Protein Deficiency and Intestinal Nematode Infection in Pregnant Mice Differentially Impact Fetal Growth through Specific Stress Hormones, Growth Factors, and Cytokines&gt;

Starr, Lisa; Scott, Marilyn; Koski, Kristine G.

doi:10.3945/jn.114.202630

Cited by 11 publications

(15 citation statements)

References 58 publications

(72 reference statements)

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“…The levels of IGF-1 increased with increasing Hb, and when the concentration of Hb exceeded a certain range, with the increase in Hb, IGF-1 decreased instead. Previous studies have shown that high Hb may impact the growth and development of children through mechanisms including inflammation, which may impair growth and development [16]. Our findings suggested that a too high of Hb is associated with reduced IGF-1 levels.…”

Section: Discussionsupporting

confidence: 52%

Relationship between hemoglobin and insulin-like growth factor-1 in children and adolescents with idiopathic short stature

Zhao

Zhang

et al. 2020

BMC Endocr Disord

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Background: The growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis is critical for the regulation of children's growth and development. Serum IGF-1 concentrations are usually low in individuals with idiopathic short stature (ISS) despite normal endogenous GH levels, and the associated underlying factors are unknown. This study aimed to explore the relationship between IGF-1 and hemoglobin (Hb) in children with ISS. Methods: A cross-sectional analysis was performed including 178 children and adolescents with ISS who were enrolled from March 2013 to February 2019. The related clinical and biochemical parameters were evaluated for each patient. Univariate analysis, smooth curve fitting and multivariate piecewise linear regression were performed. Result: The mean levels of IGF-1 standard deviation scores (SDS) and Hb were − 0.99 (− 1.60-0.09) and 131.81 ± 9.36 g/L, respectively. Univariate analysis displayed a significant positive association between Hb and IGF-1 SDS (P < 0.001). After adjusting for potential confounding factors, the positive relationship between Hb and IGF-1 SDS remained (P = 0.001). Furthermore, there was an inflection point for Hb in the curve. In a multivariate piecewise linear regression model, IGF-1 SDS was significantly positively associated with Hb when Hb concentrations were lower than 145 g/L (B 0.05; 95% CI 0.02, 0.07; P < 0.001). However, IGF-1 SDS decreased with increasing Hb levels when Hb concentrations were greater than 145 g/L (B-0.15; 95% CI-0.23, − 0.06; P = 0.001). Conclusion: This study demonstrated that Hb is associated with IGF-1 in Chinese children and adolescents with ISS. The levels of IGF-1 increased with the elevation of Hb, but when the concentration of Hb exceeded a certain range, with the increase of Hb, IGF-1 decreased instead.

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Section: Discussionsupporting

confidence: 52%

Relationship between hemoglobin and insulin-like growth factor-1 in children and adolescents with idiopathic short stature

Zhao

Zhang

et al. 2020

BMC Endocr Disord

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“…28,30,33,36 In three studies, the metabolic/nutritional exposure and the infectious exposure had additive effects without synergizing or antagonizing one another. 30,32,34 In two studies, zinc supplementation, which had no effect on its own, reversed the effect of LPS. 28,33 As already mentioned, two studies showed that maternal immune activation could reverse the effects of diabetes and iron deficiency.…”

Section: Animal Study Resultsmentioning

confidence: 99%

“…In this survey, HIV was not associated with an increased risk of spontaneous or provider-initiated PTB, consistent with Ndirangu et al 22 These findings reinforce the trend of PTB associated with small maternal stature and maternal infections demonstrated in the Tellapragada study. 25 Outcomes of maternal immune activation and metabolic abnormality in model systems A total of six studies were performed in mice, [28][29][30][31][32][33] two in rats, 34,35 and one in sheep 36 (Table 4). The rat studies both involved nutritional deficiency, while the sheep study and two of the mouse studies involved supplementation.…”

Section: Individual Studiesmentioning

confidence: 99%

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DOHaD at the intersection of maternal immune activation and maternal metabolic stress: a scoping review

Goldstein

Norris

Aronoff

2017

J Dev Orig Health Dis

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The prenatal environment is now recognized as a key driver of non-communicable disease risk later in life. Within the developmental origins of health and disease (DOHaD) paradigm, studies are increasingly identifying links between maternal morbidity during pregnancy and disease later in life for offspring. Nutrient restriction, metabolic disorders during gestation, such as diabetes or obesity, and maternal immune activation provoked by infection have been linked to adverse health outcomes for offspring later in life. These factors frequently co-occur, but the potential for compounding effects of multiple morbidities on DOHaD-related outcomes has not received adequate attention. This is of particular importance in low- or middle-income countries (LMICs), which have ongoing high rates of infectious diseases and are now experiencing transitions from undernutrition to excess adiposity. The purpose of this scoping review is to summarize studies examining the effect and interaction of co-occurring metabolic or nutritional stressors and infectious diseases during gestation on DOHaD-related health outcomes. We identified nine studies in humans - four performed in the United States and five in LMICs. The most common outcome, also in seven of nine studies, was premature birth or low birth weight. We identified nine animal studies, six in mice, two in rats and one in sheep. The interaction between metabolic/nutritional exposures and infectious exposures had varying effects including synergism, inhibition and independent actions. No human studies were specifically designed to assess the interaction of metabolic/nutritional exposures and infectious diseases. Future studies of neonatal outcomes should measure these exposures and explicitly examine their concerted effect.

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“…Specifically, mRNA expression and protein levels of FGF2 are increased in the endometrium in heifer cows fed a lower (protein 10% of dry matter) protein diet in comparison to lactating cows fed a greater (18% protein of dry matter) percentage protein diet (Pretheeban et al, 2011). Likewise, pregnant mice fed a protein deficient diet displayed an increased FGF2 concentration in the amniotic fluid (Starr et al, 2015). Complicated pregnancies involving intrauterine growth restriction have increased vasculogenesis, angiogenesis, and pseudovasculogenesis via the increased expressions of VEGF-A, FGF2, and eNOS (Barut et al, 2010).…”

Section: Discussionmentioning

confidence: 97%

Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFα expression in Sprague-Dawley rats

Vomhof-DeKrey

Darland

Ghribi

et al. 2016

Journal of Reproductive Immunology

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A maternal low-protein (LP) diet in Sprague-Dawley rats results in low birth weight, rapid adipose tissue catch-up growth, adult obesity, and insulin resistance. The placenta functions to fulfill the fetus' nutrient demands. Adequate angiogenic factor concentrations help to ensure normal growth and vasculature development of the placenta and, in turn, optimum maternal-to-fetal nutrient delivery. Maternal malnutrition creates a proinflammatory environment that leads to inhibition of placental tissue growth. Therefore, we hypothesized that a maternal LP diet will lead to abnormal angiogenesis via dysregulation of immune cells resulting in increased secretion of proinflammatory cytokines and reduced angiogenic factor expression. Sprague-Dawley dams were fed 8% LP or 20% normal protein diets for 3 weeks prior to breeding and throughout pregnancy. Placenta from dams fed a LP diet weighed less; had increased M2 macrophages producing TNFα, decreased M1 macrophages and iNKT cells; greater angiogenic factor (FGF2, VEGFR-1, IGF2) expression and protein content, and greater CD31/PECAM (platelet endothelial cell adhesion molecule) expression. Prenatal protein restriction may induce the placenta to upregulate compensatory mechanisms of angiogenesis in order to meet the nutrient demands of the fetus.

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Protein Deficiency and Intestinal Nematode Infection in Pregnant Mice Differentially Impact Fetal Growth through Specific Stress Hormones, Growth Factors, and Cytokines>

Abstract: PD and nematode infection impaired fetal mass and linear growth, respectively. Fetal mass, length, and individual organ masses were regulated by different hormones, growth factors, and cytokines.

Cited by 11 publications

References 58 publications

Relationship between hemoglobin and insulin-like growth factor-1 in children and adolescents with idiopathic short stature

Relationship between hemoglobin and insulin-like growth factor-1 in children and adolescents with idiopathic short stature

DOHaD at the intersection of maternal immune activation and maternal metabolic stress: a scoping review

Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFα expression in Sprague-Dawley rats

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