Relationship between maternal and fetal plasma glucose and insulin concentrations during graded maternal hyperglycemic states in primates.
Our goal was to conduct a controlled study using an established timed-pregnant baboon model to describe the maternal and fetal plasma glucose and insulin concentrations during graded increases in maternal circulating glucose levels. Timed-pregnant baboons were operated on during the second half of pregnancy, and after recovery from surgery, maternal glucose infusions were started. To determine changes in plasma glucose and insulin concentrations, maternal and fetal blood samples were obtained before glucose infusion and at 30-minute intervals to include 30 minutes postinfusion. Maternal plasma glucose concentrations ranged from 97 to 392 mg/dL and fetal plasma glucose concentrations from 78 to 278 mg/dL. Maternal plasma insulin concentrations ranged from 123 to 1384 U/mL, and the fetal plasma insulin concentrations from 76 to 260 U/mL. Significant correlations were noted between maternal plasma glucose and insulin concentrations (N = 10; R(2), 80%; P < 0.001), as well as maternal and fetal plasma glucose concentrations (N = 10; R(2), 97%; P < 0.001). Maternal-to-fetal glucose gradient ranged from 16 to 34% (mean, 23%) and did not correlate with maternal plasma glucose concentration. No correlation was found between fetal plasma glucose and insulin concentration. Maternal-to-fetal insulin gradient ranged from 31 to 87% (mean, 70.7%) and was significantly different from the glucose gradient ( P < 0.0001). Results from this study suggests that (1) there is a relatively steady transplacental glucose transfer during the second half of pregnancy at maternal plasma glucose concentrations ranging from 97 to 392 mg/dL; and (2) there is also a relative incapacity of the fetal pancreas, compared with the maternal pancreas, to respond to graded increases of hyperglycemia. Studies aimed at determining whether particular thresholds of maternal hyperglycemia at different gestational ages can lead to transitory hyperosmolar and polyuric fetal states could provide further insights into the mechanisms leading to idiopathic polyhydramnios.
Santolaya-Forgas
Joaquín
J
Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, Maryland 20892, USA.
Romero
Roberto
R
Wildman
Derek E
DE
Kim
Chong Jai
CJ
Mahoney
Michael
M
Mehendale
Ramakrishna
R
Burd
Laurence
L
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005333:Fetus / Q000187:drug effects; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology*; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood*; D008431:Maternal-Fetal Exchange / Q000502:physiology*; D010215:Papio; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000097:blood*
D001786:Blood Glucose; D007328:Insulin; D005947:Glucose