scholarly journals Maternal undernutrition during late gestation-induced intrauterine growth restriction in the rat is associated with impaired placental GLUT3 expression, but does not correlate with endogenous corticosterone levels

2002 ◽  
Vol 174 (1) ◽  
pp. 37-43 ◽  
Author(s):  
J Lesage ◽  
D Hahn ◽  
M Leonhardt ◽  
B Blondeau ◽  
B Breant ◽  
...  
Keyword(s):  
Body Weight ◽  
Plasma Glucose ◽  
Food Restriction ◽  
Glucose Transporter ◽  
Maternal Plasma ◽  
Plasma Corticosterone ◽  
Growth Restriction ◽  
Late Gestation ◽  
Glucose Content ◽  
Protein Levels

Fetal intrauterine growth restriction (IUGR) is a frequently occurring and serious complication of pregnancy. Infants exposed to IUGR are at risk for numerous perinatal morbidities, including hypoglycemia in the neonatal period, as well as increased risk of later physical and/or mental impairments, cardiovascular disease and non-insulin-dependent diabetes mellitus. Fetal growth restriction most often results from uteroplacental dysfunction during the later stage of pregnancy. As glucose, which is the most abundant nutrient crossing the placenta, fulfills a large portion of the fetal energy requirements during gestational development, and since impaired placental glucose transport is thought to result in growth restriction, we investigated the effects of maternal 50% food restriction (FR50) during the last week of gestation on rat placental expression of glucose transporters, GLUT1, GLUT3 and GLUT4, and on plasma glucose content in both maternal and fetal compartments. Moreover, as maternal FR50 induces fetal overexposure to glucocorticoids and since these hormones are potent regulators of placental glucose transporter expression, we investigated whether putative alterations in placental GLUT expression correlate with changes in maternal and/or fetal corticosterone levels. At term (day 21 of pregnancy), plasma glucose content was significantly reduced (P<0.05) in mothers subjected to FR50, but was not affected in fetuses. Food restriction reduced maternal body weight (P<0.001) but did not affect placental weight. Plasma corticosterone concentration, at term, was increased (P<0.05) in FR50 mothers. Fetuses from FR50 mothers showed reduced body weight (P<0.001) but higher plasma corticosterone levels (P<0.05). Adrenalectomy (ADX) followed by corticosterone supplementation of the mother prevented the FR50-induced rise in maternal plasma corticosterone at term. Food restriction performed on either sham-ADX or ADX mothers induced a similar reduction in the body weight of the pups at term (P<0.01). Moreover, plasma corticosterone levels were increased in pups from sham-ADX FR50 mothers (P<0.01) and in pups from ADX control mothers (P<0.01). Western blot analysis of placental GLUT proteins showed that maternal FR50 decreased placental GLUT3 protein levels in all experimental groups at term (P<0.05 and P<0.01), but did not affect either GLUT1 or GLUT4 protein levels. Northern blot analysis of placental GLUT expression showed that both GLUT1 and GLUT3 mRNA were not affected by the maternal feeding regimen or surgery. We concluded that prolonged maternal malnutrition during late gestation decreases maternal plasma glucose content and placental GLUT3 glucose transporter expression, but does not obviously affect fetal plasma glucose concentration. Moreover, the present results are not compatible with a role of maternal corticosterone in the development of growth-restricted rat fetuses.

Dexamethasone-Induced Intrauterine Growth Restriction Modulates Expression Of Placental Vascular Growth Factors And Fetal And Placental Growth

2021 ◽  
Author(s):  
Arias A ◽  
Schander Ja ◽  
Bariani MV ◽  
Correa F ◽  
Domínguez Rubio AP ◽  
...  
Keyword(s):  
Body Weight ◽  
Growth Retardation ◽  
Body Weight Gain ◽  
Fetal Tissue ◽  
Growth Restriction ◽  
Late Gestation ◽  
Dexamethasone Treatment ◽  
Intrauterine Growth ◽  
Beneficial Effects ◽  
Protein Levels

Abstract Prenatal exposure to glucocorticoids (GC) is a central topic of interest in medicine since GCs are essential for the maturation of fetal organs and intrauterine growth. Synthetic glucocorticoids, which are used in obstetric practice, exert beneficial effects on the fetus, but have also been reported to lead to intrauterine growth retardation (IUGR). In this study, a model of growth restriction in mice was established through maternal administration of dexamethasone during late gestation. We hypothesised that GC overexposure may adversely affect placental angiogenesis and fetal and placental growth. Female BALB/c mice were randomly assigned to control or dexamethasone treatment, either left to give birth or euthanised on days 15, 16, 17 and 18 of gestation followed by collection of maternal and fetal tissue. The IUGR rate increased to 100% in the dexamethasone group (8 mg/kg body weight on gestational days 14 and 15) and pups had clinical features of symmetrical IUGR at birth. Dexamethasone administration significantly decreased maternal body weight gain and serum corticosterone levels. Moreover, prenatal dexamethasone treatment not only induced fetal growth retardation but also decreased placental weight. In IUGR placentas, VEGFA protein levels and mRNA expression of VEGF receptors were reduced and NOS activity was lower. Maternal dexamethasone administration also reduced placental expression of the GC receptor, αGR. We demonstrated that maternal dexamethasone administration causes fetal and placental growth restriction. Furthermore, we propose that the growth retardation induced by prenatal GC overexposure may be caused, at least partially, by an altered placental angiogenic profile.

The influence of vanadate on insulin counter-regulatory hormones in obese fa/fa rats

1991 ◽  
Vol 131 (2) ◽  
pp. 185-191 ◽  
Author(s):  
S. M. Brichard ◽  
L. N. Ongemba ◽  
J. Kolanowski ◽  
J. C. Henquin
Keyword(s):  
Body Weight ◽  
Food Restriction ◽  
Body Weight Gain ◽  
Plasma Corticosterone ◽  
Plasma Glucagon ◽  
Lower Plasma ◽  
Peripheral Tissues ◽  
Insulin Resistant ◽  
Glucose Homoeostasis ◽  
Basal Plasma

ABSTRACT Vanadate has been shown to improve glucose homoeostasis in mildly glucose-intolerant and severely insulin-resistant fa/fa rats. The present study examined whether changes in insulin counter-regulatory hormones contribute to this beneficial effect of vanadate. Since oral administration of Na3VO4 caused a decrease in food intake and stopped the increase in body weight, vanadate-treated fa/fa rats were compared with both controls with food available ad libitum and pair-fed rats. Slightly lower plasma glucose levels were maintained in conjunction with markedly lower plasma insulin levels in vanadatetreated rats, and this effect was not simply due to the smaller body weight of the animals. Compared with control rats, treatment with vanadate affected neither basal plasma glucagon levels nor the increase in glucagon levels observed after insulin-induced hypoglycaemia or after i.v. injection of arginine. Compared with pair-fed rats, treatment with vanadate prevented the fall in basal plasma glucagon and its exaggerated rise in response to insulin that mere food restriction produced. Plasma corticosterone levels were high in fa/fa rats. Vanadate and pair-feeding similarly decreased basal plasma levels of corticosterone as well as nocturnal corticosteronuria. Thus the attenuation of the hypercorticism of fa/fa rats results from the reduction in body weight gain rather than from a specific action of vanadate. Vanadate did not influence urinary excretion of noradrenaline, an index of neural sympathetic activity, but prevented the increase in adrenaline excretion, an index of adrenal medulla activity, that was produced by food restriction in pair-fed rats. In conclusion, vanadate administration has no or little specific effects on three major insulin counter-regulatory hormones. This reinforces the suggestion that the beneficial effects of vanadate on glucose homoeostasis in fa/fa rats are mainly due to a correction of insulin resistance in peripheral tissues. Journal of Endocrinology (1991) 131, 185–191

Chronically altered body protein levels following lateral hypothalamic lesions in rats

1996 ◽  
Vol 270 (4) ◽  
pp. R738-R743 ◽  
Author(s):  
M. D. Hirvonen ◽  
R. E. Keesey
Keyword(s):  
Body Weight ◽  
Food Restriction ◽  
The Body ◽  
Lean Tissue ◽  
Body Protein ◽  
Protein Mass ◽  
Protein Levels ◽  
Reduced Body ◽  
Irreversible Reduction ◽  
Body Weights

Rats maintaining reduced body weights after lesions of the lateral hypothalamus (LH; LH rats) are characterized by smaller body protein masses. Two experiments were conducted to determine whether this reduced protein mass is actively defended. In the first, it was found that LH rats induced to overeat and restore body weight to the level of nonlesioned controls markedly increased their body fat without significantly increasing body protein. That is, LH rats at normal body weights were notably obese. In the second experiment, body protein losses produced by food restriction in LH rats were both relatively small and proportionally the same as those seen in similarly restricted nonlesioned controls. These observations demonstrate that LH rats retain the capacity for preserving body protein when challenged by either under- or overnutrition. The apparently irreversible reduction in the body protein mass thus appears to be the result of a specific lean tissue downregulation induced by LH damage.

scholarly journals Effect of ozone exposure on Amyotrophic Lateral Sclerosis (ALS) pathology using a mice model of TDP-43 proteinopathy

2021 ◽  
Author(s):  
Ana Rodriguez ◽  
Agueda Ferrer-Donato ◽  
Marta Cabrera-Pinto ◽  
Susana Seseña ◽  
Paloma Fernández ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Body Weight ◽  
Plasma Glucose ◽  
Motor Performance ◽  
Motor Coordination ◽  
Ozone Exposure ◽  
Mice Model ◽  
Inhibitory Peptide ◽  
Glucose Content ◽  
Lateral Sclerosis

AbstractBackgroundOzone (O3), one of the main photochemical pollutants in the atmosphere today, is a serious health risk factor. Although the effects of O3 exposure have been documented on many diseases, they have not yet been examined on Amyotrophic Lateral Sclerosis (ALS)- a fatal progressive and neurodegenerative disease.ObjectivesTo investigate the effect of the O3 exposure in a mice model of TDP-43 proteinopathy, exploring a possible association between the O3 exposure and the ALS pathogenesis.MethodsTDP-43A315T and wild-type (WT) mice were exposed to O3 (0.25 ppm) or filtered air (FA) for 15 days (4 hours/day). We assessed (1) weight loss (2) motor performance (3) plasma glucose content and (4) metabolic markers from plasma samples of the animals.ResultsThroughout the experiment, we observed a progressive decline in body weight and the motor coordination in TDP-43A315T mice compared to WT controls. Although there was a trend, there were no significant differences in the decline of body weight of TDP-43A315T mice when exposed to either FA or O3. In O3-TDP-43A315T mice, the disease duration lasted longer. In addition, O3-TDP-43A315T mice showed improvements in motor performance as well TDP-43A315T mice were hypoglycemic compared to WT mice. However, FA-TDP-43A315T mice showed lower plasma glucose levels at the disease end-stage. We found altered levels of adipokines and metabolic proteins in TDP-43A315T mice compared to WT controls. A positive correlation was found among GIP and glucagon compared to insulin concentrations in control mice. Interestingly, resistin, Gastric Inhibitory Peptide (GIP), Glucagon Like Peptide 1 (GIP-1) and insulin levels were higher in O3-TDP-43A315T mice.DiscussionWe provide new evidence about a mechanistic link between O3 exposure and the improvement of the metabolic disturbances present in TDP-43A315T mice. Further studies are needed to corroborate the obtained results as they warrant to understanding the underlying mechanisms.

Comparison of two models of intrauterine growth restriction for early catch-up growth and later development of glucose intolerance and obesity in rats

2010 ◽  
Vol 298 (1) ◽  
pp. R141-R146 ◽  
Author(s):  
Yasaman Shahkhalili ◽  
Julie Moulin ◽  
Irene Zbinden ◽  
Olivier Aprikian ◽  
Katherine Macé
Keyword(s):  
Body Weight ◽  
Birth Weight ◽  
Food Intake ◽  
Glucose Intolerance ◽  
Intrauterine Growth Restriction ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Catch Up

Two models of intrauterine growth restriction, maternal food restriction (FR), and dexamethasone (DEX) exposure were compared for early postnatal catch-up growth and later development of glucose intolerance and obesity in Sprague-Dawley rats. Mated dams were randomly divided into three groups at 10 days gestational age. Group FR was food restricted (50% of nongestating rats) during the last 11 days of gestation; Group DEX received DEX injections during the last week of gestation, and Group CON, the control group, had no intervention. Birth weight, catch-up growth, body weight, and food intake were measured in male offspring for 22 wk. Body composition, blood glucose, and plasma insulin in response to a glucose load were assessed at 8, 16, and 22 wk. Pups from both FR and DEX dams had similarly lower birth weights than CON (22% and 25%, P < 0.0001), but catch-up growth, which occurred during the suckling period, was much more rapid in FR than DEX offspring (6 vs. 25 days, 95% CI). Postweaning, there were no significant differences between groups in food intake, body weight, body fat, and plasma insulin, but baseline plasma glucose at 22 wk and 2-h glucose area-under-the-curve at 8 and 22 wk were greater only in FR vs. CON offspring ( P < 0.05), thereby contrasting with the lack of significant differences between DEX and CON. These results suggest that prenatal food restriction is a more sensitive model than DEX exposure for studies aimed at investigating the link between low birth weight, early postnatal catch-up growth, and later development of glucose intolerance.

Glucose transporter isoform-3 mutations cause early pregnancy loss and fetal growth restriction

2007 ◽  
Vol 292 (5) ◽  
pp. E1241-E1255 ◽  
Author(s):  
Amit Ganguly ◽  
Robert A. McKnight ◽  
Santanu Raychaudhuri ◽  
Bo-Chul Shin ◽  
Zhigui Ma ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Fetal Growth ◽  
Early Pregnancy ◽  
Fetal Growth Restriction ◽  
Pregnancy Loss ◽  
Glucose Transporter ◽  
Growth Restriction ◽  
Late Gestation ◽  
Null Mouse ◽  
Early Pregnancy Loss

Glucose transporter isoform-3 (GLUT3) is the trophoblastic facilitative glucose transporter. To investigate the role of this isoform in embryonic development, we created a novel GLUT3-null mouse and observed arrested early embryonic development and loss at neurulation stage when both alleles were mutated. This loss occurred despite the presence of other related isoforms, particularly GLUT1. In contrast, when a single allele was mutated, despite increased embryonic cell apoptosis, adaptive changes in the subcellular localization of GLUT3 and GLUT1 in the preimplantation embryo led to postimplantation survival. This survival was compromised by decreased GLUT3-mediated transplacental glucose transport, causing late-gestation fetal growth restriction. This yielded young male and female adults demonstrating catch-up growth, with normal basal glucose, insulin, insulin-like growth factor-I and IGF-binding protein-3 concentrations, fat and lean mass, and glucose and insulin tolerance. We conclude that GLUT3 mutations cause a gene dose-dependent early pregnancy loss or late-gestation fetal growth restriction despite the presence of embryonic and placental GLUT1 and a compensatory increase in system A amino acid placental transport. This critical life-sustaining functional role for GLUT3 in embryonic development provides the basis for investigating the existence of human GLUT3 mutations with similar consequences during early pregnancy.

scholarly journals Prepartum Maternal Plasma Glucose Concentrations and Placental Glucose Transporter mRNA Expression in Cows Carrying Somatic Cell Clone Fetuses

2011 ◽  
Vol 57 (1) ◽  
pp. 57-61 ◽  
Author(s):  
Hiroki HIRAYAMA ◽  
Ken SAWAI ◽  
Muneyuki HIRAYAMA ◽  
Tomokazu HIRAI ◽  
Soichi KAGEYAMA ◽  
...  
Keyword(s):  
Somatic Cell ◽  
Mrna Expression ◽  
Plasma Glucose ◽  
Glucose Transporter ◽  
Cell Clone ◽  
Maternal Plasma ◽  
Glucose Transporter Mrna

scholarly journals High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2140
Author(s):  
Yumiko Takahashi ◽  
Yutaka Matsunaga ◽  
Hiroki Yoshida ◽  
Terunaga Shinya ◽  
Ryo Sakaguchi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transporter ◽  
High Carbohydrate Diet ◽  
Oral Glucose ◽  
Carbohydrate Diet ◽  
Post Exercise ◽  
Glucose Administration ◽  
Protein Levels ◽  
High Carbohydrate ◽  
Glucose Transporter 2

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

scholarly journals Male Fetal Sex Affects Uteroplacental Angiogenesis in Growth Restriction Mouse Model†

2021 ◽  
Author(s):  
Jessica F Hebert ◽  
Jess A Millar ◽  
Rahul Raghavan ◽  
Amie Romney ◽  
Jason E Podrabsky ◽  
...  
Keyword(s):  
Mouse Model ◽  
Killer Cell ◽  
Receptor Activation ◽  
Growth Restriction ◽  
Late Gestation ◽  
Spiral Artery ◽  
Micro Computed Tomography ◽  
Fetal Sex ◽  
Maternal Genotype ◽  
Agt Gene

Abstract Abnormally increased angiotensin II activity related to maternal angiotensinogen (AGT) genetic variants, or aberrant receptor activation, is associated with small-for-gestational-age (SGA) babies and abnormal uterine spiral artery remodeling in humans. Our group studies a murine AGT gene titration transgenic (TG; 3-copies of the AGT gene) model, which has a 20% increase in AGT expression mimicking a common human AGT genetic variant (A[−6]G) associated with intrauterine growth restriction (IUGR) and spiral artery pathology. We hypothesized that aberrant maternal AGT expression impacts pregnancy-induced uterine spiral artery angiogenesis in this mouse model leading to IUGR. We controlled for fetal sex and fetal genotype (e.g., only 2-copy wild-type [WT] progeny from WT and TG dams were included). Uteroplacental samples from WT and TG dams from early (days 6.5 and 8.5), mid (d12.5), and late (d16.5) gestation were studied to assess uterine natural killer cell (uNK) phenotypes, decidual metrial triangle angiogenic factors, placental growth and capillary density, placental transcriptomics, and placental nutrient transport. Spiral artery architecture was evaluated at day 16.5 by contrast-perfused three-dimensional micro-computed tomography (3D microCT). Our results suggest that uteroplacental angiogenesis is significantly reduced in TG dams at day 16.5. Males from TG dams are associated with significantly reduced uteroplacental angiogenesis from early to late gestation compared with their female littermates and WT controls. Angiogenesis was not different between fetal sexes from WT dams. We conclude that male fetal sex compounds the pathologic impact of maternal genotype in this mouse model of growth restriction.

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