Effect of Maternal Exercise on Fetal and Placental Glycogen Storage in the Mature Rat

2000 ◽  
Vol 25 (6) ◽  
pp. 443-452 ◽  
Author(s):  
P.E. Houghton ◽  
M.F. Mottola ◽  
J.H. Plust ◽  
C.L. Schachter
Keyword(s):  
Fetal Liver ◽  
Weight Ratio ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Treadmill Running ◽  
Hepatic Glycogen ◽  
Sprague Dawley ◽  
Fetal Organ ◽  
Maternal Exercise ◽  
Storage Patterns

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

Effects of exercise on maternal glycogen storage patterns and fetal outcome in mature rats

1992 ◽  
Vol 70 (12) ◽  
pp. 1634-1638 ◽  
Author(s):  
M. F. Mottola ◽  
J. H. Plust ◽  
P. D. Christopher ◽  
C. L. Schachter
Keyword(s):  
Liver Glycogen ◽  
Fetal Outcome ◽  
Glycogen Storage ◽  
Treadmill Running ◽  
Sprague Dawley ◽  
Glycogen Concentration ◽  
Maternal Liver ◽  
Negative Effect ◽  
Maternal Exercise ◽  
Storage Patterns

The purpose of the present study was to examine the effects of exercise on maternal glycogen storage patterns and fetal outcome in mature (approximately 12 months of age) Sprague–Dawley rats. The exercise 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 pregnancy, which continued until day 19 of gestation. In mature animals, chronic exercise increased (p < 0.05) liver glycogen concentration in both pregnant and nonpregnant rats. In pregnant exercised animals, the glycogen concentration of the maternal liver increased almost twofold (p < 0.05) compared with the sedentary pregnant group. There was no difference in the amount of glycogen stored in the gastrocnemius or soleus muscles in response to training, pregnancy, or chronic maternal exercise in the mature rat. In the pregnant groups, there were fewer (p < 0.05) viable fetuses and more (p < 0.05) resorption sites than in young rats. In addition, exercise during pregnancy in the mature animal decreased (p < 0.05) fetal body weight. These results demonstrate that a conflict may exist between maternal exercise and fetal demands for energy in the mature rat. This conflict seems to favour the maternal system, as evidenced by the enhanced maternal liver glycogen storage and the negative effect on fetal growth.Key words: age, exercise, pregnancy, glycogen storage patterns.

Effects of maternal exercise on liver and skeletal muscle glycogen storage in pregnant rats

1991 ◽  
Vol 71 (3) ◽  
pp. 1015-1019 ◽  
Author(s):  
M. F. Mottola ◽  
P. D. Christopher
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Treadmill Running ◽  
Control Group ◽  
Skeletal Muscle Glycogen ◽  
Maternal Exercise ◽  
White Gastrocnemius

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.

Effect of maternal exercise on fetal liver glycogen late in gestation in the rat

1986 ◽  
Vol 60 (4) ◽  
pp. 1254-1258 ◽  
Author(s):  
K. I. Carlson ◽  
H. T. Yang ◽  
W. S. Bradshaw ◽  
R. K. Conlee ◽  
W. W. Winder
Keyword(s):  
Fetal Liver ◽  
Metabolic Stress ◽  
Liver Glycogen ◽  
Moderate Intensity ◽  
Blood Levels ◽  
Pregnant Rats ◽  
Maternal Liver ◽  
Maternal Exercise ◽  
Glucose Plasma ◽  
Glucagon And Insulin

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.

scholarly journals CREBH Maintains Circadian Glucose Homeostasis by Regulating Hepatic Glycogenolysis and Gluconeogenesis

2017 ◽  
Vol 37 (14) ◽  
Author(s):  
Hyunbae Kim ◽  
Ze Zheng ◽  
Paul D. Walker ◽  
Gregory Kapatos ◽  
Kezhong Zhang
Keyword(s):  
Blood Glucose ◽  
Glucose Homeostasis ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Hepatic Glycogen ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Glucose Levels ◽  
Blood Glucose Levels

ABSTRACT Cyclic AMP-responsive element binding protein, hepatocyte specific (CREBH), is a liver-enriched, endoplasmic reticulum-tethered transcription factor known to regulate the hepatic acute-phase response and lipid homeostasis. In this study, we demonstrate that CREBH functions as a circadian transcriptional regulator that plays major roles in maintaining glucose homeostasis. The proteolytic cleavage and posttranslational acetylation modification of CREBH are regulated by the circadian clock. Functionally, CREBH is required in order to maintain circadian homeostasis of hepatic glycogen storage and blood glucose levels. CREBH regulates the rhythmic expression of the genes encoding the rate-limiting enzymes for glycogenolysis and gluconeogenesis, including liver glycogen phosphorylase (PYGL), phosphoenolpyruvate carboxykinase 1 (PCK1), and the glucose-6-phosphatase catalytic subunit (G6PC). CREBH interacts with peroxisome proliferator-activated receptor α (PPARα) to synergize its transcriptional activities in hepatic gluconeogenesis. The acetylation of CREBH at lysine residue 294 controls CREBH-PPARα interaction and synergy in regulating hepatic glucose metabolism in mice. CREBH deficiency leads to reduced blood glucose levels but increases hepatic glycogen levels during the daytime or upon fasting. In summary, our studies revealed that CREBH functions as a key metabolic regulator that controls glucose homeostasis across the circadian cycle or under metabolic stress.

The glucoregulatory response to high-intensity aerobic exercise following training in rats with insulin-treated type 1 diabetes mellitus

2016 ◽  
Vol 41 (6) ◽  
pp. 631-639 ◽  
Author(s):  
Matthew W. McDonald ◽  
Michael R. Murray ◽  
Kenneth N. Grise ◽  
T. Dylan Olver ◽  
Adwitia Dey ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Blood Glucose ◽  
Type 1 Diabetes Mellitus ◽  
Acute Exercise ◽  
Aerobic Training ◽  
Glycogen Storage ◽  
Treadmill Running ◽  
Hepatic Glycogen

An acute bout of exercise elicits a rapid, potentially deleterious, reduction in blood glucose in patients with type 1 diabetes mellitus (T1DM). In the current study, we examined whether a 10-week aerobic training program could alleviate the rapid exercise-associated reduction in blood glucose through changes in the glucoregulatory hormonal response or increased hepatic glycogen storage in an insulin-treated rat model of T1DM. Thirty-two male Sprague–Dawley rats were divided evenly into 4 groups: non-T1DM sedentary (C) (n = 8), non-T1DM exercised (CX) (n = 8), T1DM sedentary (D) (n = 8), and T1DM exercised (DX) (n = 8). Exercise training consisted of treadmill running for 5 days/week (1 h, 27 m/min, 6% grade) for 10 weeks. T1DM was induced by multiple streptozotocin injections (20 mg/kg) followed by implantation of subcutaneous insulin pellets. At week 1, an acute exercise bout led to a significant reduction in blood glucose in DX (p < 0.05), whereas CX exhibited an increase in blood glucose (p < 0.05). During acute exercise, serum epinephrine was increased in both DX and CX (p < 0.05), whereas serum glucagon was increased during recovery only in CX (p < 0.01). Following aerobic training in DX, the exercise-mediated reduction in blood glucose remained; however, serum glucagon increased to the same extent as in CX (p < 0.05). DX exhibited significantly less hepatic glycogen (p < 0.001) despite elevations in glycogenic proteins in the liver (p < 0.05). Elevated serum epinephrine and decreased hepatic adrenergic receptor expression were also evident in DX (p < 0.05). In summary, despite aerobic training in DX, abrupt blood glucose reductions and hepatic glycogen deficiencies were evident. These data suggest that sympathetic overactivity may contribute to deficiencies in hepatic glycogen storage.

scholarly journals N6-methyladenosine modification governs liver glycogenesis by stabilizing the glycogen synthase 2 mRNA

2021 ◽  
Author(s):  
Xiang Zhang ◽  
Huilong Yin ◽  
Xiaofang Zhang ◽  
Xunliang Jiang ◽  
Yongkang Liu ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Molecular Mechanism ◽  
Knockout Mice ◽  
Glycogen Synthase ◽  
Critical Role ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Hepatic Glycogen

Abstract Hepatic glycogen is the main source of blood glucose and controls the intervals between meals in mammals. Hepatic glycogen storage in mammalian pups is insufficient compared to their adult counterparts; however, the detailed molecular mechanism is poorly understood. Here, we showed that, similar to glycogen storage pattern, N6-methyladenosine (m6A) modification in mRNAs gradually increases during the growth of mice in liver. Strikingly, in the liver-specific Mettl3 knockout mice, loss of m6A modification disrupts liver glycogen storage. On the mechanism, we screened and identified that glycogen synthase 2 (Gys2) plays a critical role in m6A-mediated regulation of liver glycogen storage. Furthermore, IGF2BP2, as a “reader” of m6A, stabilizes the mRNA of Gys2. More importantly, reconstitution of GYS2 rescues liver glycogenesis in Mettl3-cKO mice. Collectively, a METTL3-IGF2BP2-GYS2 axis, in which METTL3 and IGF2BP2 regulate glycogenesis as “writer” and “reader” respectively, plays a critical role on maintenance of liver glycogenesis in mammals.

scholarly journals Age-related augmentation of phosphorylase b kinase in hepatic tissue from the glycogen-storage-disease (gsd/gsd) rat

1986 ◽  
Vol 238 (3) ◽  
pp. 811-816 ◽  
Author(s):  
D G Clark ◽  
S D Neville ◽  
M Brinkman ◽  
P V Nelson ◽  
R J Illman ◽  
...  
Keyword(s):  
Food Deprivation ◽  
Glycogen Content ◽  
Storage Disease ◽  
Liver Weight ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Hepatic Tissue ◽  
Blood Metabolites ◽  
Hepatic Glycogen ◽  
Age Related

The effects of food deprivation on body weight, liver weight, hepatic glycogen content, glycogenolytic enzymes and blood metabolites were compared in young and old phosphorylase b kinase-deficient (gsd/gsd) rats. Although the concentration of glycogen in liver from 9-week-old female gsd/gsd rats (730 mumol of glucose equivalents/g wet wt.) was increased by 7-8% during starvation, total hepatic glycogen was decreased by 12% after 24 h without food. In 12-month-old male gsd/gsd rats the concentration of liver glycogen (585 mumol of glucose equiv./g wet wt.) was decreased by 16% and total hepatic glycogen by nearly 40% after food deprivation for 24 h. Phosphorylase b kinase and phosphorylase a were present at approx. 10% of the control activities in 9-week-old gsd/gsd rats, but both enzyme activities were increased more than 3-fold in 12-month-old affected rodents. It is concluded that the age-related ability to mobilize hepatic glycogen appears to result from the augmentation of phosphorylase b kinase during maturation of the gsd/gsd rat.

Does β3-adrenoreceptor blockade attenuate acute exercise-induced reductions in leptin mRNA?

1999 ◽  
Vol 87 (5) ◽  
pp. 1678-1683 ◽  
Author(s):  
S. Brooke Bramlett ◽  
Jun Zhou ◽  
Ruth B. S. Harris ◽  
Stephen L. Hendry ◽  
Trudy L. Witt ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Acute Exercise ◽  
Liver Glycogen ◽  
Treadmill Running ◽  
Control Group ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Receptor Stimulation ◽  
Exercise Induced

We investigated the effect of a single bout of exercise on leptin mRNA levels in rat white adipose tissue. Male Sprague-Dawley rats were randomly assigned to an exercise or control group. Acute exercise was performed on a rodent treadmill and was carried out to exhaustion, lasting an average of 85.5 ± 1.5 min. At the end of exercise, soleus muscle and liver glycogen were reduced by 88% ( P < 0.001). Acutely exercised animals had lower ( P< 0.05) leptin mRNA levels in retroperitoneal but not epididymal fat, and this was independent of fat pad weight. To test the hypothesis that β3-adrenergic-receptor stimulation was involved in the downregulation of leptin mRNA in retroperitoneal fat, a second experiment was performed in which rats were randomized into one of four groups: control, control + β3-antagonist, exercise, and exercise + β3-antagonist. A highly selective β3-antagonist (SR-59230A) or vehicle was given by gavage 30 min before exercise or control experiment. Exercise consisted of 55 min of treadmill running, sufficient to reduce liver and muscle glycogen by 70 and 80%, respectively (both P < 0.0001). Again, acute exercise reduced leptin mRNA in retroperitoneal fat (exercise vs. control; P < 0.05), but β3-antagonism blocked this effect (exercise + β3-antagonist vs. control + β3-antagonist; P = 0.42). Unexpectedly, exercise increased serum leptin. This would be consistent with the idea that there are releasable, preformed pools of leptin within adipocytes. We conclude that β3-receptor stimulation is a mechanism by which acute exercise downregulates retroperitoneal adipose tissue leptin mRNA in vivo.

scholarly journals Effects in vivo of food deprivation and 3-mercaptopicolinate in the glycogen-storage-disease (gsd/gsd) rat

1985 ◽  
Vol 231 (3) ◽  
pp. 755-759 ◽  
Author(s):  
D G Clark ◽  
M Brinkman ◽  
S D Neville ◽  
W D Haynes
Keyword(s):  
Blood Glucose ◽  
Food Deprivation ◽  
Intraperitoneal Injection ◽  
Storage Disease ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Hepatic Glycogen ◽  
Glycogen Stores ◽  
Female Control

Intraperitoneal injection of 3-mercaptopicolinate into 24 h-food-deprived 27-week-old female control (GSD/GSD) rats lowered the concentration of circulating glucose by 66%, but glycerol and lactate concentrations were increased up to 3- and 4-fold respectively. In phosphorylase b kinase-deficient (gsd/gsd) rats the corresponding changes for blood glucose, lactate and glycerol were half those observed in the controls. Although the concentration of liver glycogen (approx. 12%, w/w) in the gsd/gsd rats was not altered during food deprivation, total hepatic glycogen was decreased by 17%. It is suggested that the gradual breakdown of the extensive hepatic glycogen stores during starvation assists in the maintenance of normoglycaemia in the gsd/gsd rat.

scholarly journals Effects of glucose ingestion at different frequencies on glycogen recovery in mice during the early hours post exercise

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yutaka Matsunaga ◽  
Kenya Takahashi ◽  
Yumiko Takahashi ◽  
Hideo Hatta
Keyword(s):  
Muscle Glycogen ◽  
Blood Glucose Concentration ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Carbohydrate Intake ◽  
Treadmill Running ◽  
Plasma Insulin Concentration ◽  
Post Exercise ◽  
Glycogen Concentration ◽  
Glucose Ingestion

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.

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