Peptide Medix product catalog

ET
Editorial Team
August 16, 2026 5 min read

Diabetes and metabolism peptide research centres on three reagent groups: the islet hormones and their processing fragments, the incretin axis that has reshaped the field over the past decade, and the adipokines and hepatokines that link fat and liver to glucose handling. Our diabetes topic page collects the peptide standards, antisera, tracers and immunoassay kits used across that literature. This guide explains which families sit inside the topic, what each is ordered for, and which reagent format answers which question.

What sits under the diabetes topic

A family is filed here when its parent peptide is produced by the pancreatic islet, acts on glucose or lipid metabolism, or is used as a marker of metabolic state in animal and cell models. That includes hormones secreted by beta, alpha, delta and PP cells; gut-derived incretins and their analogs; adipose- and liver-derived signalling peptides; and the myokines that connect exercise physiology to metabolic phenotyping. Heavy overlap exists with obesity — leptin, ghrelin and amylin sit in both — and with cardiovascular work through apelin and adrenomedullin. Every item is supplied for in-vitro and approved animal research only.

Islet hormones and processing markers

  • Insulin — human, rat, mouse, bovine and porcine sequences, plus proinsulin and analog standards. The species distinction matters: rodents express two insulin genes, and immunoassays calibrated on human insulin misreport rodent samples.
  • C-peptide — the connecting peptide released stoichiometrically with insulin and cleared more slowly, which makes it the preferred index of endogenous secretion when exogenous insulin is present in a model.
  • Glucagon — the alpha-cell counter-regulatory hormone; assays here are notoriously cross-reactive with other proglucagon products, so antibody specificity is the critical spec.
  • Amylin (IAPP) — co-secreted with insulin; also the amyloidogenic peptide of islet amyloid, so both soluble standards and aggregation-competent preparations are ordered.
  • Somatostatin and pancreatic polypeptide — the delta- and PP-cell hormones, used both as standards and as immunohistochemical markers for islet composition.
  • Preptin — a proIGF-2-derived peptide co-secreted from beta cells, a smaller but active literature.

The incretin axis

This is the fastest-moving part of the topic, and the reason many laboratories arrive at the catalog at all:

  • GLP-1 — GLP-1(7–36)amide and GLP-1(7–37) as active forms, the inactive (9–36) metabolite, and the antagonist exendin(9–39). The incretin pathway hub maps the whole axis.
  • GIP — glucose-dependent insulinotropic polypeptide, the second incretin, now central to dual-agonist pharmacology.
  • Exendin and lixisenatide — the Gila monster-derived agonist lineage and its clinical descendants, ordered as reference standards.
  • Oxyntomodulin and glicentin — the other proglucagon products; distinguishing them from glucagon is the central analytical problem in this family.
  • GLP-2 — the intestinotrophic sibling peptide, studied in gut adaptation rather than glycaemia.
  • Secretin and PYY — gut hormones frequently measured alongside the incretins in nutrient-challenge protocols.

Adipokines, hepatokines and myokines

  • Adiponectin — the insulin-sensitising adipokine; supplied as fragments and standards, with the caveat that the native protein circulates as multimers that fragment standards cannot reproduce.
  • Leptin and resistin — the classical adipokines linking adiposity to insulin action.
  • Ghrelin and obestatin — the acylated and unacylated ghrelin forms have different activities, and the octanoyl modification is labile, so sample handling determines what you measure.
  • FGF-19 and FGF-23 — endocrine FGFs governing bile-acid and phosphate metabolism respectively, both now standard in metabolic phenotyping panels.
  • Betatrophin (ANGPTL8) — beta-cell proliferation claims for this protein were retracted, but it remains an actively studied lipid-metabolism regulator; a good example of why catalog inclusion is about research use, not settled biology.
  • Irisin and FNDC5 — the exercise-induced myokine and its precursor, where antibody specificity has been the subject of published controversy.
  • Visfatin, vaspin and nesfatin — adipose-derived peptides with metabolic and appetite-related literatures.
  • INSL5 — a colonic enteroendocrine peptide of the relaxin superfamily, studied in gut–metabolic signalling.

Which formats the diabetes topic contains

Synthetic peptide standards serve as assay calibrators, receptor agonists and antagonists. ELISA, EIA and RIA kits carry most of the workload in this topic — insulin, C-peptide, GLP-1, glucagon and adipokine quantitation in plasma and islet supernatant is routine, and kit choice defines your data quality. Polyclonal antisera support islet immunohistochemistry and Western detection. Labeled peptides supply I-125 tracers for classical RIA and fluorescent GLP-1 analogs for receptor-trafficking imaging. Magnetic beads underpin multiplex metabolic panels.

How laboratories choose within a family

Four decisions recur. Species is first and most consequential — human-calibrated insulin and leptin assays systematically misreport rodent samples; check species reactivity on every item. Processing state is second: total versus active GLP-1, acylated versus unacylated ghrelin, intact versus C-terminal FGF-23. Choose the analyte, then the kit. Cross-reactivity is third and is the defining problem of the proglucagon family; a glucagon assay that cross-reacts with glicentin will overstate glucagon in gut-rich samples. Fourth, peptide plus antibody versus a kit: for concentration in a sample, a validated kit is faster and more reproducible; for mechanism, localisation or custom assay development, order the components separately.

Handling notes for this topic

Two issues cause most avoidable failures. Active GLP-1 and GIP are cleaved by DPP-4 within minutes in collected blood, so plasma for active-form assays needs a DPP-4 inhibitor at collection — no reagent choice compensates for that. Acyl-ghrelin loses its octanoyl group unless samples are acidified and protease-inhibited. Beyond that, standard practice applies: sealed lyophilised vials at −20 °C, gentle reconstitution, single-use aliquots, no repeated freeze–thaw. Amylin and other aggregation-prone sequences need particular care with solvent choice — see peptide solubility, the storage guide and the COA guide.

Where to go next

Browse the full diabetes topic, the pancreas and islets hub or the incretin pathway hub. Adjacent guides cover the obesity and appetite section, which shares the adipokine families, and the assay kit type guide for choosing between ELISA, EIA and RIA formats.

Frequently Asked Questions

Why measure C-peptide instead of insulin?
C-peptide is released in equal molar amounts with insulin but cleared far more slowly and is not extracted by the liver on first pass, so it tracks endogenous secretion more faithfully. It is also unaffected by exogenous insulin administered in a model, which insulin assays cannot distinguish from endogenous hormone.
What is the difference between total and active GLP-1 assays?
Active assays detect only GLP-1(7–36)amide and (7–37); total assays also detect the DPP-4-cleaved (9–36) metabolite, giving values several-fold higher. Neither is wrong — they answer different questions. Active-form measurement additionally requires a DPP-4 inhibitor in the collection tube, or the analyte degrades before analysis.
Can I use a human insulin ELISA on mouse plasma?
Generally not without validation. Mouse insulin 1 and insulin 2 differ from human insulin at several residues, and human-calibrated antibodies show variable and often poor recognition. Use a rodent-specific kit, and check whether it reports both mouse insulin isoforms or only one.
Why are glucagon assays considered unreliable?
Because proglucagon is processed differently in pancreas and gut, producing glucagon, glicentin, oxyntomodulin and major proglucagon fragment — all sharing sequence. Antibodies raised against the mid-region cross-react broadly. Sandwich assays requiring both the N- and C-terminus of glucagon are substantially more specific; check the epitope specification before ordering.
How should ghrelin samples be collected?
For acyl-ghrelin, collect into EDTA with a protease inhibitor, acidify promptly, and keep cold — the octanoyl ester on Ser3 hydrolyses quickly at neutral pH, converting acyl to des-acyl ghrelin and shifting your ratio. Total ghrelin assays are more forgiving but answer a different question.
Are these reagents suitable for studying diabetes in people?
No. Everything in the research catalog is supplied for in-vitro assays and approved animal research. Several molecules here have approved therapeutic counterparts, but catalog material is not manufactured to pharmaceutical standards and is not for human, veterinary or diagnostic use.

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