The insulin-like effects of mouse growth hormone on adipose tissue from virgin and pregnant mice.

The abilities of mouse prolactin (mPRL), growth hormone (mGH), placental lactogen (mPL)-I, and mPL-II to stimulate glucose oxidation were investigated, using adipose tissue from both virgin and pregnant mice. In separate experiments, adipose tissue segments from the parametrial fat pads of virgin and pregnant mice were collected on days 7, 13, and 17 of gestation. Tissue segments were first preincubated at 37 degrees C for 3 hours in Krebs-Ringer-HEPES (KRH) buffer without any added hormones. Following the preincubation, mPRL, mGH, recombinant mPL-I, mPL-II (1 microgram/mL), and porcine insulin (plns) (1 ng/L) were added to the incubations, along with 0.5 microCi/mL D-[U-14C]glucose, and incubated for an additional 2 hours. After the second incubation, the 14CO2 produced by the oxidation of the D-[U-14C]glucose was collected and counted. Both mGH and plns significantly stimulated glucose oxidation in adipose tissue from virgin and pregnant mice. However, mPRL, mPL-I, and mPL-II failed to stimulate glucose oxidation in adipose tissue from either virgin or pregnant mice. Preincubating adipose tissue, from day 13 of gestation, with 0.5 microgram/mL epinephrine (Epn) increased basal glucose oxidation and decreased both mGH- and plns-stimulated glucose oxidation. Preincubating adipose tissue, from day 13 of gestation, with 0.11 microgram/mL dexamethasone (Dex) significantly decreased the ability of the tissue to oxidize glucose. However, the Dex-treated tissue retained its ability to increase glucose oxidation in response to mGH and plns. These results indicate that mGH, but not mPRL, mPL-I, or mPL-II, has insulin-like effects on adipose tissue, and that mGH and plns may affect glucose oxidation through similar pathways.