The role of prolactin in the pathogenesis of autoimmune disease

Berczi, István

doi:10.1007/bf02915460

Cited by 14 publications

(3 citation statements)

References 116 publications

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“…There is increasing evidence that prolactin functions also as an immunostimulatory molecule and, therefore, has the potential to contribute to the pathogenesis of autoimmune diseases (14)(15)(16)(17)(18)(19)(20)(21). An association between SLE and elevated prolactin levels has been suggested (22)(23)(24)(25)(26)(27)(28)(29); attempts to correlate prolactin levels with either global lupus activity (30)(31)(32)(33)(34)(35)(36) or specific organ involvement (37,38), however, have yielded varying results.…”

Section: Introductionmentioning

confidence: 99%

Bromocriptine restores tolerance in estrogen-treated mice

Peeva¹,

Grimaldi²,

Spatz³

et al. 2000

J. Clin. Invest.

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Section: Introductionmentioning

confidence: 99%

Bromocriptine restores tolerance in estrogen-treated mice

Peeva¹,

Grimaldi²,

Spatz³

et al. 2000

J. Clin. Invest.

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“…[2,3]. Bromocriptine administered s.c. inhibits prolactin secretion only, thus lowering its immunostimulatory effects and dampening the autoimmune reaction [1,2], while i.p. bromocriptine induces a hyperglycemic effect that counteracts its beneficial action on the immune system.…”

Section: Discussionmentioning

confidence: 99%

“…beneficial effect of bromocriptine, a D2-dopaminergic agonist, has been described in various rodent models of autoimmune diseases, such as arthritis and uveitis, which do not involve alterations of glucose homeostasis [1]. Attenuation of these diseases reflected the ability of the dopaminergic agonist to suppress pituitary secretion of the immunostimulatory hormone, prolactin.…”

Section: Introductionmentioning

confidence: 99%

Bromocriptine-Induced Hyperglycemia in Nonobese Diabetic Mice: Kinetics and Mechanisms of Action

Durant¹,

Coulaud²,

Homo‐Delarche³

2007

Rev Diabet Stud

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■ AbstractThe effects of bromocriptine (10 mg/kg), known to inhibit prolactin secretion and lower autoimmune processes, were studied on glucose homeostasis in non-fasted non-obese diabetic mice, a spontaneous model of type 1 diabetes. Hyperglycemia was observed 120 and 240 min after i.p. but not s.c. injection. Bromocriptine administration i.p. led to rapid and marked hyperglycemia characterized by sexual dimorphism with males having higher glycemia than females. Bromocriptine induced a rapid but transient decrease in insulinemia in males only and biphasic increases in glucagon levels and a sustained stimulatory effect on circulating corticosterone in both sexes. Bromocriptine-induced hyperglycemia involved D2-dopaminergic receptors, as demonstrated by the inhibitory effect of the D2-dopamine antagonist, metoclopramide (10 mg/kg). Simultaneous injection of bromocriptine and metoclopramide also blocked the rise in blood corticosterone. In conclusion, by inducing hyperglycemia, i.p. bromocriptine administration to prediabetic autoimmune mice may counteract its beneficial antiimmunostimulatory effects.

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