A study to determine if acute maternal and fetal hyperglycemia/insulinemia induces leptin production during pregnancy.
BACKGROUND
In pregnant primates, the effect of post-prandial hyperglycemic or insulinemic states on leptin production is not known. Our goal was to conduct a controlled study using an established pregnant baboon model ( PAPIO ANUBIS) to determine whether acute glucose changes would have an effect on maternal or fetal plasma leptin levels.


METHODS
Two animals were operated on at 138 and 140 days of gestation (term approximately 184 days) by placing 4 cannulae in the maternal aorta, inferior vena cava, fetal carotid artery, and the amniotic cavity. At 145 and 150 days, glucose infusions were started via the maternal femoral vein. Animal 1 received 7.5 gm of glucose over a 2-hour period at 145 th day. Animal 2 received 20 gm of glucose over a 1-hour period at 150th day. Both animals remained ad libitum throughout the experiments. Maternal and fetal blood samples were obtained from the arterial lines before the glucose infusion and at half hour intervals to include 30 minutes post-infusion.


RESULTS
Significant changes from baseline concentrations were observed for maternal and fetal glucose and insulin concentrations in response to both glucose challenges. Maternal and fetal plasma leptin concentrations did not correlate with glucose or insulin changes.


CONCLUSIONS
This preliminary study demonstrated that in primates, acute changes in circulating maternal or fetal glucose or insulin concentration do not affect maternal or fetal plasma leptin concentrations. These results suggest that alterations in leptin secretion by the maternal-placental-fetal unit may only occur in pathological states.
Santolaya-Forgas
J
J
Center for Fetal Medicine and Prenatal Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. jsantolaya@partners.org
Mehta
S H
SH
Castracane
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VD
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000378:metabolism* / Q000473:pathology*; D005865:Gestational Age; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology; D006943:Hyperglycemia / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D020738:Leptin / Q000096:biosynthesis*; D010215:Papio / Q000378:metabolism*; D011247:Pregnancy
D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D005947:Glucose