Diurnal changes in the brain glycogen

1958 ◽  
Vol 14 (12) ◽  
pp. 452-452 ◽  
Author(s):  
D. Svorad
Keyword(s):  
Diurnal Changes ◽  
Brain Glycogen ◽  
The Brain

scholarly journals Glycogen as a Putative Target for Diagnosis and Therapy in Brain Pathologies

2011 ◽  
Vol 2011 ◽  
pp. 1-17 ◽  
Author(s):  
Jean-François Cloix ◽  
Tobias Hévor
Keyword(s):  
Chronic Conditions ◽  
Glycogen Content ◽  
Glycogen Synthesis ◽  
Therapeutic Approaches ◽  
Brain Glycogen ◽  
Putative Target ◽  
Glucose Polymer ◽  
Energy Store ◽  
High Level ◽  
The Brain

Brain glycogen, a glucose polymer, is now considered as a functional energy store to the brain. Indeed, when neurons outpace their own possibilities to provide themselves with energy, astrocytic metabolism is in charge of feeding neurons, since brain glycogen synthesis is mainly due to astrocyte. Therefore, malfunctions or perturbations of astrocytic glycogen content, synthesis, or mobilization may be involved in processes of brain pathologies. This is the case, for example, in epilepsies and gliomas, two different situations in which, brain needs high level of energy during acute or chronic conditions. The purpose of the present paper is to demonstrate how brain glycogen might be relevant in these two pathologies and to pinpoint the possibilities of considering glycogen as a tool for diagnostic and therapeutic approaches in brain pathologies.

Seasonal changes in glycogen content and Na+-K+-ATPase activity in the brain of crucian carp

2006 ◽  
Vol 291 (5) ◽  
pp. R1482-R1489 ◽  
Author(s):  
Matti Vornanen ◽  
Vesa Paajanen
Keyword(s):  
Atpase Activity ◽  
Seasonal Changes ◽  
Crucian Carp ◽  
Glycogen Content ◽  
Hill Coefficient ◽  
Ouabain Binding ◽  
Brain Glycogen ◽  
Na Pump ◽  
Glycogen Stores ◽  
The Brain

Changes in the number of Na+-K+-ATPase α-subunits, Na+-K+-ATPase activity and glycogen content of the crucian carp ( Carassius carassius) brain were examined to elucidate relative roles of energy demand and supply in adaptation to seasonal anoxia. Fish were collected monthly around the year from the wild for immediate laboratory assays. Equilibrium dissociation constant and Hill coefficient of [3H]ouabain binding to brain homogenates were 12.87 ± 2.86 nM and −1.18 ± 0.07 in June and 11.93 ± 2.81 nM and −1.17 ± 0.06 in February ( P > 0.05), respectively, suggesting little changes in Na+-K+-ATPase α-subunit composition of the brain between summer and winter. The number of [3H]ouabain binding sites and Na-K-ATPase activity varied seasonally ( P < 0.001) but did not show clear connection to seasonal changes in oxygen content of the fish habitat. Six weeks’ exposure of fish to anoxia in the laboratory did not affect Na+-K+-ATPase activity ( P > 0.05) confirming the anoxia resistance of the carp brain Na pump. Although anoxia did not suppress the Na pump, direct Q10 effect on Na+-K+-ATPase at low temperatures resulted in 10 times lower catalytic activity in winter than in summer. Brain glycogen content showed clear seasonal cycling with the peak value of 203.7 ± 16.1 μM/g in February and a 15 times lower minimum (12.9 ± 1.2) in July. In winter glycogen stores are 15 times larger and ATP requirements of Na+-K+-ATPase at least 10 times less than in summer. Accordingly, brain glycogen stores are sufficient to fuel brain function for about 8 min in summer and 16 h in winter, meaning about 150-fold extension of brain anoxia tolerance by seasonal changes in energy supply-demand ratio.

Conversion of glucose to glycogen after ingestion of a high-carbohydrate diet

1960 ◽  
Vol 198 (4) ◽  
pp. 787-792 ◽  
Author(s):  
A. Chari-Bitron ◽  
S. Lepkovsky ◽  
R. M. Lemmon ◽  
M. K. Dimick
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Content ◽  
Intermediate Compound ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
Experimental Conditions ◽  
Brain Glycogen ◽  
High Carbohydrate ◽  
The Brain

The glycogen content of nine tissues of trained-fed rats was investigated at fasting and at different times after eating with and without water. With the exception of the brain and muscles, the tissues contained little or no glycogen at fasting and accumulated variable amounts during the course of digestion with peak accumulation in most cases 4–7 hours after the commencement of feeding. The brain glycogen did not vary in the rats in spite of the different experimental conditions of this study. The amount of muscle glycogen in the fed rats was the same or slightly more than the amount found in the fasting rats. The fasting liver incorporated C14 substrates into glycogen while it was decreasing in amounts. Fasting muscles incorporated C14 substrates almost as fast as fed muscles indicating that muscle glycogen behaved as an intermediate compound and was metabolized as fast as formed. Accumulation of glycogen in the mesenteric, renal and subcutaneous fatty tissues was decreased by a) feeding without water and b) excessive deposits of fat in the fatty tissues.

scholarly journals Cerebral glycogen in humans following acute and recurrent hypoglycemia: Implications on a role in hypoglycemia unawareness

2016 ◽  
Vol 37 (8) ◽  
pp. 2883-2893 ◽  
Author(s):  
Gülin Öz ◽  
Mauro DiNuzzo ◽  
Anjali Kumar ◽  
Amir Moheet ◽  
Ameer Khowaja ◽  
...  
Keyword(s):  
Occipital Lobe ◽  
Biophysical Model ◽  
Resonance Spectroscopy ◽  
Hypoglycemic Episode ◽  
Hypoglycemia Unawareness ◽  
Brain Glycogen ◽  
Acute Hypoglycemia ◽  
The Brain ◽  
Recurrent Hypoglycemia

Supercompensated brain glycogen levels may contribute to the development of hypoglycemia-associated autonomic failure (HAAF) following recurrent hypoglycemia (RH) by providing energy for the brain during subsequent periods of hypoglycemia. To assess the role of glycogen supercompensation in the generation of HAAF, we estimated the level of brain glycogen following RH and acute hypoglycemia (AH). After undergoing 3 hyperinsulinemic, euglycemic and 3 hyperinsulinemic, hypoglycemic clamps (RH) on separate occasions at least 1 month apart, five healthy volunteers received [1-13C]glucose intravenously over 80+ h while maintaining euglycemia. 13C-glycogen levels in the occipital lobe were measured by 13C magnetic resonance spectroscopy at ∼8, 20, 32, 44, 56, 68 and 80 h at 4 T and glycogen levels estimated by fitting the data with a biophysical model that takes into account the tiered glycogen structure. Similarly, prior 13C-glycogen data obtained following a single hypoglycemic episode (AH) were fitted with the same model. Glycogen levels did not significantly increase after RH relative to after euglycemia, while they increased by ∼16% after AH relative to after euglycemia. These data suggest that glycogen supercompensation may be blunted with repeated hypoglycemic episodes. A causal relationship between glycogen supercompensation and generation of HAAF remains to be established.

scholarly journals The Photoreceptors of Lampreys

1935 ◽  
Vol 12 (3) ◽  
pp. 254-270
Author(s):  
J. Z. YOUNG
Keyword(s):  
Colour Change ◽  
Diurnal Changes ◽  
Posterior Pituitary ◽  
Nervous Control ◽  
Pineal Complex ◽  
Artificial Illumination ◽  
Pituitary Secretion ◽  
Set Up ◽  
The Brain ◽  
Illumination Removal

1. Illumination of the dorsal region of the head of an ammocoete larva is followed by movements of the animal, but only after exposure for longer periods than are necessary to elicit responses from the tail. 2. Since this reaction persists unaffected after removal of the pineal and paired eyes, it is concluded that it is produced by the direct effect of light on some tissue in the brain. 3. Larval and adult L. planeri show very pronounced daily rhythms of colour change, becoming pale at night and dark during the daytime. 4. Continuous artificial illumination of the animals produces maximal darkening and stops the diurnal rhythm. 5. When animals are left in total darkness the diurnal changes usually persist, though diminished in extent; sometimes the melanophores come to rest in the expanded phase. 6. Since section or faradic stimulation of spinal nerves is not followed by local changes in the melanophores, it is concluded that these are not under nervous control. 7. After removal of either the whole pituitary complex or its pars nervosa and intermedia the animals become maximally pale, and remain so indefinitely in spite of changes of illumination. 8. Injection of extracts of mammalian posterior pituitary lobe causes darkening of such hypophysectomised lampreys. 9. Pituitrin was also found to be capable of maintaining the expansion of isolated melanophores. 10. After removal of the pineal complex from ammocoetes the rhythms of colour change were interrupted, the melanophores remaining in the expanded phase under all conditions of illumination. Removal of the pineal of adult L. planeri disturbed the colour rhythm, which was then completely abolished if the paired eyes were also removed. 11. Thus the paling of an ammocoete when it passes from light to darkness is probably due to the inhibition of posterior pituitary secretion by nervous impulses set up by the change of illumination of the pineal complex.

scholarly journals Physiological Responses to Hypoxia in the Absence of Brain Glycogen

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Taylor Zike ◽  
Justin J. Crowder ◽  
Bartholomew A. Pederson
Keyword(s):  
Survival Time ◽  
Motor Coordination ◽  
Glycogen Synthase ◽  
Acute Hypoxia ◽  
Protective Role ◽  
Vaginal Birth ◽  
Sleep Regulation ◽  
Brain Glycogen ◽  
Obstructive Sleep ◽  
The Brain

Background and Hypothesis: Glycogen is a highly branched polymer of glucose and is an important form of energy storage in mammals. The brain is able to form glycogen in astrocytes and neurons via glycogen synthase and branching enzyme. Once formed, brain glycogen functions as the only stored energy source for these cells. Various physiological roles for brain glycogen have been hypothesized, including memory consolidation and sleep regulation, as well as a protective role during various physiological stressors, such as hypoglycemia and hypoxia. For instance, rat brain glycogen levels were decreased 10 minutes after vaginal birth, but not after a C-section. This suggested that cerebral hypoxia experienced during vaginal birth induced the utilization of brain glycogen to minimize neurodegeneration during the hypoxic event. Symptoms of hypoxia can range from tachycardia, tachypnea, shortness of breath, and diaphoresis to confusion, loss of motor coordination and cognitive function, neurodegeneration, and brain death. The many causes of hypoxia include lungs diseases (COPD, pneumonia, pulmonary edema), CNS depressants (opiates), heart problems (CHF), anemia, and obstructive sleep apnea (OSA). We hypothesized that the lack of brain glycogen would cause a noticeable detrimental effect to the survival time and physiologic functions of mice exposed to acute hypoxia. Experimental Design or Project Methods: We subjected mice, with or without glycogen synthase disrupted in the brain, to carbon dioxide- or nitrogen-induced hypoxia and monitored effects on brain glycogen levels, behavior, and survival time. Results: We found that mice lacking brain glycogen exhibited the characteristic physiologic responses to hypoxia, but expired ~50% sooner than mice with brain glycogen. Conclusion and Potential Impact: These results provide evidence that brain glycogen is imperative in responding to hypoxic events. Further, these findings suggest that brain glycogen may protect patients with OSA against other comorbidities, especially neurodegeneration and cognitive impairment.

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