The Experts below are selected from a list of 24 Experts worldwide ranked by ideXlab platform

Cynthia A. Thomson - One of the best experts on this subject based on the ideXlab platform.

  • Gestational Diabetes Mellitus
    Obstetrics Gynecology, 1996
    Co-Authors: Deborah Pesicka, Judith Riley, Cynthia A. Thomson
    Abstract:

    Gestational Diabetes Mellitus (GDM) is carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. GDM is usually identified in mid- to late-pregnancy and seems to relate to increased levels of anti-insulinemic hormones—specifically estrogen, prolactin, progesterone, cortisol, and Human Placenta Lactogen. If GDM is not controlled, there is increased risk for large babies, and labor or postpartum complications. GDM generally poses little threat for congenital anomalies.

Deborah Pesicka - One of the best experts on this subject based on the ideXlab platform.

  • Gestational Diabetes Mellitus
    Obstetrics Gynecology, 1996
    Co-Authors: Deborah Pesicka, Judith Riley, Cynthia A. Thomson
    Abstract:

    Gestational Diabetes Mellitus (GDM) is carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. GDM is usually identified in mid- to late-pregnancy and seems to relate to increased levels of anti-insulinemic hormones—specifically estrogen, prolactin, progesterone, cortisol, and Human Placenta Lactogen. If GDM is not controlled, there is increased risk for large babies, and labor or postpartum complications. GDM generally poses little threat for congenital anomalies.

Martin Akilla Awe - One of the best experts on this subject based on the ideXlab platform.

  • Placental peptides metabolism and maternal factors as predictors of risk of gestational diabetes in pregnant women. A case-control study.
    PloS one, 2017
    Co-Authors: Robert A. Ngala, Linda Ahenkorah Fondjo, Peter Gmagna, Frank Naku Ghartey, Martin Akilla Awe
    Abstract:

    Background Gestational diabetes is a risk factor for perinatal complications; include shoulder dystocia, birth injuries such as bone fractures and nerve palsies. It is associated with later development of type 2 diabetes, the risk of macrosomia and other long-term health effects of infants born to diabetic mothers. The study assesses Placental peptides and maternal factors as potential predictors of gestational diabetes among pregnant women. Material and methods A total of 200 pregnant women were recruited for the study, 150 pregnant women without pre gestational diabetes including 50 women with low risk factors of diabetes as controls and 50 other pregnant women with pregestational diabetes as control. Fasting blood glucose and the lipid profile were determined by enzymatic methods using Envoy® 500 reagents (Vital Diagnostics, USA). Glycated haemoglobin was assessed using the Cation Exchange resin method. Leptin and the Human Placenta Lactogen were assayed using the Sandwich-ELISA technique. Beta chorionic gonadotrophin, insulin, progesterone and estradiol were determined using chemilumiscence imunoassay technique on MAGLUMI 600 analyzer. Anthropometry, including BMI and blood pressure were also measured. Results Fasting plasma glucose (FBG), insulin, insulin resistance, glycated haemoglobin and Human Placenta Lactogen(HPL)were significantly (p 0.05) in estradiol, insulin, insulin resistance and HPL between the pregnant women who developed gestational diabetes and those who did not. Leptin, progesterone and FBG were significantly increased in those who developed GDM. The risk of developing gestational diabetes increased with overweight (OR = 1.76, P = 0.370) and family history of diabetes (OR = 2.18, P = 0.282). Conclusion Leptin, progesterone, estradiol estimated in this study were increased in the gestational diabetes mellitus women and fairly predicted gestational diabetes in the non-diabetics pregnant women. Obesity, aging and family history of diabetes were strongly predictive of gestational diabetes.

Judith Riley - One of the best experts on this subject based on the ideXlab platform.

  • Gestational Diabetes Mellitus
    Obstetrics Gynecology, 1996
    Co-Authors: Deborah Pesicka, Judith Riley, Cynthia A. Thomson
    Abstract:

    Gestational Diabetes Mellitus (GDM) is carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. GDM is usually identified in mid- to late-pregnancy and seems to relate to increased levels of anti-insulinemic hormones—specifically estrogen, prolactin, progesterone, cortisol, and Human Placenta Lactogen. If GDM is not controlled, there is increased risk for large babies, and labor or postpartum complications. GDM generally poses little threat for congenital anomalies.

K Bridget Brosnihan - One of the best experts on this subject based on the ideXlab platform.

  • Angiotensin II and angiotensin-(1-7) decrease sFlt1 release in normal but not preeclamptic chorionic villi: an in vitro study
    Reproductive Biology and Endocrinology, 2010
    Co-Authors: Lauren Anton, David C Merrill, Liomar Aa Neves, Courtney Gruver, Cheryl Moorefield, K Bridget Brosnihan
    Abstract:

    Background During preeclampsia, Placental angiogenesis is impaired. Factors released from the Placenta including vascular endothelial growth factor (VEGF), Placental growth factor (PLGF), soluble VEGF receptor 1 (sFlt1), and soluble endoglin (sEng) are regulatory molecules of Placental development and function. While the renin angiotensin system has been shown to regulate angiogenic factors in other research fields, these mechanisms have not been extensively studied during pregnancy. Methods We evaluated the effects of angiotensin II (Ang II) and angiotensin-(1-7) [Ang-(1-7)] on the release of VEGF, PLGF, sFlt1, and sEng from Placental chorionic villi (CV). CV were collected from nulliparous third-trimester normotensive and preeclamptic subjects. CV were incubated for 0, 2, 4, and 16 hours with or without Ang II (1 nM and 1 microM) or Ang-(1-7) (1 nM and 1 microM). The release of VEGF, PLGF, sFlt1, sEng, lactate dehydrogenase (LDH), and Human Placenta Lactogen (HPL) was measured by ELISA. Results The release of sFlt1, PLGF, sEng from normal and preeclamptic CV increased over time. Release of sFlt1 and sEng was significantly higher from preeclamptic CV. VEGF was below the detectable level of the assay in normal and preeclamptic CV. After 2 hours, sFlt1 release from normal CV was significantly inhibited with Ang II (1 nM and 1 microM) and Ang-(1-7) (1 nM and 1 microM). There was a time-dependent increase in HPL indicating that the CV were functioning normally. Conclusions Our study demonstrates a critical inhibitory role of angiotensin peptides on sFlt1 in normal pregnancy. Loss of this regulation in preeclampsia may allow sFlt1 to increase resulting in anti-angiogenesis and end organ damage in the mother.