | Carrier Free,Bioactive,ActiBioPure™,Azide Free,High Performance,His Tag,PBS Only,≥95%(SDS-PAGE) | Used for IL-6 stimulation and inflammatory metabolic abnormality model construction | |
Recombinant IL-6 | Recombinant Human IL-6 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,PBS Only,≥95%(SDS-PAGE) | Used for inflammatory stimulation experiments in human cells | |
Recombinant IL-6 | Recombinant Mouse IL-6 Protein | ActiBioPure™, Bioactive, Animal Free, Carrier Free, Azide Free, High performance, ≥96%(SDS-PAGE&HPLC) | Used for IL-6 stimulation experiments in mouse systems | |
Recombinant IL-6 | Recombinant Rat IL-6 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,Azide Free,High Performance,PBS Only,≥96%(SDS-PAGE&HPLC) | Used for IL-6 functional studies in rat systems | |
IL-6 inhibition/blocking | IL-6-IN-1 |
| Used for IL-6 signaling intervention studies | |
CRP detection | Human C Reactive Protein (CRP) ELISA Kit | BioReagent | Used for CRP detection in human samples and evaluation of systemic inflammatory burden | |
CRP detection | Human C-Reactive Protein/CRP ELISA Kit | BioReagent | Used for human CRP quantification | |
hs-CRP detection | Human Hypersensitive C Reactive Protein (hs-CRP) ELISA Kit | BioReagent | Used for refined low-grade inflammation detection; suitable for metabolic syndrome and cardiovascular risk analysis | |
hs-CRP detection | Rabbit hypersensitive C Reactive Protein (hs-CRP) ELISA Kit | BioReagent | Used for hs-CRP detection in rabbit samples | |
CRP detection | Rat C Reactive Protein (CRP) ELISA Kit | BioReagent | Used for rat CRP detection | |
hs-CRP detection | Rat Hypersensitive C Reactive Protein (hs-CRP) ELISA Kit | BioReagent | Used for low-grade inflammation detection in rats | |
CRP detection | Mouse C Reactive Protein (CRP) ELISA Kit | BioReagent | Used for mouse CRP detection | |
hs-CRP detection | Mouse Hypersensitive C Reactive Protein (hs-CRP) ELISA Kit | BioReagent | Used for low-grade inflammation and cardiometabolic risk analysis in mice | |
CRP detection | Monkey C Reactive Protein (CRP) ELISA Kit | BioReagent | Used for CRP detection in monkey samples |
7 Common Questions
7.1 Can normal fasting blood glucose exclude metabolic syndrome risk?
No. In early insulin resistance, blood glucose can be maintained within the normal range through compensatory insulin secretion. Fasting insulin, HOMA-IR, TG, adiponectin, leptin, and inflammatory cytokines are recommended for simultaneous detection.
7.2 Why should HOMA-IR be analyzed together with adipokines?
HOMA-IR reflects the degree of insulin resistance but does not explain its cause. Adiponectin, leptin, and resistin reflect adipose tissue endocrine function and help determine whether insulin resistance is associated with adipose tissue dysfunction.
7.3 What does decreased adiponectin indicate?
Decreased adiponectin usually indicates weakened protective secretory function of adipose tissue and is often associated with insulin resistance, elevated TG, increased FFA, and chronic inflammation. If high-molecular-weight adiponectin is also decreased, insulin sensitivity-related risk is clearer.
7.4 Does increased leptin indicate metabolic improvement?
No. In obesity and metabolic syndrome, leptin is often elevated, but it usually suggests increased fat mass or leptin resistance. Leptin should be analyzed together with adiponectin. An increased leptin/adiponectin ratio better indicates adipose tissue functional imbalance.
Metabolic syndrome biomarker analysis should center on insulin resistance while incorporating the adipokine network, chronic inflammation, blood glucose and lipid markers, adipose tissue inflammation, hepatic lipid metabolism, and cardiometabolic risk. Insulin and HOMA-IR are used to determine the compensatory state of glucose metabolism. Adiponectin, leptin, and resistin are used to evaluate adipose tissue endocrine function. CRP, IL-6, TNF-α, and MCP-1 are used to identify systemic inflammation and adipose tissue inflammation. TG, FFA, hepatic TG, ApoB, and oxLDL further connect lipotoxicity, fatty liver, and vascular risk.
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