Table 1.
Interaction with other hormones and systems.
| Interacting partners | Effect | Reference |
|---|---|---|
| Leptin | • Leptin reduces endocannabinoid levels in the hypothalamus | (30–33) |
| • Leptin-deficient animals reduce food intake in response to a CB1 antagonist | ||
| • Leptin-deficient animals have high endocannabinoid levels | ||
| • Anorexia nervosa patients have high circulating endocannabinoid levels | ||
| Ghrelin | • Ghrelin increases endocannabinoid levels in the hypothalamus | (28) |
| • Intact CB1 is necessary for ghrelin appetite and AMPK effects in the hypothalamus | ||
| Adiponectin | • CB1 antagonist increases adiponectin levels | (30, 34) |
| • The beneficial effects of CB1 antagonist are partly (but not fully) via adiponectin | ||
| NPY, αMSH | • Anandamide increases hypothalamic neuropeptide Y, an effect inhibited by cannabinoid antagonists | (35–36) |
| • α-MSH and the cannabinoid system have been shown to decrease food intake synergistically | ||
| Orexin | • Orexin receptor, OX1R, was shown to heterodimerise with the CB1 receptor, leading to increased orexin effects | (25, 37) |
| Glucocorticoids | • Glucocorticoids release endocannabinoids in the hypothalamus | (38, 39, 82) |
| Neurotransmitters | • The endocannabinoid system influences the release of various neurotransmitters, including GABA, noradrenaline, dopamine, glutamate and acetylcholine | (29, 40, 41) |
| • A direct interaction of dopamine receptors and CB1 has been suggested |