Table 2.
Association between pharmacological activity, central and peripheral levels of metabolic regulation.
| Effects | ||
|---|---|---|
| Central | Peripheral | |
| D2/3 antagonism | ↑ Food intake | ↑ Insulin secretion |
| ↑hypohalamic AMPK | ↑ Proliferation and survival of beta cells | |
| ↑EPS | Deplete insulin stores (chronic) | |
| ↑ Catecholamine release | ||
| ↑ Prolactin | ||
| 5-HT1 partial agonism | ↓ Food intake | ↓ Insulin secretion |
| ↓ EPS | ↓ Glucose uptake (adipose tissue) | |
| ↓ Prolactin | ||
| 5-HT2A antagonism | ↑Food intake | ↓ Insulin secretion |
| ↓ EPS | ↑ Hepatic insulin sensitivity | |
| ↓ Prolactin | ↓ Glucose uptake (skeletal muscle) | |
| ↓Adipose tissue lipogenesis | ||
| 5-HT2C antagonism | ↑ Food intake | ↑ Insulin secretion(?) |
| ANS disruption | ||
| H1 antagonism | ↑ Food intake | ↓ Hepatic insulin sensitivity |
| ↑ hypothalamic AMPK | ↓ Glucose uptake (adipose tissue, skeletal muscle) | |
| ↑ Sedation | ↑ Adipose tissue lipogenesis | |
| ANS disruption | ↑ Fructose absorption | |
| ↑ Atherosclerosis | ||
| M3 antagonism | ↑ Food intake | ↓ Insulin secretion |
| ↓ EPS | ↓ Adipose tissue lipogenesis | |
| ANS disruption | ↓ Glucose uptake (skeletal muscle) | |
| alpha1 antagonism | ↑ Food intake | ↓ Hepatic insulin sensitivity |
| ↑ hypothalamic AMPK | ↓ Peripheral vascular resistance | |
| ↑ Sedation | ↓ Glucose uptake (adipose tissue, skeletal muscle) | |
| ANS disruption | ||
| alpha2 antagonism | ↓ Food intake | ↑ Insulin secretion |
| ↓Adipose tissue lipogenesis | ||
| ↑ Catecholamine release | ||