George M Butterstein1, Colin Hirst1,2, V Daniel Castracane3,4,5. 1. Department of Biological Sciences, Union College, Schenectady, NY, USA. 2. Heart Lung Vascular Institute, University of Tennessee Medical Center, Knoxville, TN, 37920, USA. 3. Department of Obstetrics and Gynecology, Texas Tech University Health Sciences Center at the Permian Basin, Odessa, TX, USA. daniel.castracane@ttuhsc.edu. 4. Department of Obstetrics and Gynecology, Texas Tech University Health Sciences Center, Amarillo, TX, USA. daniel.castracane@ttuhsc.edu. 5. Texas Tech University Health Sciences Center, Lubbock, TX, USA. daniel.castracane@ttuhsc.edu.
Abstract
PURPOSE: This study was designed to determine whether there is a role of the placenta in the regulation of maternal serum leptin levels in the pregnant rat. METHODS: We have adjusted the number of fetal-placental implants on day 9 in the pregnant rat by aspirating fetal-placental units to adjust the number to 1-2, 4-5 per rat or >10 in controls. Serum levels of leptin and progesterone were determined by radioimmunoassay. A separate group of pregnant rats were ovariectomized and maintained with progesterone silastic capsules (10, 20 or 40 mm). RESULTS: In the pregnant rats with varied fetal-placental implant numbers, the maternal serum leptin were greatest in the group with the smallest number (1-2) of implants; intermediate in the midgroup (4-5 implants); and lowest in the group with a full complement of implantations (>10) (p < 0.001). Serum progesterone levels are lowest in the 1-2 implantation group. In the ovariectomized rats there was a stepwise decline in serum leptin (p < 0.05) as the dose of progesterone increased (p < 0.01). Both of these studies suggest that progesterone suppressed maternal serum leptin levels. CONCLUSIONS: Increasing placental mass is not associated with increasing maternal serum leptin levels in the pregnant rat; the contrary condition is observed with the least placental implants having the highest leptin levels. Progesterone seems to suppress serum leptin levels in several physiological models.
PURPOSE: This study was designed to determine whether there is a role of the placenta in the regulation of maternal serum leptin levels in the pregnant rat. METHODS: We have adjusted the number of fetal-placental implants on day 9 in the pregnant rat by aspirating fetal-placental units to adjust the number to 1-2, 4-5 per rat or >10 in controls. Serum levels of leptin and progesterone were determined by radioimmunoassay. A separate group of pregnant rats were ovariectomized and maintained with progesterone silastic capsules (10, 20 or 40 mm). RESULTS: In the pregnant rats with varied fetal-placental implant numbers, the maternal serum leptin were greatest in the group with the smallest number (1-2) of implants; intermediate in the midgroup (4-5 implants); and lowest in the group with a full complement of implantations (>10) (p < 0.001). Serum progesterone levels are lowest in the 1-2 implantation group. In the ovariectomized rats there was a stepwise decline in serum leptin (p < 0.05) as the dose of progesterone increased (p < 0.01). Both of these studies suggest that progesterone suppressed maternal serum leptin levels. CONCLUSIONS: Increasing placental mass is not associated with increasing maternal serum leptin levels in the pregnant rat; the contrary condition is observed with the least placental implants having the highest leptin levels. Progesterone seems to suppress serum leptin levels in several physiological models.