Circadian rhythm of liver glycogen metabolism in rats: effects of hypothalamic lesions

1980 ◽  
Vol 238 (1) ◽  
pp. E21-E25 ◽  
Author(s):  
K. Ishikawa ◽  
T. Shimazu

The effects of electrolytic lesions of the suprachiasmatic nucleus (SCN) and ventromedial nucleus (VMH) of the hypothalamus on the circadian rhythm of liver glycogen metabolism were studied in rats fed during the dark period (2000–0800 h). Bilateral lesions of the SCN did not affect appreciably the circadian rhythmicity in three parameters of liver glycogen metabolism, i.e., glycogen content and glycogen synthetase I and phosphorylase a activities. In contrast, bilateral lesions of the VMH resulted in almost complete loss of circadian rhythmicity in phosphorylase a activity by lowering the high activity normally observed in late evening. VMH lesions also reduced the amplitudes of the rhythms of synthetase I activity and glycogen content, but did not abolish their rhythmicities. These results suggest that the integrity of the VMH, rather than the SCN, is important for regulation or expression of the food-triggered circadian rhythm of liver phosphorylase a activity. The implication of the lateral hypothalamic nucleus in regulation of the circadian rhythm of liver synthetase I is also discussed.

1991 ◽  
Vol 71 (5) ◽  
pp. 1694-1699 ◽  
Author(s):  
Z. V. Kendrick ◽  
G. S. Ellis

The effect of 17 beta-estradiol 3-benzoate (10 micrograms.0.1 ml sunflower oil-1.100 g body wt-1) on exercise performance, tissue glycogen utilization, and lipid availability was determined in male rats. In experiment 1, estradiol or oil was administered 1 h or 1–6 days before a treadmill run to exhaustion. No differences in body weight between oil- and estradiol-administered animals were observed during the 6-day treatment. Animals receiving estradiol for 3–6 days ran significantly longer and completed more work than oil-administered animals. Significant degradation of red and white vastus muscle, myocardial, and liver glycogen was observed in all animals run to exhaustion. In experiment 2, animals were administered estradiol for 5 days and then run for 2 h. The submaximal run for 2 h significantly reduced tissue glycogen content in red and white vastus muscle, heart, and liver of oil-administered animals. The latter effect was attenuated in both vastus muscles, liver, and myocardial tissues in the estradiol-administered animals. Estradiol administration significantly increased plasma fatty acids and lowered plasma lactate during the submaximal run. These data indicate that when body weight remained constant between groups of male rats, estradiol administration for 3–6 days increased exercise performance. Furthermore, estradiol administration for 5 days resulted in greater lipid availability and less tissue glycogen utilization during submaximal running for 2 h.


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.


1973 ◽  
Vol 136 (1) ◽  
pp. 115-124 ◽  
Author(s):  
Robert J. Bonney ◽  
Harold A. Hopkins ◽  
P. Roy Walker ◽  
Van R. Potter

Intact rats trained on a controlled feeding and lighting schedule designated ‘8+16’ exhibited diurnal oscillations in liver weight, glucokinase activity and liver glycogen content. Glucokinase activity expressed as units/g of liver decreased to 30% of that from unoperated controls during the first 48h after partial hepatectomy and returned to near normal values in 2 weeks. When the glucokinase activity was expressed as units/liver per 100g body wt., a decrease to 50% of control activity was observed between 24 and 48h after the operation. A similar pattern was found for pyruvate kinase type I. In contrast, pyruvate kinase type III activity increased after partial hepatectomy. It is suggested that the newly divided cells after partial hepatectomy do not synthesize glucokinase and pyruvate kinase I but do synthesize pyruvate kinase III. Glycogen was found to accumulate as early as 24h after partial hepatectomy, and normal concentrations were reached after 48h if the operation was performed at times other than during the feeding periods.


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.


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.


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

2021 ◽  
Vol 22 (2) ◽  
pp. 759
Author(s):  
Karen P. Briski ◽  
Mostafa M. H. Ibrahim ◽  
A. S. M. Hasan Mahmood ◽  
Ayed A. Alshamrani

The catecholamine norepinephrine (NE) links hindbrain metabolic-sensory neurons with key glucostatic control structures in the brain, including the ventromedial hypothalamic nucleus (VMN). In the brain, the glycogen reserve is maintained within the astrocyte cell compartment as an alternative energy source to blood-derived glucose. VMN astrocytes are direct targets for metabolic stimulus-driven noradrenergic signaling due to their adrenergic receptor expression (AR). The current review discusses recent affirmative evidence that neuro-metabolic stability in the VMN may be shaped by NE influence on astrocyte glycogen metabolism and glycogen-derived substrate fuel supply. Noradrenergic modulation of estrogen receptor (ER) control of VMN glycogen phosphorylase (GP) isoform expression supports the interaction of catecholamine and estradiol signals in shaping the physiological stimulus-specific control of astrocyte glycogen mobilization. Sex-dimorphic NE control of glycogen synthase and GP brain versus muscle type proteins may be due, in part, to the dissimilar noradrenergic governance of astrocyte AR and ER variant profiles in males versus females. Forthcoming advances in the understanding of the molecular mechanistic framework for catecholamine stimulus integration with other regulatory inputs to VMN astrocytes will undoubtedly reveal useful new molecular targets in each sex for glycogen mediated defense of neuronal metabolic equilibrium during neuro-glucopenia.


Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 976
Author(s):  
Natalia N. Bezborodkina ◽  
Sergey V. Okovityi ◽  
Boris N. Kudryavtsev

Chronic hepatitises of various etiologies are widespread liver diseases in humans. Their final stage, liver cirrhosis (LC), is considered to be one of the main causes of hepatocellular carcinoma (HCC). About 80–90% of all HCC cases develop in LC patients, which suggests that cirrhotic conditions play a crucial role in the process of hepatocarcinogenesis. Carbohydrate metabolism in LC undergoes profound disturbances characterized by altered glycogen metabolism. Unfortunately, data on the glycogen content in LC are few and contradictory. In this study, the material was obtained from liver biopsies of patients with LC of viral and alcohol etiology and from the liver tissue of rats with CCl4-induced LC. The activity of glycogen phosphorylase (GP), glycogen synthase (GS), and glucose-6-phosphatase (G6Pase) was investigated in human and rat liver tissue by biochemical methods. Total glycogen and its labile and stable fractions were measured in isolated individual hepatocytes, using the cytofluorometry technique of PAS reaction in situ. The development of LC in human and rat liver was accompanied by an increase in fibrous tissue (20- and 8.8-fold), an increase in the dry mass of hepatocytes (by 25.6% and 23.7%), and a decrease in the number of hepatocytes (by 50% and 28%), respectively. The rearrangement of the liver parenchyma was combined with changes in glycogen metabolism. The present study showed a significant increase in the glycogen content in the hepatocytes of the human and the rat cirrhotic liver, by 255% and 210%, respectively. An increased glycogen content in cells of the cirrhotic liver can be explained by a decrease in glycogenolysis due to a decreased activity of G6Pase and GP.


1967 ◽  
Vol 39 (3) ◽  
pp. 415-NP ◽  
Author(s):  
H. M. RADFORD

SUMMARY Electrolytic lesions were made in the hypothalamus of 41 Merino ewes which were subsequently observed for 2–16 months. Ovarian inactivity resulted from bilateral medial and ventral lesions placed immediately posterior to the optic chiasma (four ewes) or immediately anterior to the mammillary body (five ewes). Failure to show oestrus while apparently still ovulating regularly was a feature in another four ewes in which bilateral medial and ventral lesions were placed between the sites already described. Small bilateral lesions in these ventral regions led initially to ovarian inactivity, but final re-establishment of apparently normal reproductive activity in three ewes. Bilateral lesions in regions other than those described above resulted in no apparent change in reproductive activity (eight ewes). Similarly, unilateral or asymmetrical lesions in the remaining 17 ewes failed to affect their reproductive activity. The results are consistent with the hypothesis that in sheep a region of the median eminence responsible for the production of gonadotrophin-releasing factors requires neural inputs traversing both anterior and posterior hypothalamic areas.


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