Obesity, insulin resistance, and placental dysfunction—fetal growth

2020 ◽  
pp. 191-197
Author(s):  
Mariam Al Beloushi ◽  
Anjum Doshani ◽  
Justin C. Konje
2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Samantha C. Lean ◽  
Alexander E. P. Heazell ◽  
Mark R. Dilworth ◽  
Tracey A. Mills ◽  
Rebecca L. Jones

2013 ◽  
Vol 25 (1) ◽  
pp. 228
Author(s):  
P. Peugnet ◽  
A. Tarrade ◽  
C. Sandersen ◽  
M. Dahirel ◽  
D. Guillaume ◽  
...  

In equids, the size of the uterus determines fetal intrauterine development, which in turn affects postnatal insulin sensitivity and growth rate. We induced intrauterine growth enhancement through embryo transfer using Pony (P), Saddlebred (S), and Draft (D) horses and studied growth and insulin sensitivity in foals from birth to one year of age. Control pregnancies of S-in-S (n = 14) and P-in-P (n = 10) were obtained by AI. Enhanced fetal growth was obtained by transferring S (S-in-D, n = 7) and P embryos (P-in-D, n = 5) into D mares. From birth to weaning (180 days), each foal was kept with its surrogate P, S, or D dam. At 3, 140, and 380 days, glucose clearance and pancreatic beta cell response to exogenous glucose were assessed with an intravenous glucose tolerance test (IVGTT). At 200 days, the euglycemic-hyperinsulinemic clamp method was used to determine the sensitivity and responsiveness of tissues to exogenous insulin. Plasma T3, T4, and IGF1 were assayed at 3 and 180 days. Data were analysed using one-way ANOVA and Tukey post hoc tests. S-in-S were heavier and taller than P-in-P from birth to 380 days (P < 0.001). Before weaning, plasma concentrations of several hormones involved in growth were lower in S-in-S than P-in-P (at 3 and 180 days, respectively, T3: P = 0.08 and P = 0.02, T4: P < 0.001 and P = 0.06, IGF1: P = 0.04 and P < 0.001). No difference was found in glucose regulation between these groups. In contrast, post-weaning insulin resistance was observed in P-in-P at 200 days (P < 0.001) and confirmed at 380 days where they exhibited slower glucose clearance (P = 0.03) associated with higher fasting glucose (P < 0.001) than S-in-S. Fetal growth was not enhanced in S-in-D with no difference in height and weight at birth. Although S-in-D grew faster from 30 to 140 days, growth rates were not different from S-in-S after weaning, weaning coinciding with lower T3 (P < 0.001) in S-in-D than in S-in-S. Glucose regulation was not different between the two groups, but insulin remains to be assayed at 140 and 380 days. Fetal growth was enhanced in P-in-D: at birth, they were heavier (P = 0.01) and taller (P < 0.001) than P-in-P. Growth of P-in-D was faster until weaning. No more difference, however, was observed between P-in-D and P-in-P at 380 days. Plasma concentrations of T3 (P = 0.03) and those of T4 (P < 0.001) were lower at 3 days and T3 was still lower at 180 days (P < 0.001) in P-in-D compared with P-in-P. Moreover, P-in-D developed early insulin resistance: insulin secretion was higher in P-in-D compared with P-in-P (P = 0.002) after IVGTT at 3 days. At 200 days, however, P-in-D and P-in-P had the same sensitivity to insulin. There was no difference in glucose clearance rates at 380 days, but P-in-D had lower fasting glucose (P < 0.001) than P-in-P. Insulin assays at 140 and 380 days are pending. In conclusion, these data indicate that transfer of a small breed embryo into a large breed mare and subsequent suckling by the recipient mare can enhance fetal and postnatal growth and affect the foal’s glycaemia and sensitivity to insulin at birth and in subsequent months. Ongoing work includes analyses of milk samples and effects on general health.


Diabetes ◽  
2002 ◽  
Vol 51 (12) ◽  
pp. 3473-3478 ◽  
Author(s):  
D. Jaquet ◽  
D. A. Tregouet ◽  
T. Godefroy ◽  
V. Nicaud ◽  
D. Chevenne ◽  
...  

World Science ◽  
2019 ◽  
Vol 2 (9(49)) ◽  
pp. 4-8
Author(s):  
V. V. Lazurenko ◽  
I. B. Borzenko ◽  
D. Yu. Tertyshnik

The purpose of the study is to evaluate the effect of placental dysfunction caused by gestational endotheliopathy on the course of labor and the condition of the newborn. The first group consisted of 70 patients with placental dysfunction with gestational endotheliopathy confirmed by laboratory-instrumental findings in the first trimester of pregnancy. The control group included 30 pregnant women with physiological gestational course. PD secondary to GE leads to preterm birth, fetal distress, increases the percentage of caesarean section, contributes to the delay of fetal growth and birth weight, poor infant status and perinatal complications.


2021 ◽  
Author(s):  
Irving L. M. H. Aye ◽  
Fredrick J. Rosario ◽  
Anita Kramer ◽  
Oddrun Kristiansen ◽  
Trond M. Michelsen ◽  
...  

ABSTRACTIn pregnancy, adiponectin serves as an endocrine link between maternal adipose tissue, placental function and fetal growth, with low adiponectin promoting placental function and fetal growth. Circulating adiponectin levels are decreased in obese pregnant women and in gestational diabetes, which is believed to contribute to the insulin resistance and increased risk of fetal overgrowth associated with these conditions. However, the molecular mechanisms governing adiponectin secretion from maternal adipose tissues in pregnancy are poorly understood. Using visceral adipose tissue from lean and obese pregnant mice, we show that obesity in pregnancy is associated with adipose tissue inflammation, ER stress, insulin resistance, increased adiponectin ubiquitination and decreased total abundance of adiponectin. Moreover, adiponectin ubiquitination was increased in visceral fat of obese pregnant women as compared to lean pregnant women. We further observed that insulin prevents, whereas ER stress and inflammation promote, adiponectin ubiquitination and degradation in differentiated 3T3-L1 adipocytes. We have identified key molecular pathways regulating adiponectin secretion in pregnancy. This information will help us better understand the mechanisms controlling maternal insulin resistance and fetal growth in pregnancy and may provide a foundation for the development of strategies aimed at improving adiponectin production in pregnant women with obesity or gestational diabetes.


2006 ◽  
Vol 66 (S 01) ◽  
Author(s):  
MB Langbein ◽  
R Strick ◽  
PL Strissel ◽  
N Vogt ◽  
MW Beckmann ◽  
...  

Hypertension ◽  
2019 ◽  
Vol 74 (5) ◽  
pp. 1136-1143 ◽  
Author(s):  
Marie Austdal ◽  
Gabriela Brettas Silva ◽  
Sophie Bowe ◽  
Liv Cecilie Vestrheim Thomsen ◽  
Line Haugstad Tangerås ◽  
...  

Clinical end-stage parameters define the pregnancy disorders preeclampsia and fetal growth restriction while classification of the underlying placental dysfunction is missing and urgently needed. Flt-1 (FMS-like tyrosine kinase receptor 1) is the most promising placenta-derived predictive biomarker for preeclampsia. We aimed to classify placental dysfunction in preeclampsia and fetal growth restriction at delivery by metabolic profiling and authenticate the biomarker Flt-1 for placental dysfunction. We studied 143 pregnancies with or without preeclampsia and/or fetal growth restriction delivered by cesarean section. Metabolic placenta profiles were created by high-resolution magic angle spinning nuclear magnetic resonance spectroscopy and the resulting placental phenotypes obtained by hierarchical clustering. Placental Flt-1 expression (membrane-bound and soluble isoforms combined) and maternal serum Flt-1 expression (soluble isoforms) were analyzed by immunohistochemistry and ELISA, respectively. We identified 3 distinct placenta groups by 21 metabolites and diagnostic outcome parameters; normal placentas, moderate placental dysfunction, and severe placental dysfunction. Increased placental Flt-1 was associated with severe placental dysfunction, and increased serum Flt-1 was associated with moderate and severe placental dysfunction. The preeclamptic pregnancies with and without placental dysfunction could be distinguished by 5 metabolites and placental Flt-1. Placental Flt-1 alone could separate normal pregnancies with and without placental dysfunction. In conclusion, metabolomics could classify placental dysfunction and provide information not identified by traditional diagnostics and metabolites with biomarker potential were identified. Flt-1 was confirmed as precision biomarker for placental dysfunction, substantiating its usefulness for identification of high-risk pregnancies for preeclampsia and fetal growth restriction with placental involvement.


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