Body-Fat Metabolism: AOD-9604 & GH Fragment 176–191 — study-led overview

Research groups have explored growth-hormone–derived fragments for effects on fat metabolism. This plain-English overview summarises what studies report about AOD-9604 and GH Fragment 176–191, what models were used, and where evidence is still limited.

Key takeaways

• Most findings come from animal models and ex vivo adipose-tissue experiments; controlled human efficacy data are limited and mixed.
• AOD-9604 has been reported to reduce weight gain and increase fat oxidation/lipolysis in obese mice; mechanistic work points to β₃-adrenergic pathways. Human trials mainly report safety/tolerability, with inconsistent weight outcomes.
• GH Fragment 176–191 is frequently described as antilipogenic in preclinical systems; some studies did not see direct lipolysis under their conditions.

What researchers measure

Typical readouts include body-weight change, indirect calorimetry (fat oxidation), plasma glycerol/FFA (lipolysis indices), and adipose-tissue assays (lipolytic vs. lipogenic enzyme activity). In ex vivo work, investigators test isolated human or rodent adipose tissue to observe shifts in lipolysis or lipogenesis under controlled conditions.

Study snapshots (models → what was measured → one-line summary)

• Obese mice (in vivo): Chronic AOD-9604 reduced weight gain, increased fat oxidation and lipolysis; β₃-AR involvement suggested. Endocrinology, 2001 · AJP-Endocrinol Metab, 2001
• Rodent & human adipose (ex vivo): AOD peptides increased lipolysis and reduced lipogenesis; obese-animal weight gain attenuated. AJP-Endocrinol Metab, 2000
• GH Fragment 176–191 (rat adipose): Antilipogenic activity observed; no significant direct lipolysis under assay conditions. Endocrinology, 1993
• Reviews/overviews: Narrative and mechanistic discussions place hGH fragments within broader fat-metabolism research. Front Endocrinol, 2022
• Human trials (AOD-9604): Safety/tolerability reported across multiple RCTs; weight-loss efficacy signals inconsistent across studies and protocols. J Endocrinol Metab, 2013 · J Endocrinol Metab, 2014

How to read these results

Findings are model-dependent. Rodent energy balance, strain, housing and diet can shift outcomes; adipose depots (subcutaneous vs. visceral) also respond differently. Chromatography and assay methods matter: two labs can measure related endpoints and still report different magnitudes. For human relevance, controlled trials with clear endpoints are the critical step.

What remains uncertain

• Human efficacy: large, well-controlled trials with agreed endpoints are limited; results to date are mixed.
• Standardisation: formulations, dosing paradigms and outcome measures vary across studies.
• Mechanisms in humans: β₃-adrenergic signalling is implicated preclinically; confirmation and relevance in human metabolism require further work.

Further reading

1. Heffernan et al. (2001) Endocrinology — obese mice & β₃-AR work.
2. Heffernan et al. (2001) AJP-Endocrinol Metab — fat oxidation & lipolysis in vivo.
3. Heffernan et al. (2000) AJP-Endocrinol Metab — ex vivo human/rodent adipose assays.
4. Wu et al. (1993) Endocrinology — 176–191 antilipogenic, non-lipolytic in assay.
5. Habibullah et al. (2022) Review — GH fragment biology overview.
6. Stier et al. (2013) — AOD-9604 safety/tolerability across RCTs.

Internal links

• QC Hub — chromatograms, method notes, and batch documents.
• All research materials — browse catalogue.

Updated: 02 Oct 2025