Molecule guides
Obesity and Appetite Reagents: Which Families, Antisera and Kits to Order
A circuit, not a tissue: peripheral hunger and satiety signals, the hypothalamic neuropeptides they act on, and the adipokines — mapped to the reagents that study them.
This topic is defined by a circuit, not by a single organ. Signals from adipose tissue and the gut inform the hypothalamic arcuate nucleus about energy availability, and there two antagonistic neuronal groups — NPY/AgRP against POMC/CART — determine feeding behaviour through the melanocortin receptors. Everything researchers use along that pathway — immunoassay kits, tracers, antisera and peptide standards — is gathered on our obesity topic page. Below we go through the families in the topic, why laboratories buy each one, and which format answers which question.
What the obesity topic covers
A family belongs in this section when published models show the parent peptide affecting energy expenditure, food intake or adipose biology. In practice that spans satiety and hunger signals from the periphery, neuropeptides of the hypothalamus, the melanocortin system, the adipokines, and the newer browning-related peptides and myokines. The overlap with neighbouring topics is intentional and large: adiponectin and leptin are shared with diabetes, while galanin, orexin and NPY are also listed under neuropeptides. Every product is for in-vitro use and approved animal research, and none of it is a weight-management product.
Signals from the periphery: hunger, satiety, adiposity
- Leptin — the fat-derived adiposity signal whose discovery founded this field; available as recombinant standards, fragments and antagonists, together with the kits and antisera used for measuring it in rodent plasma.
- Ghrelin — the one circulating orexigenic hormone that is firmly established. Receptor activity belongs to the octanoylated form, while des-acyl ghrelin supports a separate literature of its own.
- Obestatin — encoded on the same preproghrelin transcript, with a contested anorexigenic literature; a good example of a family included because it is actively studied rather than because the biology is agreed.
- PYY — PYY(3–36) is the Y2-selective satiety species, while intact PYY(1–36) has a different receptor preference, so the fragment always needs stating.
- Amylin and oxyntomodulin — satiety peptides released alongside other hormones and now pivotal to research on combination pharmacology.
- CCK — the first satiety hormone identified; the standard active species is sulfated CCK-8, and losing the sulfate abolishes potency at CCK-A.
- GLP-1 — acts on appetite in addition to glucose control; the incretin pathway hub covers it.
Hypothalamic and melanocortin families
- NPY — the most powerful orexigenic peptide yet characterised, with Y1-, Y2- and Y5-selective fragments available for taking the circuit apart.
- AgRP — a natural inverse agonist at MC3R and MC4R, co-expressed with NPY; the fragment normally used is AgRP(83–132).
- POMC, MSH and melanocortin — the anorexigenic branch. Of all the nodes implicated in monogenic obesity, α-MSH acting at MC4R is the best validated, and receptor-selective analogues are listed on the family page.
- CART — co-expressed with POMC; CART(55–102) is the fragment most often used as the active form.
- MCH — melanin-concentrating hormone, an appetite-stimulating peptide from the lateral hypothalamus.
- Orexin — orexin-A and orexin-B tie arousal to feeding and sit at the interface between sleep and metabolism.
- Galanin and spexin — pull in opposite directions on energy balance and macronutrient choice; spexin is a newer arrival whose literature is growing fast.
- Nesfatin-1, neuromedin U and neuromedin S — anorexigenic hypothalamic peptides used in receptor studies and for mapping circuits.
- GnIH/RFRP — connects energy status with the reproductive axis, and is ordered where a study spans both.
Families from adipose tissue, muscle and browning research
- Adiponectin and resistin — the original adipokines; note that adiponectin's activity depends on which multimeric form it is in, something no peptide fragment can mimic.
- Adipocyte-derived factors — a catch-all family page collecting the less well studied peptides secreted from fat.
- Irisin and FNDC5 — the browning candidate induced by exercise, and the protein it derives from. Since the specificity of antibodies in this family has been challenged in print, blocking-peptide controls and validated reagents matter more here than they usually would.
- Meteorin-like (Metrnl) and musclin — myokines studied in exercise adaptation and thermogenesis.
- Apelin and adropin — metabolic peptides forming the bridge between this topic and cardiovascular research.
- Visfatin and vaspin — fat-derived peptides featuring in insulin-sensitivity studies.
Formats found in the obesity topic
Synthetic peptide standards dominate here: receptor pharmacology, assay calibration and central administration in rodents all start from them, and receptor-selective fragments are the main way of distinguishing melanocortin-receptor from Y-receptor effects. Adipokines, PYY, ghrelin and leptin in plasma are measured with EIA and ELISA kits. Polyclonal antisera are used for hypothalamic immunohistochemistry, where co-staining POMC/CART with NPY/AgRP markers is standard practice. Labelled peptides supply fluorescent ligands for receptor-trafficking imaging and tracers for binding assays, while magnetic beads underpin multiplex metabolic panels.
Choosing within a family
Fragment choice comes first and goes wrong most often: CART(55–102) is not CART(62–102), AgRP(83–132) is not intact AgRP, and PYY(3–36) is not PYY(1–36). Substituting one for another changes the pharmacology, not just the potency. Next comes modification: amidated C-termini, acylated ghrelin and sulfated CCK-8 are functional requirements rather than optional extras — see C-terminal amidation. Species follows, because human and rodent sequences diverge in several of these families and antibody cross-reactivity should never be assumed, so check species reactivity. Finally, if you need a concentration from a sample, a validated kit beats assembling components; if you need mechanism or localisation, buy the antiserum and the peptide separately.
Handling notes specific to this topic
Three cautions stand out. Acyl-ghrelin is delicate — acidify and add protease inhibitors, or what you actually quantify is des-acyl ghrelin. Amylin is amyloidogenic and therefore aggregates, so prepare solutions fresh in appropriate solvents and expect irreproducibility from stock that has been standing (see peptide solubility). And peptides destined for central administration should have their vehicle compatibility confirmed in advance rather than discovered during the experiment. Otherwise the normal workflow applies: vials sealed at −20 °C, aliquots for single use, and minimal freeze–thaw; the storage, aliquoting and COA guides give the detail.
Where to look next
Look through the whole obesity topic, the melanocortin pathway hub or the adipose tissue hub. Also useful are the metabolism and diabetes section and the neuropeptide section, with which most of the hypothalamic families are shared.
Questions
PYY(1–36) or PYY(3–36) — which do I need?
They are different reagents, not two grades of the same one. Cleavage by DPP-4 yields PYY(3–36), the Y2-selective species that satiety studies use; the intact PYY(1–36) retains activity at Y1 and produces a different profile in feeding experiments. Always specify the fragment. Both are catalogued because both are used in published work.
Why must CCK be supplied sulfated?
Because binding with high affinity at CCK-A depends on the sulfate group on the tyrosine at position 7 counting in from the C-terminus. Without it, CCK-8 retains activity at CCK-B but is almost powerless at CCK-A. Since acidic conditions readily remove the sulfate, confirm it on the COA rather than taking it for granted.
Can peptide standards be used for central administration work?
Within an approved animal protocol they are the standard tool, but check three things first: solubility at your intended concentration, endotoxin status, and whether the peptide is compatible with your vehicle. Unless an individual item states otherwise, research-grade peptides are neither endotoxin-controlled nor sterile — which is a real consideration for intracerebroventricular work.
What makes irisin contentious?
Two things. The antibodies used in the early measurements were later shown to bind unrelated proteins, and the start codon of human FNDC5 is atypical. None of that means the protein is not real, and research continues, but reagent validation deserves more attention here than elsewhere: where a conclusion depends on absolute quantitation, use blocking-peptide controls and antibodies that have been validated by mass spectrometry.
Is α-MSH enough, or do I need selective melanocortin ligands?
Because α-MSH acts at MC1R, MC3R, MC4R and MC5R without discrimination, it cannot attribute an effect on feeding to a single receptor. That is precisely why the melanocortin family page also lists selective antagonists and agonists: use α-MSH as the natural ligand, and the selective tools to establish which receptor is responsible.
Are these peptides intended for weight loss?
They are not. Everything in the research catalog is for in-vitro assays and approved animal studies. A few of the molecules in this topic have licensed therapeutic equivalents, yet catalog material is not produced to pharmaceutical standards.