What does dopamine do in the liver?

[Alien Cockroach]

Dopaminergic receptors generally seem to either raise or lower intracellular levels of cAMP through second-messenger systems. Now, one object of curiosity that I have had on my mind lately is this: what exactly is its function in the human liver?

 

[Hercules Rockefeller]

Dopamine is a neurotransmitter for the sympathetic nervous system. I can’t remember off-hand what physiological actions it mediates outside the CNS, but I do seem to remember that dopamine plays an important role in mediating vasodilation in a couple of different organs. Its peripheral effects are exploited therapeutically. Dopamine is also a precursor for adrenaline and noradrenaline.

 

[Alien Cockroach]

Yes, I am familiar with the catecholamines. Maybe it's the D1 receptor I'm thinking of. I simply remember some little tidbit regarding dopamine and the liver. I think it had something to do with lipolysis.

 

[Hercules Rockefeller]

Well, that's enough information to do some specific searches, isn't it? :shrug: How about this....

Bromocriptine/SKF38393 treatment ameliorates dyslipidemia in ob/ob mice.
Metabolism. 1999 Aug;48(8):1033-40.
Zhang et al.

Our previous studies have shown that the dopaminergic D1 receptor agonist SKF38393 (SKF) plus the D2 receptor agonist bromocriptine (BC) act synergistically to reduce obesity in obese C57BL/6J (ob/ob) mice. The present study investigated the effects of this combination on dyslipidemia in ob/ob mice. Female ob/ob mice were treated daily with vehicle or SKF (20 mg/kg body weight [BW]) plus BC (16 mg/kg BW [BC/SKF]) for 14 days. The animals were then used for the characterization of plasma lipoprotein profiles, hepatic triacylglycerol synthesis and secretion, adipocyte lipolysis, adipose and muscle lipoprotein lipase (LPL) activity, and muscle triglyceride (TG) content. The treatment significantly reduced plasma glucose 54%, TG 41%, cholesterol 21%, phospholipid 20%, and free fatty acid (FFA) 36% (P < .01). Hepatic triacylglycerol synthesis was 55% lower in treated mice versus control mice (P < .01). The cell size of isolated adipocytes was significantly reduced (41%) by treatment. LPL activity was increased in soleus skeletal muscle (25%, P < .05) but was sharply reduced in adipose tissue (91%, P < .01) in treated versus control mice. The TG content of hindlimb muscle was about 49% lower in treated versus control mice (P < .05). The basal and isoproterenol-stimulated lipolytic rate was decreased (approximately 53%) in adipocytes from treated animals compared with the control (P < .01). In conclusion, BC/SKF normalized the hypertriglyceridemia likely via its simultaneous antilipogenic action in liver tissue and antilipolytic action in adipose tissue. Decreased plasma flux of FFA partially contributed to the reduced hepatic lipogenesis, plasma very-low-density lipoprotein (VLDL)-TG, and TG in skeletal muscle. The above-described effects of BC/SKF treatment are largely independent of its effect to normalize hyperphagia in ob/ob mice.