Effect of the ovarian hormones on GLUT4 expression and contraction-stimulated glucose uptake.
Level 5 - mechanism / opinion, no new human data
Animal research (Sprague-Dawley rat model)
PubMed 11934680 · doi:10.1152/ajpendo.00184.2001
What was done
Female Sprague-Dawley rats received either sham surgery (control, C) or ovariectomy followed by 15-day timed-release pellet implantation of placebo (O), 17β-estradiol (E), progesterone (P), physiological progesterone plus estradiol (P + E), or progesterone plus high-dose estradiol (P + HiE). On day 15, animals received an intraperitoneal injection of 2-deoxy-[14C]glucose and were subjected to either 30 minutes of treadmill running (0.35 m/s) or 30 minutes of sedentary cage rest. Glucose uptake, glycogen content, and GLUT4 protein levels were measured in red and white quadriceps.
What was found
Basal glucose uptake and resting glycogen levels did not differ between treatment groups in red or white quadriceps. During exercise, red quadriceps glucose uptake decreased (P < 0.05) in O, P, and P + E rats compared with C rats, while E and P + HiE treatments restored uptake. Postexercise red quadriceps glycogen content was higher (P < 0.05) in E and P + HiE rats compared with O and P rats. Progesterone treatment alone (P rats) reduced GLUT4 content in red quadriceps by 21% (P < 0.05) compared with C rats, but estrogen deficiency did not alter total GLUT4 protein content.
Why it matters
This study shows that estradiol is required to maintain contraction-stimulated glucose uptake and spare muscle glycogen during aerobic exercise in females, operating via mechanisms independent of total GLUT4 protein abundance.
Limits
The study was conducted in female rats and may not directly translate to human physiology. The abstract does not report the total animal sample size. It examined a single 30-minute exercise duration and did not measure GLUT4 translocation to the plasma membrane.
Cited by
- supports Progesterone induces hyperinsulinemia, acts on the pancreas and liver, and antagonizes GLUT4 receptor translocation in skeletal muscle to deposit body fat.