scholarly journals The effect of fasting on the glycogen metabolism in heat-acclimated rats

2008 ◽  
Vol 60 (1) ◽  
pp. 49-58 ◽  
Author(s):  
Biljana Miova ◽  
Suzana Dinevska-Kjovkarevska ◽  
S. Mitev ◽  
Mirsada Dervisevic

We investigated the influence of successive fasting for 24,48,72, and 96 h on some key enzymes and substrates of liver, kidney, and muscle in control and heat-acclimated (30days at 35 ? 1?C)rats. Short-term fasting (for 24 and 48 h)resulted in decrease of liver glycogen content, blood glucose level, and concentration of glucose-6-phosphate, as well as increase of glucose-6-phosphatase activity, regardless of the previous temperature of acclimation. During a period of prolonged fasting (for 72 and 96 h),there was a rebound of liver glycogen content only in animals kept at room temperature. Fasting induced increase of renal glycogen content in animals kept at room temperature and increase of renal glucose-6-phosphatase activity in both experimental groups. As for muscle metabolism, endogenous nutrition resulted in decrease of muscle glycogen content in heat-acclimated animals. Activity of muscle glycogen phosphorylase (a+b)was decreased in the control and increased in heat-acclimated animals. The obtained results indicate that the examined carbohydrate-related parameters show time-dependent changes during 4 days of fasting. Twenty-four- and 48-h fasting intensifies glycogenolytic processes, while 72- and 96-h fasting intensifies gluconeogenic processes, doing so to a lesser extent in heat-acclimated animals. The changes caused by the fasting were modified by acclimation to moderate heat, primarily in the liver and to a lesser extent in the kidney and muscle.

2019 ◽  
pp. 17-24
Author(s):  
Daphna Atar-Zwillenberg ◽  
Michael Atar ◽  
Gianni Morson ◽  
Udo Spornitz

The hormonal regulation of amphibian glycogen metabolism was studied in Xenopus laevis as a typical member of the anurans (tailless amphibians).The main focus of this study was given to the effects of various hormones on the glycogen/glucose balance in adult toads. We determined biochemically the liver and muscle glycogen contents as well as the blood glucose and lipid levels for a number of hormones and also diabetes inducing substances. Additionally, we examined ultrastructure changes in hepatocytes induced by the various treatments, and also investigated the activity of carbohydrate-relevant enzymes by histochemistry. With one exception, the liver glycogen content of Xenopus remained basically unchanged by the treatments or was even slightly enhanced. Only human chorionic gonadotropin, through which the vitellogenic response is triggered, prompts a significant decrease of liver glycogen in females. Under the same conditions the male liver glycogen content remained stable. Muscle glycogen contents were not affected by any of the treatments. Blood glucose and lipid levels on the other hand were elevated considerably in both sexes after application of either epinephrine or cortisol. The ultrastructural examination revealed a proliferation of Rough Endoplasmic Reticulum (RER) in hepatocytes from epinephrine treated toads of both sexes as well as from HCG treated females. By histochemistry, we detected an elevated glucose-6-phosphatase activity in the hepatocytes from toads treated with either epinephrine or cortisol. These treatments also led to enhanced glycogen phosphorylase activity in males, and to a slightly elevated glyceraldehyde-3-phosphate dehydrogenase activity in females. Our results show that the hepatic glycogen is extremely stable in adult Xenopus. Only vitellogenesis causes a marked utilization of glycogen. Since the blood glucose levels are elevated in epinephrine or cortisol treated toads without the liver glycogen being affected, we conclude that either protein and/or lipid metabolism are involved in carbohydrate metabolism in Xenopus laevis.


2000 ◽  
Vol 278 (1) ◽  
pp. E65-E75 ◽  
Author(s):  
Anna Casey ◽  
Rob Mann ◽  
Katie Banister ◽  
John Fox ◽  
Peter G. Morris ◽  
...  

This study investigated the effect of carbohydrate (CHO) ingestion on postexercise glycogen resynthesis, measured simultaneously in liver and muscle ( n = 6) by 13C magnetic resonance spectroscopy, and subsequent exercise capacity ( n = 10). Subjects cycled at 70% maximal oxygen uptake for 83 ± 8 min on six separate occasions. At the end of exercise, subjects ingested 1 g/kg body mass (BM) glucose, sucrose, or placebo (control). Resynthesis of glycogen over a 4-h period after treatment ingestion was measured on the first three occasions, and subsequent exercise capacity was measured on occasions four through six. No glycogen was resynthesized during the control trial. Liver glycogen resynthesis was evident after glucose (13 ± 8 g) and sucrose (25 ± 5 g) ingestion, both of which were different from control ( P < 0.01). No significant differences in muscle glycogen resynthesis were found among trials. A relationship between the CHO load (g) and change in liver glycogen content (g) was evident after 30, 90, 150, and 210 min of recovery ( r = 0.59–0.79, P< 0.05). Furthermore, a modest relationship existed between change in liver glycogen content (g) and subsequent exercise capacity ( r= 0.53, P < 0.05). However, no significant difference in mean exercise time was found (control: 35 ± 5, glucose: 40 ± 5, and sucrose: 46 ± 6 min). Therefore, 1 g/kg BM glucose or sucrose is sufficient to initiate postexercise liver glycogen resynthesis, which contributes to subsequent exercise capacity, but not muscle glycogen resynthesis.


2016 ◽  
Vol 120 (11) ◽  
pp. 1328-1334 ◽  
Author(s):  
Cas J. Fuchs ◽  
Javier T. Gonzalez ◽  
Milou Beelen ◽  
Naomi M. Cermak ◽  
Fiona E. Smith ◽  
...  

The purpose of this study was to assess the effects of sucrose vs. glucose ingestion on postexercise liver and muscle glycogen repletion. Fifteen well-trained male cyclists completed two test days. Each test day started with glycogen-depleting exercise, followed by 5 h of recovery, during which subjects ingested 1.5 g·kg−1·h−1 sucrose or glucose. Blood was sampled frequently and 13C magnetic resonance spectroscopy and imaging were employed 0, 120, and 300 min postexercise to determine liver and muscle glycogen concentrations and liver volume. Results were as follows: Postexercise muscle glycogen concentrations increased significantly from 85 ± 27 (SD) vs. 86 ± 35 mmol/l to 140 ± 23 vs. 136 ± 26 mmol/l following sucrose and glucose ingestion, respectively (no differences between treatments: P = 0.673). Postexercise liver glycogen concentrations increased significantly from 183 ± 47 vs. 167 ± 65 mmol/l to 280 ± 72 vs. 234 ± 81 mmol/l following sucrose and glucose ingestion, respectively (time × treatment, P = 0.051). Liver volume increased significantly over the 300-min period after sucrose ingestion only (time × treatment, P = 0.001). As a result, total liver glycogen content increased during postexercise recovery to a greater extent in the sucrose treatment (from 53.6 ± 16.2 to 86.8 ± 29.0 g) compared with the glucose treatment (49.3 ± 25.5 to 65.7 ± 27.1 g; time × treatment, P < 0.001), equating to a 3.4 g/h (95% confidence interval: 1.6-5.1 g/h) greater repletion rate with sucrose vs. glucose ingestion. In conclusion, sucrose ingestion (1.5 g·kg−1·h−1) further accelerates postexercise liver, but not muscle glycogen repletion compared with glucose ingestion in trained athletes.


1990 ◽  
Vol 259 (5) ◽  
pp. E692-E698 ◽  
Author(s):  
O. Ljungqvist ◽  
P. O. Boija ◽  
H. Esahili ◽  
M. Larsson ◽  
J. Ware

Liver glycogen content, blood glucose, insulin, glucagon, and epinephrine were determined during 1 h hemorrhagic hypotension at 60 mmHg and 23 h thereafter in fed and two groups of 24-h food-deprived rats receiving either no infusion or 30% glucose intravenously during hemorrhage. Liver glycogen content was reduced by greater than 90% after 24-h food deprivation. Fed and food-deprived rats given glucose developed similar and substantial elevations of blood glucose during hemorrhage, whereas changes in blood glucose were modest in food-deprived rats given no infusion. In fed rats, liver glycogen was reduced by 60% during the 1-h bleed, but within 2 h after hemorrhage repletion of liver glycogen content commenced. By 6 h, approximately 75% of the glycogen lost during hemorrhage had been restored, and 23 h after hemorrhage liver glycogen content was six times greater compared with nonbled controls. Although glycogen levels increased after hemorrhage in food-deprived animals, the increase was negligible compared with that found in fed rats. Infusion of glucose during hemorrhage or adrenergic blockade after hemorrhage did not alter glycogen repletion in food-deprived rats. Posthemorrhage fed animals had high levels of insulin, glucagon, and epinephrine during hemorrhage, whereas insulin levels remained low in food-deprived rats despite exogenously induced hyperglycemia. It is concluded that rapid and substantial glycogen repletion can occur even immediately poststress. The conditions seem to be related to the nutritional state at the time of the insult.


2006 ◽  
Vol 395 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Gretchen E. Parker ◽  
Bartholomew A. Pederson ◽  
Mariko Obayashi ◽  
Jill M. Schroeder ◽  
Robert A. Harris ◽  
...  

Glycogen, a branched polymer of glucose, forms an energy re-serve in numerous organisms. In mammals, the two largest glyco-gen stores are in skeletal muscle and liver, which express tissue-specific glycogen synthase isoforms. MGSKO mice, in which mGys1 (mouse glycogen synthase) is disrupted, are devoid of muscle glycogen [Pederson, Chen, Schroeder, Shou, DePaoli-Roach and Roach (2004) Mol. Cell. Biol. 24, 7179–7187]. The GSL30 mouse line hyper-accumulates glycogen in muscle [Manchester, Skurat, Roach, Hauschka and Lawrence (1996) Proc. Natl. Acad. Sci. U.S.A. 93, 10707–10711]. We performed a microarray analysis of mRNA from the anterior tibialis, medial gastrocnemius and liver of MGSKO mice, and from the gastroc-nemius of GSL30 mice. In MGSKO mice, transcripts of 79 genes varied in their expression in the same direction in both the anterior tibialis and gastrocnemius. These included several genes encoding proteins proximally involved in glycogen metabolism. The Ppp1r1a [protein phosphatase 1 regulatory (inhibitor) sub-unit 1A] gene underwent the greatest amount of downregulation. In muscle, the downregulation of Pfkfb1 and Pfkfb3, encoding isoforms of 6-phosphofructo-2-kinase/fructose-2,6-bisphospha-tase, is consistent with decreased glycolysis. Pathways for branched-chain amino acid, and ketone body utilization appear to be downregulated, as is the capacity to form the gluconeogenic precursors alanine, lactate and glutamine. Expression changes among several members of the Wnt signalling pathway were identified, suggesting an as yet unexplained role in glycogen meta-bolism. In liver, the upregulation of Pfkfb1 and Pfkfb3 expression is consistent with increased glycolysis, perhaps as an adaptation to altered muscle metabolism. By comparing changes in muscle expression between MGSKO and GSL30 mice, we found a subset of 44 genes, the expression of which varied as a function of muscle glycogen content. These genes are candidates for regulation by glycogen levels. Particularly interesting is the observation that 11 of these genes encode cardiac or slow-twitch isoforms of muscle contractile proteins, and are upregulated in muscle that has a greater oxidative capacity in MGSKO mice.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1801-P
Author(s):  
KRISTINA WARDELMANN ◽  
JOSÉ PEDRO CASTRO ◽  
MICHAELA RATH ◽  
JÜRGEN WEIß ◽  
ANNETTE SCHUERMANN ◽  
...  

1992 ◽  
Vol 267 (35) ◽  
pp. 25129-25134 ◽  
Author(s):  
A.M. Gómez-Foix ◽  
W.S. Coats ◽  
S Baqué ◽  
T Alam ◽  
R.D. Gerard ◽  
...  

1960 ◽  
Vol 38 (1) ◽  
pp. 553-558 ◽  
Author(s):  
Violet M. Chang ◽  
D. R. Idler

Liver glycogen levels were determined for a pure stock of sockeye salmon (Oncorhynchus nerka) taken at three locations during spawning migration. The liver glycogen content of the male was found to be consistently greater than that of the female throughout the entire river migration. In both sexes liver glycogen decreased during the earlier phase of migration, but increased during the later stage so that the levels at the spawning grounds were approximately twice those at the mouth of the river. The changes which occur are discussed in relation to sex differences, energy expenditures, and plasma steroid hormone levels.


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