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DOI: 10.1055/s-2005-862886
Prolactin an diabetogenic hormone?
Hyperprolactinemia has been reported to be associated with abnormalities in carbohydrate metabolism, body fat and fat deposition. In patients with prolactinoma (8 of 12) we could demonstrate decreased insulin sensitivity as determined by reduced whole body glucose uptake during the euglycemic-hyperinsulinemic clamp. However, in insulin resistant (n=12) and insulin sensitive individuals (n=14) without type 2 diabetes as well as in patints with type 2 diabetes, prolactin (PRL) serum concentrations were in the normal range without any significant differences between the groups.
In an attempt to investigate whether elevated PRL concentrations could induce insulin resistance in vitro, we determined the influence of PRL on insulin-stimulated (100nM) glucose uptake into isolated human adipocytes. First, we confirmed that the short isoform of prolactin receptors was detected on human adipocytes.
In physiological concentration (20ng/ml) prolactin showed no influence on glucose uptake, whereas in hyperprolactinemic concentrations we detected a significant dose dependent decrease of insulin stimulated glucose uptake to about 60% of the maximal insulin stimulated glucose uptake at 100 ng/ml PRL concentration and to 50% at 200ng/ml PRL concentration respectively.
Our data demonstrate that hyperprolactinemia could induce insulin resistance in patients with prolactinoma as well as in primary human adipocyte culture in vitro, suggesting a potential diabetogenic role of hyperprolactinemia.