Adipose Tissue

Androgen Receptor

The receptor every anabolic-androgenic steroid is designed to hit. Binding moves it into the nucleus where it switches on genes for muscle protein synthesis, and in other tissues for hair loss, prostate growth and oil production.

Beta-3 Adrenergic Receptor

The fat-cell adrenergic receptor. Activating it releases stored fat and raises heat production without the heart-rate effect of beta-1. It is the claimed target of the GH fragments that are supposed to burn fat without growing anything.

Estrogen Receptor alpha

The estrogen receptor that dominates breast tissue, liver and the pituitary feedback loop. Gynecomastia and much of the negative feedback on LH run through it.

GIP Receptor

The second incretin receptor. Adding it to GLP-1 agonism is what separates tirzepatide from semaglutide: more energy expenditure and a direct effect on fat tissue, on top of the appetite drop.

Glucagon Receptor

Glucagon's receptor. Agonising it raises energy expenditure and burns liver fat, which is why the triple agonists add it. It also raises blood glucose, which is the tension every dual and triple agonist has to balance.

Glucocorticoid Receptor

The cortisol receptor. Some androgens bind it too, and whether they act as agonist or blocker at a given tissue is a large part of why compounds with similar AR affinity feel so different.

Growth Hormone Receptor

Where growth hormone itself acts. Binding pairs the receptor and fires JAK2/STAT5, which in the liver means IGF-1 output and in fat means lipolysis. Injected GH works here; secretagogues work one step upstream.