Sexual Function & Performance
12/08/2026
Peptides and growth factors are biological signalling molecules that can influence how cells obtain, store and use energy. Research is investigating how specific molecules interact with pathways involved in glucose utilisation, insulin signalling, mitochondrial function, fatty-acid metabolism, energy expenditure, appetite regulation and cellular energy homeostasis.
Energy metabolism involves a complex network of processes through which the body converts nutrients into usable energy. At the cellular level, mitochondria play a central role in producing ATP through oxidative metabolism, while glucose and fatty acids provide important energy substrates.
Research into peptides and metabolic signalling explores pathways relevant to:
It is important to distinguish between different types of biological compounds. IGF-1 is a peptide growth factor involved in growth and metabolic signalling, while GLP-1 is an endogenous incretin hormone involved in glucose regulation and energy balance. Retatrutide is an experimental multi-receptor agonist targeting GLP-1, GIP and glucagon receptors. MOTS-c is a mitochondria-derived peptide being investigated in metabolic research, while AOD-9604 is a synthetic peptide fragment derived from human growth hormone that has primarily been investigated in relation to lipid metabolism.
The strength and type of evidence therefore varies considerably between compounds.
Insulin-like growth factor-1 (IGF-1) is a peptide growth factor involved in growth, development, cellular proliferation and metabolism. IGF-1 binds primarily to the IGF-1 receptor (IGF-1R), activating intracellular signalling pathways including PI3K/Akt and MAPK.
IGF-1 signalling interacts with pathways involved in glucose metabolism, protein synthesis and nutrient utilisation. Its biological effects are closely connected with the broader growth-hormone/IGF-1 axis, which contributes to the regulation of growth and metabolic processes.
At the cellular level, IGF-1 signalling can influence glucose transport and utilisation as well as anabolic processes that require cellular energy.
The broader research pathway can therefore be summarised as:
IGF-1 → IGF-1R → PI3K/Akt & MAPK signalling → glucose utilisation / protein synthesis → cellular growth & metabolic activity
IGF-1 should not simply be characterised as an “energy-boosting” molecule. Its physiological effects are considerably broader and include growth, anabolic signalling and glucose regulation.
The distinction between physiological IGF-1 signalling and therapeutic administration is particularly important because systemic manipulation of the IGF-1 pathway can produce effects beyond those observed in isolated cellular or experimental models.
Glucagon-like peptide-1 (GLP-1) is an endogenous peptide hormone involved in glucose regulation, insulin secretion, appetite and energy balance.
GLP-1 receptor activation influences pancreatic β-cells and other tissues, increasing glucose-dependent insulin secretion and reducing glucagon secretion when glucose concentrations are elevated. GLP-1 signalling also influences gastric emptying and central appetite regulation.
The broader physiological pathway can therefore be summarised as:
GLP-1 → GLP-1 receptor → insulin/glucagon regulation → glucose homeostasis → appetite & energy balance
GLP-1 receptor signalling has been extensively investigated in humans and forms the basis of established pharmacological treatments for metabolic disease.
However, GLP-1 signalling should not be described simply as increasing cellular ATP production. Its principal metabolic effects involve glucose regulation, appetite, gastrointestinal signalling and whole-body energy balance.
This distinction is important when interpreting research because changes in appetite, food intake or body weight are different biological outcomes from directly increasing mitochondrial ATP production.
Retatrutide (LY3437943) is an experimental peptide that activates three metabolic hormone receptors:
Retatrutide is sometimes referred to informally as “GLP-3” because of its triple-receptor activity. However, GLP-3 is not the formal name of a naturally occurring human hormone. Retatrutide is the scientifically appropriate name for the compound.
Retatrutide has attracted considerable research interest because it combines incretin signalling with glucagon-receptor activation. Research has investigated its effects on glucose regulation, insulin signalling, appetite, body weight, lipid metabolism and energy expenditure.
The three receptor pathways contribute different biological signals. GLP-1 and GIP signalling can influence glucose-dependent insulin secretion, appetite and nutrient handling, while glucagon-receptor activation is associated with effects on hepatic metabolism, lipid utilisation and energy expenditure.
The broader research pathway can therefore be summarised as:
GLP-1R + GIPR + glucagon receptor → integrated metabolic signalling → glucose regulation + appetite regulation + lipid metabolism + energy expenditure
Human clinical research has investigated retatrutide in people with obesity and type 2 diabetes, with studies reporting substantial changes in body weight and metabolic measures.
This makes retatrutide particularly relevant to research examining how multiple metabolic pathways can be targeted simultaneously.
However, retatrutide remains an investigational compound, and evidence concerning retatrutide should not automatically be applied to other compounds simply because they are marketed as “GLP-3” or described as triple agonists.
For energy-metabolism research, retatrutide is therefore relevant as an example of how multiple hormonal signalling pathways can be manipulated to influence energy balance, nutrient utilisation and metabolic regulation.
MOTS-c is a mitochondria-derived peptide that has attracted interest in experimental research examining metabolic regulation.
Preclinical research has investigated MOTS-c in relation to glucose metabolism, insulin sensitivity, AMPK signalling, exercise-related metabolic adaptation and cellular stress responses.
AMPK is an important cellular energy sensor that responds to changes in the balance between cellular energy demand and energy availability. AMPK activation can influence processes including glucose uptake, fatty-acid oxidation and cellular energy homeostasis.
The proposed research pathway can therefore be summarised as:
MOTS-c → metabolic signalling / AMPK-related pathways → glucose utilisation & fatty-acid metabolism → cellular energy homeostasis
MOTS-c is particularly interesting because it links mitochondrial biology with broader metabolic signalling.
However, the majority of evidence remains preclinical. Findings observed in cellular and animal models do not establish that administration of MOTS-c improves mitochondrial energy production, exercise capacity or metabolic health in humans.
MOTS-c should therefore be regarded as an experimental metabolic research peptide, rather than an established metabolic treatment.
AOD-9604 is a synthetic peptide fragment derived from the C-terminal region of human growth hormone. It has primarily been investigated in relation to lipid metabolism and fat mobilisation.
Experimental research has examined whether AOD-9604 can influence lipolysis and aspects of adipose-tissue lipid accumulation.
The proposed metabolic pathway can therefore be simplified as:
AOD-9604 → adipose-tissue signalling → lipolysis / lipid metabolism → altered energy-substrate availability
Research interest in AOD-9604 has largely focused on its potential effects on fat metabolism rather than direct stimulation of mitochondrial ATP production.
It is therefore more accurate to describe AOD-9604 as an experimental peptide investigated in relation to lipid metabolism than as a compound that directly “boosts metabolism.”
Evidence for clinically meaningful effects in humans remains limited, and findings from experimental models should not automatically be interpreted as evidence of increased whole-body energy expenditure or improved metabolic health.
| Peptide / growth factor | Biological pathway investigated | Primary research area |
|---|---|---|
| IGF-1 | IGF-1R, PI3K/Akt, MAPK, glucose & anabolic signalling | Growth & metabolism |
| GLP-1 | Insulin, glucagon, appetite & glucose regulation | Glucose & energy balance |
| GLP-3 | GLP-1R + GIPR + glucagon receptor | Glucose, lipid & energy metabolism |
| MOTS-c | AMPK-related metabolic signalling | Mitochondrial & metabolic research |
| AOD-9604 | Lipolysis & lipid metabolism | Fat metabolism |
| BPC-157 | Cellular and vascular signalling | Primarily tissue repair |
Research into how the body produces and uses energy involves several interconnected biological systems.
Mitochondria are central to aerobic energy production, converting energy stored in nutrients into ATP through processes including the citric-acid cycle and oxidative phosphorylation.
Glucose metabolism determines how carbohydrates are taken up, broken down and ultimately used to generate energy or stored for later use.
Fat metabolism provides another major energy source, with fatty acids being mobilised from adipose tissue and oxidised within mitochondria.
Metabolic signalling pathways help cells determine whether nutrients and energy are abundant or limited. Pathways involving insulin, IGF-1, AMPK, GLP-1, GIP and glucagon help coordinate these responses.
Peptides can interact with these systems at different levels.
Some influence hormonal regulation.
Some affect glucose utilisation.
Some influence lipid mobilisation and oxidation.
Others are being investigated as potential mitochondrial signalling molecules.
These mechanisms should not be treated as interchangeable.
An increase in glucose uptake, for example, does not necessarily mean that an individual will experience greater physical energy. Similarly, increased lipolysis does not automatically demonstrate increased whole-body fat loss.
Likewise, an experimental effect on mitochondrial signalling does not establish improved mitochondrial function in humans.
The phrase “increases energy” can describe several very different biological outcomes, including:
These outcomes are not equivalent.
For this reason, research should be described in terms of the specific metabolic pathway and measurable outcome being investigated, rather than broadly stating that a peptide “boosts energy” or “increases metabolism.”
Beauregard, N., McInnis, K., Goldfield, G.S. and Doucet, É. (2024) ‘Energy balance and obesity: the emerging role of glucagon like peptide-1 receptor agonists’, Current Opinion in Clinical Nutrition and Metabolic Care, 27(6), pp. 472–478. doi:10.1097/MCO.0000000000001064.
Bajaj, H.S. et al. (2026) ‘Efficacy and safety of retatrutide, a GIP, GLP-1, and glucagon receptor agonist, in people with type 2 diabetes and inadequate glycaemic control with diet and exercise (TRANSCEND-T2D-1): a double-blind, randomised, phase 3 trial’, The Lancet. doi:10.1016/S0140-6736(26)00967-0.
Feng, Y. et al. (2025) ‘Endurance training enhances skeletal muscle mitochondrial respiration by promoting MOTS-c secretion’, Free Radical Biology and Medicine. doi:10.1016/j.freeradbiomed.2024.12.038.
Jastreboff, A.M. et al. (2023) ‘Triple-Hormone-Receptor Agonist Retatrutide for Obesity — A Phase 2 Trial’, New England Journal of Medicine, 389(6), pp. 514–526. doi:10.1056/NEJMoa2301972.
Khan, M.Z., Zugaza, J.L. and Torres-Aleman, I. (2025) ‘The signaling landscape of insulin-like growth factor 1’, Journal of Biological Chemistry, 301(1), 108047. doi:10.1016/j.jbc.2024.108047.
Lu, H. et al. (2024) ‘The mitochondrial genome-encoded peptide MOTS-c interacts with Bcl-2 to alleviate nonalcoholic steatohepatitis progression’, Cell Reports, 43(1), 113587. doi:10.1016/j.celrep.2023.113587.
Rosenstock, J. et al. (2023) ‘Retatrutide, a GIP, GLP-1 and glucagon receptor agonist, for people with type 2 diabetes: a randomised, double-blind, placebo and active-controlled, parallel-group, phase 2 trial conducted in the USA’, The Lancet, 402(10401), pp. 529–544. doi:10.1016/S0140-6736(23)01053-X.
Tarasov, A. et al. (2024) ‘The impact of GLP-1 signalling on the energy metabolism of pancreatic islet β-cells and extrapancreatic tissues’, Peptides, 178, 171243. doi:10.1016/j.peptides.2024.171243.
Zhang et al. (2024) ‘The correlation between mitochondrial derived peptide (MDP) and metabolic states: a systematic review and meta-analysis’.
The evidence surrounding metabolic peptides exists across several levels.
Cellular studies can identify molecular pathways and determine how a compound interacts with specific receptors or signalling systems.
Animal studies can investigate whole-tissue and whole-organism metabolic responses, including glucose regulation, lipid metabolism and energy expenditure.
Human metabolic studies can determine whether those biological effects translate into measurable changes in glucose control, substrate utilisation, body composition or energy expenditure.
Controlled clinical trials are ultimately required to establish whether manipulating a particular pathway produces meaningful clinical benefits and has an acceptable safety profile.
The evidence base is therefore not uniform.
GLP-1 signalling and GLP-1-based therapies have an extensive human research base.
Retatrutide has also progressed into human clinical research, making it considerably more clinically investigated than several experimental mitochondrial peptides.
MOTS-c remains predominantly an experimental research area, with much of the evidence coming from preclinical models.
AOD-9604 has primarily been investigated in relation to lipid metabolism, but evidence for meaningful clinical effects remains limited.
IGF-1 has a substantial physiological and clinical research literature, although its systemic effects mean that it should not simply be treated as an energy-enhancing compound.
BPC-157 is included for comparison because it is frequently discussed alongside experimental peptides, but its primary research focus is tissue repair and cellular signalling rather than energy metabolism itself.
Changes in metabolic signalling do not automatically translate into improved physical performance.
A compound may alter glucose uptake without improving exercise capacity.
A compound may increase lipolysis without producing clinically meaningful fat loss.
A compound may influence mitochondrial signalling without demonstrating increased ATP production in humans.
Similarly, reducing appetite and food intake can produce substantial changes in body weight without directly increasing the efficiency of cellular energy production.
The biological mechanism and the clinical outcome therefore need to be considered separately.
For research purposes, it is more accurate to state that a compound “has been investigated in relation to glucose metabolism,” “has been studied for effects on lipid metabolism,” or “has demonstrated metabolic effects in preclinical models” than to describe it broadly as an “energy booster.”
The information presented on this page summarises published scientific research and is provided for educational purposes.
Evidence varies considerably between compounds and between biological outcomes. Laboratory, cell-culture and animal studies can provide evidence for mechanisms of action but do not establish that a compound is safe or effective as a treatment in humans.
In particular, evidence that a peptide influences glucose metabolism, mitochondrial signalling, lipolysis or another metabolic pathway does not demonstrate that administration of that peptide will increase energy production, improve exercise performance or produce beneficial changes in human metabolism.
IGF-1, GLP-1, retatrutide, MOTS-c, AOD-9604 and other experimental peptides should therefore be considered according to their individual evidence bases rather than being treated as equivalent metabolic agents.
Retatrutide is sometimes referred to as “GLP-3” in informal or commercial contexts, but retatrutide is the appropriate scientific name for the investigational triple-receptor agonist. The term “GLP-3” should not be interpreted as evidence of a distinct, naturally occurring human GLP-3 hormone.
Experimental peptides and growth factors should not be assumed to be safe or effective for personal use. The information above is not medical advice or a recommendation for treatment.
