Obesity &
Adipokine
Research Assays
Validated sandwich ELISA kits for adipose-derived hormones and metabolic inflammation biomarkers Adiponectin, Leptin, Resistin, Visfatin, Ghrelin, FGF-21, TNF-a, IL-6, and FABP4. Multi-species validated. Essential for obesity mechanism studies, GLP-1 response monitoring, and metabolic syndrome characterisation.
Browse Adipokine Assays Adipokine BiologyAdipokine Biology & Obesity Research
Adipose tissue is an active endocrine organ, secreting a range of bioactive proteins collectively termed adipokines that regulate energy homeostasis, insulin sensitivity, appetite, inflammation, and vascular biology. In obesity, dysfunctional adipose tissue produces an altered adipokine profile: low adiponectin, high leptin (with hypothalamic resistance), elevated resistin, and increased inflammatory cytokines. This adipokine dysregulation is mechanistically linked to insulin resistance, type 2 diabetes, NAFLD, and cardiovascular disease making adipokine quantification central to both obesity pathophysiology research and GLP-1 agonist mechanism-of-action studies.
Adipokines act locally within adipose tissue, systemically via the circulation, and centrally in the hypothalamus. Their measurement in serum/plasma provides an integrated readout of adipose tissue function. Key adipokines studied in obesity research fall into three functional groups: insulin-sensitising adipokines (Adiponectin), appetite-regulating hormones (Leptin, Ghrelin), and pro-inflammatory adipokines (Resistin, Visfatin/NAMPT, TNF-a, IL-6).
GLP-1 receptor agonists (Tirzepatide, Semaglutide, Liraglutide) exert metabolic effects beyond glucose control improving adipokine profiles, reducing hepatic fat, and modulating adipose tissue inflammation. Pairing GLP-1 drug PK ELISA with adipokine biomarker panels enables researchers to correlate drug exposure with metabolic response, a design increasingly used in mechanism-of-action studies and clinical pharmacodynamics.
Adipose-Derived Hormone ELISA Kits
Sandwich ELISA kits for quantification of core adipokines in serum, plasma, tissue lysate, and cell culture supernatant. Validated in human, rat, and mouse. No cross-reactivity between adipokines confirmed in panel studies.
The most abundant adipokine in circulation (2 20 g/mL). Secreted predominantly by healthy, small adipocytes. Inversely correlated with adiposity levels fall in obesity, T2DM, and metabolic syndrome, and rise with weight loss and GLP-1 agonist therapy. Acts via AdipoR1/R2 to activate AMPK (insulin-sensitising, fatty acid oxidation) and PPAR-a in liver and muscle. High-molecular-weight (HMW) adiponectin is the most biologically active form. Low adiponectin is an independent predictor of T2DM and cardiovascular risk.
Secreted by adipocytes in proportion to fat mass. Signals to hypothalamic arcuate nucleus via LepRb to suppress appetite and increase energy expenditure. In obesity, circulating leptin is paradoxically elevated but central hypothalamic signalling is impaired (leptin resistance). Monitoring leptin alongside GLP-1 drug levels and adiponectin provides an integrated metabolic readout. The Adiponectin:Leptin ratio (A/L) =1.0 is a validated marker of insulin resistance.
Cysteine-rich protein secreted by adipocytes (rodents) and macrophages/monocytes (humans). In rodent models, resistin is directly linked to insulin resistance via IRS-1 phosphorylation interference. In humans, resistin is more relevant as a pro-inflammatory mediator elevated in obesity, T2DM, and inflammatory states. Also elevated in NAFLD and NASH. Useful complement to adiponectin in metabolic syndrome panels.
Secreted predominantly by visceral adipose tissue (hence Visfatin). The same protein is NAMPT the rate-limiting enzyme in the NAD+ biosynthesis salvage pathway. Elevated in visceral obesity, T2DM, metabolic syndrome, and inflammatory conditions. Circulating visfatin/NAMPT correlates better with visceral fat than BMI, making it a useful marker for visceral adiposity specifically. Also exhibits pro-inflammatory cytokine-like activity.
Secreted primarily by stomach X/A-like cells. The only known orexigenic (appetite-stimulating) gut hormone rises before meals, falls after eating. Acts on hypothalamic GHS-R1a to promote hunger and fat deposition. Ghrelin falls significantly with GLP-1 agonist therapy and bariatric surgery, contributing to appetite suppression beyond GLP-1R signalling. Total vs acylated (active) ghrelin measurement provides different biological insights.
Adipocyte Fatty Acid Binding Protein 4 intracellular lipid chaperone released into circulation by adipocytes and macrophages. Circulating FABP4 is elevated in obesity, metabolic syndrome, and T2DM. Mediates crosstalk between adipose tissue and the liver/vasculature. FABP4 is an emerging predictive biomarker for T2DM and cardiovascular risk, independent of conventional markers. Also elevated in NAFLD and acts as a mechanistic link between adiposity and hepatic lipid accumulation.
Inflammatory & Crossover Biomarkers
Obesity-associated chronic low-grade inflammation drives insulin resistance, NAFLD progression, and cardiovascular risk. The inflammatory biomarkers below are measurable in circulation and serve as mechanistic readouts of adipose tissue-mediated inflammatory signalling.
Tumour Necrosis Factor-alpha secreted by activated macrophages within adipose tissue (ATMs) in obesity. TNF-a impairs insulin signalling via serine phosphorylation of IRS-1, promotes lipolysis releasing excess FFAs, and drives NAFLD progression. Krishgen TNF-a ELISA is calibrated against NIBSC/WHO International Reference Standard enabling accurate cross-study comparisons and regulatory-grade reporting. Key GLP-1 mechanism-of-action endpoint: semaglutide and tirzepatide reduce adipose tissue TNF-a expression in preclinical models.
Interleukin-6 dual pro- and anti-inflammatory cytokine with complex metabolic roles. In obesity, IL-6 secreted by adipose tissue drives hepatic acute-phase protein production (CRP, fibrinogen) and contributes to insulin resistance via JAK-STAT3 pathway interference. However, muscle-secreted IL-6 during exercise has insulin-sensitising effects context matters. NIBSC/WHO-calibrated Krishgen IL-6 ELISA is validated in human serum, plasma, tissue lysate, and cell supernatant.
Fibroblast Growth Factor 21 secreted primarily by the liver in response to fasting, carbohydrate excess, and hepatic stress. A key regulator of adipose tissue browning, hepatic lipid oxidation, and insulin sensitisation. FGF-21 is elevated in NAFLD and NASH (a diagnostic biomarker) and is also a GLP-1 co-target several next-generation metabolic therapies combine GLP-1R agonism with FGF-21R agonism (e.g., efruxifermin, pegozafermin). FGF-21 monitoring links obesity adipokine biology with hepatotoxicity and drug response endpoints.
Endogenous GLP-1 (7-36 amide active; 7-37 amide active; 9-36 amide inactive) is secreted by intestinal L-cells postprandially. Note: These endogenous GLP-1 ELISA measure your patient's own GLP-1, not the drug. They are relevant for studying natural incretin physiology, L-cell function, and baseline GLP-1 secretion in T2DM vs healthy subjects. They do not measure Semaglutide, Liraglutide, or Tirzepatide which require dedicated drug ELISA (KBI5030, KBI5020, KOD1027).
Pairing GLP-1 Drug PK with Adipokine Endpoints
GLP-1 agonist mechanism-of-action studies benefit from simultaneous measurement of drug exposure (drug PK ELISA) and metabolic/inflammatory response (adipokine biomarker ELISA). The table below shows a recommended multi-assay panel design for GLP-1 mechanism studies.
| Assay Purpose | Biomarker | Expected Response to GLP-1 Agonist | Krishgen Kit |
|---|---|---|---|
| Drug Exposure | Tirzepatide / Semaglutide / Liraglutide | Primary PK endpoint confirms drug present and quantifies exposure | KOD1027 / KBI5030 / KBI5020 |
| Insulin Sensitisation | Adiponectin | Increases particularly HMW form; marks improved insulin sensitivity | Search Catalogue |
| Appetite Regulation | Leptin | Decreases with weight loss; leptin sensitivity may improve | Search Catalogue |
| Appetite Regulation | Ghrelin | Decreases contributes to appetite suppression beyond GLP-1R agonism | Search Catalogue |
| Inflammation | TNF-a | Decreases reflects reduced adipose tissue macrophage activation | NIBSC-calibrated |
| Inflammation | IL-6 | Decreases in adipose compartment; hepatic IL-6 may normalise | NIBSC-calibrated |
| Hepatic Response | FGF-21 | May decrease as hepatic steatosis improves; GLP-1/FGF-21 combo context | Hepatotoxicity Page |
| Visceral Adiposity | Visfatin / NAMPT | Decreases with visceral fat reduction | Search Catalogue |
Obesity & Adipokine Assay Reference Table
All Krishgen ELISA kits for obesity and metabolic research. Sandwich ELISA, validated in human, rat, and mouse. CoA and validation data on request.
| Biomarker | Function | Disease Relevance | Format | Species | Link |
|---|---|---|---|---|---|
AdiponectinInsulin-sensitising adipokine | AMPK activation lipid oxidation anti-inflammatory | MetSynT2DMNAFLD | Sandwich ELISA | Human / Rat / Mouse | Search |
LeptinAppetite / energy homeostasis | Hypothalamic satiety signalling via LepRb | ObesityLeptin resistance | Sandwich ELISA | Human / Rat / Mouse | Search |
ResistinPro-inflammatory adipokine | Insulin resistance IRS-1 serine phosphorylation | T2DMNAFLDInflammation | Sandwich ELISA | Human / Rat / Mouse | Search |
Visfatin / NAMPTVisceral adipose marker | NAD+ biosynthesis visceral adiposity marker | Visceral obesityInflammation | Sandwich ELISA | Human / Rat / Mouse | Search |
Ghrelin (Total)Orexigenic gut hormone | GHS-R1a activation hunger stimulation | AppetiteGLP-1 response | Sandwich ELISA | Human / Rat / Mouse | Search |
FABP4 / aP2Adipocyte lipid chaperone | Adipose-liver-vascular lipid crosstalk | MetSynCV riskNAFLD | Sandwich ELISA | Human / Rat / Mouse | Search |
TNF-aPro-inflammatory cytokine | Adipose macrophage output IRS-1 inhibition | Obesity inflammationInsulin resistance | Sandwich ELISA (NIBSC) | Human / Rat / Mouse | View |
IL-6Pleiotropic cytokine | Hepatic acute-phase response adipose inflammation | Metabolic inflammationCRP induction | Sandwich ELISA (NIBSC) | Human / Rat / Mouse | View |
FGF-21Hepatokine steatosis marker | Adipose browning hepatic lipid oxidation | NAFLDNASHGLP-1 target | Sandwich ELISA | Human / Rat / Mouse | View |
GLP-1 (Total + Active)Endogenous incretin | L-cell secretion incretin physiology | T2DMIncretin deficiency | Sandwich ELISA | Human / Rat / Mouse | Search |
Frequently Asked Questions
The A/L ratio (adiponectin g/mL leptin ng/mL) is a validated index of insulin resistance values below 1.0 indicate high metabolic risk, independent of BMI. Requires validated, specific ELISA for both markers measured in the same sample. Krishgen provides both assays in the same validated platform for human, rat, and mouse.
No they are entirely different assays for different analytes. Drug ELISA (KBI5030 Semaglutide, KOD1027 Tirzepatide, etc.) detect the pharmaceutical compound. Endogenous GLP-1 ELISA detect the naturally secreted hormone from intestinal L-cells. Both are useful in GLP-1 agonist mechanism studies but must not be confused or substituted for each other.
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Our scientific team can advise on adipokine panel design, multi-analyte studies, and GLP-1 mechanism-of-action study protocols.
