scholarly journals AMINOCUANIDINE IMPROVES FETAL GROWTH IN STREPTOZOTOCIN-INDUCED MATERNAL DIABETES

1987 ◽  
Vol 21 (4) ◽  
pp. 214A-214A
Author(s):  
Robert E Greenberg ◽  
Tracy Dunham ◽  
James Wogenrich
Keyword(s):  
Fetal Growth ◽  
Maternal Diabetes

Effects of Maternal Diabetes on Fetal Expression of Insulin-Like Growth Factor and Insulin-Like Growth Factor Binding Protein MRNAs in the Rat

1995 ◽  
Vol 147 (2) ◽  
pp. R5-R8 ◽  
Author(s):  
Randal D. Streck ◽  
Veeraramani S. Rajaratnam ◽  
Renata B. Fishman ◽  
Peggy J. Webb
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fetal Growth ◽  
Fetal Liver ◽  
Expression Patterns ◽  
Maternal Diabetes ◽  
Limb Bud ◽  
Insulin Like Growth Factor ◽  
Igf Binding Proteins ◽  
Increased Risk

ABSTRACT Matemal diabetes is associated in humans and rats with an increased risk for fetal growth abnormalities and malformations. Therefore, the effect of maternal diabetes on expression of genes that regulate fetal growth and differentiation is of considerable interest. Developmental growth is regulated in part by the expression and availability of insulin-like growth factors (IGFs). Postnatal expression of a subset of the IGFs and IGF binding proteins (IGFBPs) has been demonstrated to be regulated in response to diabetes and other metabolic conditions. We used in situ hybridization to analyze the effect of maternal diabetes, induced by streptozotocin (STZ) prior to mating, upon prenatal rat IGF and IGFBP mRNA expression. At gestational day (GD) 14, the most striking effect of maternal diabetes on fetal IGF/IGFBP gene expression was a marked increase in the abundance of IGFBP-1 mRNA within the liver primordia of fetuses isolated from diabetic dams compared to age-matched controls. This upregulation cannot be entirely due to the approximately one-half-day delay in fetal development (based on limb bud staging) associated with maternal diabetes, as there was no gross difference in the level of IGFBP-1 mRNA between GD13 and GD14 control fetal livers. In contrast, the fetal mRNA expression patterns of IGF-I, IGF-II and IGFBP-2, -3, -4, -5 and -6 were not grossly altered by maternal diabetes. These data are consistent with the hypothesis that IGFBP-1 produced within the fetal liver and secreted into fetal circulation may play a role in regulating rat fetal growth.

Maternal Diabetes in Rats: II. Effects on Fetal Growth and Protein Turnover

Diabetes ◽  
1988 ◽  
Vol 37 (12) ◽  
pp. 1671-1677 ◽  
Author(s):  
J. P. Canavan ◽  
D. F. Goldspink
Keyword(s):  
Fetal Growth ◽  
Protein Turnover ◽  
Maternal Diabetes

Maternal diabetes in rats. II. Effects on fetal growth and protein turnover

Diabetes ◽  
1988 ◽  
Vol 37 (12) ◽  
pp. 1671-1677 ◽  
Author(s):  
J. P. Canavan ◽  
D. F. Goldspink
Keyword(s):  
Fetal Growth ◽  
Protein Turnover ◽  
Maternal Diabetes

scholarly journals Placental glycogen stores and fetal growth: insights from genetic mouse models

Reproduction ◽  
2020 ◽  
Vol 159 (6) ◽  
pp. R213-R235 ◽  
Author(s):  
Simon J Tunster ◽  
Erica D Watson ◽  
Abigail L Fowden ◽  
Graham J Burton
Keyword(s):  
Mouse Models ◽  
Fetal Growth ◽  
Maternal Diabetes ◽  
Glycogen Storage ◽  
Waste Products ◽  
And Function ◽  
Glycogen Stores ◽  
The Relationship ◽  
Genetic Mouse Models

The placenta performs a range of crucial functions that support fetal growth during pregnancy, including facilitating the supply of oxygen and nutrients to the fetus, removal of waste products from the fetus and the endocrine modulation of maternal physiology. The placenta also stores glucose in the form of glycogen, the function of which remains unknown. Aberrant placental glycogen storage in humans is associated with maternal diabetes during pregnancy and pre-eclampsia, thus linking placental glycogen storage and metabolism to pathological pregnancies. To understand the role of placental glycogen in normal and complicated pregnancies, we must turn to animal models. Over 40 targeted mutations in mice demonstrate the defects in placental cells that store glycogen and suggest that placental glycogen represents a source of readily mobilized glucose required during periods of high fetal demand. However, direct functional evidence is currently lacking. Here, we evaluate these genetic mouse models with placental phenotypes that implicate glycogen trophoblast cell differentiation and function to illuminate the common molecular pathways that emerge and to better understand the relationship between placental glycogen and fetal growth. We highlight the current limitations in exploring the key questions regarding placental glycogen storage and metabolism and define how to experimentally overcome these constraints.

MATERNAL DIABETES INDUCES UPREGULATION OF HEPATIC INSULIN-LIKE GROWTH FACTOR BINDING PROTEIN-1 MRNA EXPRESSION, GROWTH RETARDATION AND DEVELOPMENTAL DELAY AT THE SAME STAGE OF RAT FETAL DEVELOPMENT

1997 ◽  
Vol 152 (1) ◽  
pp. R1-R6 ◽  
Author(s):  
Veeraramani S. Rajaratnam ◽  
Peggy J. Webb ◽  
Renata B. Fishman ◽  
Randal D. Streck
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Developmental Delay ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Fetal Development ◽  
Growth And Development ◽  
Maternal Diabetes ◽  
Insulin Like Growth Factor ◽  
Factor Binding

ABSTRACT Since maternal diabetes is associated with fetal growth abnormalities in humans and rats, effects of maternal diabetes on fetal expression of genes regulating growth are of interest. Increased expression of Insulin-Like Growth Factor Binding Protein-1 (IGFBP-1) is associated with several examples of growth retardation and is upregulated in response to diabetes. As we have shown previously, IGFBP-1 expression is upregulated in gestational day (GD) 14 rat fetuses in response to maternal diabetes. Here we analyze the effect of streptozotocin-induced maternal diabetes on IGFBP-1 mRNA expression during GD12-16 of rat fetal development, using in situ hybridization. IGFBP-1 mRNA was more abundant in GD12-14 fetal livers from diabetic dams than in livers of age-matched controls. This upregulation is not due to the approximately 1-day fetal developmental delay associated with maternal diabetes, as there is no gross difference in the level of IGFBP-1 mRNA in GD13 vs GD12 or GD14 vs GD13 control fetal livers. At GD15-16, however, we detected little difference in IGFBP-1 expression between experimental and control fetuses. This transient period of maternal diabetes-stimulated IGFBP-1 mRNA expression (GD12-14) is coincident with the sensitive period for maternal diabetes-induced defects in fetal growth and development, suggesting that IGFBP-1 is involved in the regulation of fetal growth and development in response to the maternal condition.

scholarly journals Maternal Glucose Concentration Influences Fetal Growth, Gestation, and Pregnancy Complications

2001 ◽  
Vol 154 (6) ◽  
pp. 514-520 ◽  
Author(s):  
Theresa O. Scholl ◽  
MaryFran Sowers ◽  
Xinhua Chen ◽  
Carine Lenders
Keyword(s):  
Fetal Growth ◽  
Glucose Concentration ◽  
Maternal Diabetes ◽  
Maternal Complications ◽  
Very Preterm ◽  
Lower Glucose ◽  
Increased Risk ◽  
Placental Inflammation ◽  
High Concentrations ◽  
Maternal Glucose

Abstract Using 1990–1995 data, the authors examined the influence of post-challenge maternal glucose concentration on pregnancy outcome in 1,157 nondiabetic US gravidas. After control for potential confounding variables and comparing gravidas with lower glucose concentrations (<99 mg/dl) with the others, they found that mean birth weight increased by 50 g and 200 g with glucose concentrations of 99–130 mg/dl and >130 mg/dl, respectively. Increased maternal glucose concentration also was associated with an increased risk of large-for-gestation fetuses (p for trend < 0.001) and a decreased risk of fetal growth restriction (p for trend < 0.05). The association between glucose and gestation was inverse and significantly shortened when glucose concentrations were higher. Maternal complications increased twofold or more with high glucose concentrations and included cesarean section and clinical chorioamnionitis. Chorioamnionitis in combination with high maternal glucose concentration increased the risk of very preterm delivery almost 12-fold. These observations extend Pedersen's hypothesis—that high concentrations of maternal glucose give rise to increased nutrient transfer to the fetus and increase fetal growth, beyond the model of maternal diabetes (Acta Endocrinol 1954;16:330–42). They raise the question of whether higher, but seemingly normal maternal glucose concentration predisposes to or is a marker for placental inflammation and infection.

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