Does acute endogenous hyperprolactinemia affect intravenous glucose tolerance in humans?
To investigate whether acute endogenous hyperprolactinemia (h-PRL) influences glucose tolerance in humans, two intravenous glucose tolerance tests were performed in healthy subjects and in patients with untreated type 2 diabetes. One of the tests was carried out during h-PRL induced by oral priming with 10 mg metoclopramide (MET). The other was performed during normoprolactinemia (n-PRL) prevailing after oral priming with placebo. The glucose disappearance rates (Kg) were compared in the n-PRL and h-PRL states. In eight healthy subjects with high Kg values (greater than or equal to 1.2) during n-PRL, the glucose tolerance decreased during MET-induced h-PRL. This was reflected by a Kg fall from 2.0 +/- 0.4 during n-PRL to 1.3 +/- 0.3 during h-PRL (P less than 0.01). It is unlikely that this Kg decline could have been caused by prolactin-induced changes in serum levels of insulin, cortisol, or growth hormone (GH), since these hormones showed glucose-elicited response patterns that were similar in the n-PRL and h-PRL states. It is also improbable that MET per se could have caused Kg to fall, inasmuch as MET left Kg unaffected when oral pretreatment with bromocriptine prevented MET from inducing h-PRL in an additional five healthy subjects with high Kg values.(ABSTRACT TRUNCATED AT 250 WORDS)
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D001971:Bromocriptine / Q000494:pharmacology; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology; D008875:Middle Aged; D011388:Prolactin / Q000097:blood*
D001971:Bromocriptine; D011388:Prolactin; D008787:Metoclopramide