Table 1.

Summary of mechanisms of dopamine-mediated modulation of β-cell activity, insulin, and glucagon secretion [6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33].

Mechanism	Effect	Consequences
Interference with insulin-containing grain trafficking (Dopamine-containing vesicles)	Blunt insulin release	Improvement in insulin sensitivity (e.g., insulin-resistant, obese patients) Deterioration of glucose control (non-insulin-resistant patients)
Impaired intra-pancreatic dopamine catabolism (Monoaminoxidases)	Catecholamine-induced (alpha and D2/D3 receptors) suppression of insulin synthesis and secretion	Hyperglycemia
Meal-induced intestinal synthesis of dopamine	Anti-incretin effect	Blunt insulin response after meal and post-prandial hyperglycemia
Enhancement of alpha-cell activity (High-dose dopamine)	Glucagon secretion	Fasting hyperglycemia (hepatic gluconeogenesis and glycogenolysis)
Suppression of prolactin release	Suppression of prolactin-induced insulin release	Hyperglycemia
Reduction in growth hormone	Amelioration of insulin release and peripheral insulin resistance	Improvement in glucose control (e.g., acromegaly)

Table 1 summarizes the mechanisms by which dopamine affects β-cell activity, insulin, and glucagon secretion. Each mechanism is associated with specific effects and potentially relevant clinical consequences in terms of the progression of diabetes and deterioration of glucose control.