Glycogen Storage in Fetuses of Trained Pregnant Rats

1997 ◽  
Vol 22 (4) ◽  
pp. 384-393 ◽  
Author(s):  
Pamela E. Houghton ◽  
Michelle F. Mottola ◽  
Jamie Mezzapelli ◽  
Richard Vandermolen ◽  
Paul D. Christopher

The purpose was to determine if running 30 m/min on a 10° incline, 60 min/day for 5 days/week altered fetal glycogen storage in prepregnancy trained rats. Animals that exercised for 3 weeks prior to pregnancy either continued the same exercise program until Day 19 of gestation (pregnant running group [PR]), or ceased exercising at conception (pregnant controls [PC]). A separate set of animals did not exercise either before or during pregnancy (pregnant nonrunning control group [PNRC]). On Day 20 of gestation, fetal organs and placenta were weighed and analyzed for glycogen concentration. Glycogen concentrations were not different in either fetal liver, heart, or placenta of PR rats compared to PNRC animals. However, fetal liver glycogen concentration was significantly lower in the fetal heart and liver of PC animals compared to glycogen measured in both PNRC and PR animals (p < .0.5). These results suggest that exercise of this intensity does not compromise fetal glycogen storage in trained pregnant rats. However, chronic prepregnancy exercise and then abrupt cessation of exercise at conception may compromise fetal growth and development. Key words: exercise training, pregnancy, fetal glycogen

1991 ◽  
Vol 71 (3) ◽  
pp. 1015-1019 ◽  
Author(s):  
M. F. Mottola ◽  
P. D. Christopher

To examine the effects of maternal exercise on liver and skeletal muscle glycogen storage, female Sprague-Dawley rats were randomly divided into control, nonpregnant runner, pregnant nonrunning control, pregnant runner, and prepregnant exercised control groups. The exercise consisted of treadmill running at 30 m/min on a 10 degree incline for 60 min, 5 days/wk. Pregnancy alone, on day 20 of gestation, decreased maternal liver glycogen content and increased red and white gastrocnemius muscle glycogen storage above control values (P less than 0.05). In contrast, exercise in nonpregnant animals augmented liver glycogen storage and also increased red and white gastrocnemius glycogen content (P less than 0.05). By combining exercise and pregnancy, the decrease in liver glycogen storage in the pregnant nonexercised condition was prevented in the pregnant runner group and more glycogen was stored in both the red and white portions of the gastrocnemius than all other groups (P less than 0.05). Fetal body weight was greatest (P less than 0.05) in the pregnant runner group and lowest (P less than 0.05) in the prepregnant exercise control group. These results demonstrate that chronic maternal exercise may change maternal glycogen storage patterns in the liver and skeletal muscle with some alteration in fetal outcome.


1986 ◽  
Vol 60 (4) ◽  
pp. 1254-1258 ◽  
Author(s):  
K. I. Carlson ◽  
H. T. Yang ◽  
W. S. Bradshaw ◽  
R. K. Conlee ◽  
W. W. Winder

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22–60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.


2015 ◽  
Vol 128 (10) ◽  
pp. 707-713 ◽  
Author(s):  
Mavin Macauley ◽  
Fiona E Smith ◽  
Peter E Thelwall ◽  
Kieren G Hollingsworth ◽  
Roy Taylor

In health, food carbohydrate is stored as glycogen in muscle and liver, preventing a deleterious rise in osmotically active plasma glucose after eating. Glycogen concentrations increase sequentially after each meal to peak in the evening, and fall to fasting levels thereafter. Skeletal muscle accounts for the larger part of this diurnal buffering capacity with liver also contributing. The effectiveness of this diurnal mechanism has not been previously studied in Type 2 diabetes. We have quantified the changes in muscle and liver glycogen concentration with 13C magnetic resonance spectroscopy at 3.0 T before and after three meals consumed at 4 h intervals. We studied 40 (25 males; 15 females) well-controlled Type 2 diabetes subjects on metformin only (HbA1c (glycated haemoglobin) 6.4±0.07% or 47±0.8 mmol/mol) and 14 (8 males; 6 females) glucose-tolerant controls matched for age, weight and body mass index (BMI). Muscle glycogen concentration increased by 17% after day-long eating in the control group (68.1±4.8 to 79.7±4.2 mmol/l; P=0.006), and this change inversely correlated with homoeostatic model assessment of insulin resistance [HOMA-IR] (r=−0.56; P=0.02). There was no change in muscle glycogen in the Type 2 diabetes group after day-long eating (68.3±2.6 to 67.1±2.0 mmol/mol; P=0.62). Liver glycogen rose similarly in normal control (325.9±25.0 to 388.1±30.3 mmol/l; P=0.005) and Type 2 diabetes groups (296.1±16.0 to 350.5±6.7 mmol/l; P<0.0001). In early Type 2 diabetes, the major physiological mechanism for skeletal muscle postprandial glycogen storage is completely inactive. This is directly related to insulin resistance, although liver glycogen storage is normal.


2003 ◽  
Vol 176 (2) ◽  
pp. 247-255 ◽  
Author(s):  
MR Pickard ◽  
AJ Leonard ◽  
LM Ogilvie ◽  
PR Edwards ◽  
IM Evans ◽  
...  

Maternal hypothyroidism impairs fetal growth in the rat, but the mechanisms by which this occurs are unknown. Since the fetus derives its glucose supply from the mother, and maternal thyroidectomy may disturb maternal and placental glucose metabolism, we postulated that maternal and/or placental glucose metabolic compromise may contribute to fetal growth retardation in hypothyroid dams. Feto-placental growth, tissue glycogen stores and glucose levels in sera and amniotic fluid were determined in rat dams partially thyroidectomized (TX) before pregnancy and in euthyroid controls. Fetal body weight at 16, 19 and 21 days gestation (d.g.) was related to pre-mating maternal serum total thyroxine (TT(4)) levels; permanent fetal growth retardation occurred in severely (TX(s); pre-mating maternal serum TT(4) 16.19 nM) - but not in moderately (TX(m)) - hypothyroid dams. In TX(s) dams, glycogen concentration was elevated in maternal liver and in the fetal side of the placenta at 16 and 19 d.g., and in the maternal side of the placenta at 19 and 21 d.g., despite maternal euglycemia. In contrast, fetal liver glycogen concentration was deficient in TX(m) dams at 19 d.g. and in TX(s) dams at 19 and 21 d.g., and fetal hypoglycemia occurred in TX(s) dams at 21 d.g. Multiple regression analyses indicate that these fetal deficits are strongly associated with the retardation in fetal growth, while the elevated maternal liver and placental glycogen concentrations have no impact on fetal growth near term. The mechanisms by which severe maternal hypothyroidism permanently retards rat fetal growth remain to be determined.


2020 ◽  
Vol 11 (3) ◽  
pp. 2866-2878
Author(s):  
Abdel-Rahman Tawfik ◽  
Nouf Bader Alduweesh ◽  
Zeinab Abdel-Hameid Mohamed ◽  
Abdel Rahman Sayed Sultan ◽  
Heba Ali Abd El-Rahman

Diclofenac (DCF) is one of the most generally utilized non-steroidal antiinflammatory therapies during the world for different diseases curing in post pubertal ladies. Be that as it may, constrained data is accessible with respect to its security during pregnancy and teratogenicity. The present study was done to investigate the histopathological impact of diclofenac potassium (DP) on some vital maternal and fetal tissues, placenta and liver during two different periods of gestation. In this study 30 pregnant rats have been used and divided into 3 groups (ten for each one); group 1 (control), group 2 treated with 15.4 mg/kg of diclofenac potassium during organogenesis period, and group 3 subjected during fetal developmental period with the same dosage. At the 20 gestation day the rats were anesthetized and dissected, histopathological studies on placenta, maternal liver, and fetal liver have been done. Our results revealed moderate to severe histopathological alternations in all examined tissues like disorganization of tissue architecture, vacuolation, lymphatic infiltration, apoptosis and more changes. There is a harmful effect of the DP on the placenta tissue and also the liver tissue of the fetus, and on this we recommend that you use the DP with caution during pregnancy at the possible lowest effective dose and for the shortest duration.


2000 ◽  
Vol 25 (6) ◽  
pp. 443-452 ◽  
Author(s):  
P.E. Houghton ◽  
M.F. Mottola ◽  
J.H. Plust ◽  
C.L. Schachter

The purpose was to determine the effects of exercise on fetal and placental glycogen storage patterns at 20 days gestation (term 21 days) in mature (approximately 12 months of age) Sprague-Dawley rats. The exercise protocol consisted of treadmill running at 30 m min−1, on a 10 incline, for 60 min, 5 days per week, for 4 weeks prior to conception, which continued until day 19 of pregnancy. Exercise produced a significant reduction in fetal body weight, placental weight, and fetal organ weights (heart, kidney, brain, and liver) compared to sedentary control animals (p < .05). However, when fetal body size was taken into account, these differences disappeared, except for the fetal brain:body weight ratio, which was larger in the exercised animals compared to controls (p < .05). Fetal liver glycogen concentrations were significantly lower in exercised animals compared to nonrunning control animals (p < .05). These results demonstrate that exercise of mature rats may compromise fetal development and hepatic glycogen storage in the fetus. Key words: age, exercise, pregnancy, fetal glycogen storage patterns


Author(s):  
Yutaka Matsunaga ◽  
Kenya Takahashi ◽  
Yumiko Takahashi ◽  
Hideo Hatta

Abstract Background When a high-carbohydrate diet is ingested, whether as small frequent snacks or as large meals, there is no difference between the two with respect to post-exercise glycogen storage for a period of 24 h. However, the effect of carbohydrate intake frequency on glycogen recovery a few hours after exercise is not clear. Athletes need to recover glycogen quickly after physical exercise as they sometimes exercise multiple times a day. The aim of this study was to determine the effect of carbohydrate intake at different frequencies on glycogen recovery during the first few hours after exercise. Methods After 120 min of fasting, 6-week-old male ICR mice were subjected to treadmill running exercise (20 m/min for 60 min) to decrease the levels of muscle and liver glycogen. Mice were then given glucose as a bolus (1.2 mg/g of body weight [BW], immediately after exercise) or as a pulse (1.2 mg/g of BW, every 15 min × 4 times). Following this, the blood, tissue, and exhaled gas samples were collected. Results In the bolus group, blood glucose concentration was significantly lower and plasma insulin concentration was significantly higher than those in the pulse group (p < 0.05). The plantaris muscle glycogen concentration in the bolus group was 25.3% higher than that in the pulse group at 60 min after glucose ingestion (p < 0.05). Liver glycogen concentration in the pulse group was significantly higher than that in the bolus group at 120 min after glucose ingestion (p < 0.05). Conclusions The present study showed that ingesting a large amount of glucose immediately after exercise increased insulin secretion and enhanced muscle glycogen recovery, whereas frequent and small amounts of glucose intake was shown to enhance liver glycogen recovery.


2012 ◽  
Vol 55 (2) ◽  
pp. 251-256
Author(s):  
Isabela Lovizutto Iessi ◽  
Aline Bueno ◽  
Yuri Karen Sinzato ◽  
Ana Paula Machado Spada ◽  
Marilza Vieira Cunha Rudge ◽  
...  

1988 ◽  
Vol 256 (2) ◽  
pp. 487-491 ◽  
Author(s):  
A Zorzano ◽  
E Herrera

1. Incorporation of gluconeogenic precursors into blood glucose and hepatic glycogen and acylglycerol glycerol was examined in 24 h-fasted virgin rats by using a flooding procedure for substrate administration. At 10 min after their intravenous injection, the conversion of alanine or glycerol into liver glycogen or acylglycerol glycerol was proportional to glucose synthesis. 2. In 24 h-fasted 21-day-pregnant rats, the incorporation of alanine and glycerol into hepatic acylglycerol glycerol was markedly enhanced compared with the control group. In addition, during fasting at late pregnancy, the proportion of substrates directed to acylglycerol glycerol as compared with the fraction incorporated into glucose was augmented. 3. In pentobarbital-treated fasted rats, the incorporation of both alanine and pyruvate into circulating glucose and into hepatic glycogen and acylglycerol glycerol was increased. Pentobarbital treatment increased the proportion of substrates incorporated into liver glycogen, compared with the fraction appearing in circulating glucose. These changes were concomitant with a marked accumulation of glycogen. 4. The data indicate that, during fasting, gluconeogenesis provides glucose as well as hepatic glycogen and acylglycerol glycerol, independently of whether the substrates enter gluconeogenesis at the level of pyruvate or dihydroxyacetone phosphate.


Open Medicine ◽  
2007 ◽  
Vol 2 (4) ◽  
pp. 447-457 ◽  
Author(s):  
Sebahat Turgut ◽  
Yaşar Enli ◽  
Gülten Emmungil ◽  
Günfer Turgut ◽  
Süleyman Demir ◽  
...  

AbstractIn the current study, we examined the effects of Cd on Cd, Cu, Zn and Fe levels in placenta and maternal and fetal plasma and tissues, the placental weight, total fetal and maternal body weights, and fetal and maternal tissue weights during pregnancy. A total of 21 adult female rats were treated during gestation with drinking water containing one of the following: 70 mg/L of CdCl2, a combination of 70 mg/L of CdCl2 and 70 mg/L of CuSO4, or no addition (control). Placenta Cu and Fe levels, fetal liver and kidney Cu levels, and fetal liver tissue weights were lower in the group administered Cd than in the control group. Also, Cd levels in the placenta, maternal and fetal liver, and maternal kidney were higher in the group treated with Cd than in controls. In the group administered both Cd and Cu, fetal body and tissue weights did not change, but Cd levels in the placenta, maternal and fetal liver, and maternal kidneys were higher than in controls. Zn and Fe levels in the maternal kidney and fetal liver were also lower in this group. Cd exposure during pregnancy resulted in Cd accumulation in maternal and fetal tissues during pregnancy and a decrease in the total weight of fetuses, and the combination of Cd and Cu caused some changes in the both maternal and fetal levels of Cu, Zn, and Fe, but it did not cause changes in the total fetal body weight or the weights of individual tissues.


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