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Results for “LIVER GLYCOGEN”

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At least 73 records · Page 4Linked to original sources
PubMed1998

Human liver glycogen metabolism assessed with a 13C-enriched diet and a 13CO2 breath test.

BACKGROUND: Adequate liver glycogen stores to maintain hepatic glucose output by glycogenolysis in the post-absorptive state are essential to prevent protein loss through gluconeogenesis. There are no simple techniques to monitor liver glycogen use. METHODS: In this study, we labelled liver glycogen with naturally 13C-enriched carbohydrate and measured the pattern of 13CO2 excretion and the post-prandial time during which oxidation of 13C-labelled liver glycogen was demonstrable by 13CO2 enrichment in breath. Two experiments were performed in 24 healthy volunteers. RESULTS: In the first experiment we observed that breath 13CO2 enrichment returned to baseline values at 20.3 (SD 2.3, n = 12) hours post-prandially, indicating exhaustion of the 13C-labelled liver glycogen at that time. In a second experiment, breath 13CO2 enrichment in the early hours of the post-prandial phase was studied. After a steep decline, which started 2-4 h after the last meal, the 13CO2 enrichment reached a plateau phase 6 h post-prandially. This plateau phase lasted for about 6-8 h, suggesting steady-state glycogenolysis during this period. The plateau phase was followed by a further decline in 13CO2 excretion, suggesting a gradually diminishing contribution of 13C-labelled liver glycogen to substrate oxidation. CONCLUSION: It is possible to label liver glycogen with a diet of naturally 13C-enriched carbohydrate. The oxidation of the labelled liver glycogen can be monitored by measuring 13C-enrichment in breath CO2.

Adult↗
PubMed2000

Melatonin increases muscle and liver glycogen content in nonexercised and exercised rats.

The effects of melatonin on several parameters of carbohydrate and lipid metabolism were investigated in exercised and nonexercised rats. Animals were run to exhaustion on a rodent treadmill at 24 m/min and a 12% slope. Exercise resulted in a significant hypoglycemia and increased plasma levels of lactate and beta-hydroxybutyrate, together with a significant reduction of glycogen in muscle and liver. Muscle and liver glycogen content was elevated and plasma free fatty acid decreased in nonexercised animals receiving melatonin (0.5 or 2.0 mg/kg i.p). Melatonin at 2.0 mg/kg reduced plasma lactate and increased lactate concentration in liver. When compared to untreated exercised animals glycemia and muscle and liver glycogen content were significantly higher in melatonin-treated exercised animals, while plasma and liver lactate and plasma beta-hydroxybutyrate were significantly reduced. Our data indicate that melatonin preserves glycogen stores in exercised rats through changes in carbohydrate and lipid utilization.

Animals↗
PubMed1984

The effects of psychosomatic stress at the end of pregnancy on maternal and fetal plasma cortisol levels and liver glycogen in guinea-pigs.

Plasma cortisol and liver glycogen were measured in the mother, fetus and newborn of guinea-pig after a stress on days 60 and 67 of gestation (parturition occurring on day 68); at those times, the animals were held for 3 h in the dark and subjected to a flash of 75 J intensity every 10 sec. In comparison with the controls, stress increased plasma cortisol in both mothers and fetuses. While it decreased maternal liver glycogen on day 60, it increased fetal liver glycogen at the same stage. Glycemia decreased in mothers after stress, although at delivery females previously stressed on day 60 showed hyperglycemia.

Animals↗
PubMed1989

[Liver glycogen and glucose tolerance in rats with prenatal development under hypoglycemic conditions].

Insulin injections to pregnant rats (1 ME/100 g body weight) induced obvious hypoglycaemia of the mother and its foetus, an increase of glycogen in the liver of foetus. At the reproductive age and the beginning of ageing of the litter, hyperglycaemia and a decrease of liver glycogen were observed. At the beginning of puberty, the glycaemic curves had a diabetic character. The adequate supply of foetus with glucose through the mother blood seems to be an important factor, determining the normal development of neuroendocrine regulation mechanisms of the carbohydrate metabolism.

Aging↗
PubMed1992

Effect of growth hormone on liver glycogen accumulation in suckling rats.

The regulation of liver glycogen turnover in the neonatal period differs from that of the adult state. Little is also known about the regulation exerted by GH in the first period of life. To shed light on the regulation of glycogen production and in particular to study the role of GH on liver glycogen accumulation, we investigated the effect of GH administration in control or GH-deficient neonatal rats. A slow-release GH preparation was injected subcutaneously on days 9 and 12 of life, in normal and neonatally treated rats with thyroxine or cortisol. Seventy-two hours after the last GH administration, liver glycogen was increased without concomitant elevation of plasma insulin and corticosterone levels and in addition without sequential inactivation of glycogen synthase. These data strongly suggest that the current concepts on the regulation of the hepatic synthesis of glycogen should be revised.

Animals↗
PubMed1988

Liver glycogen in gangrenous intestinal obstruction.

Considerable drops in liver glycogen contents of guinea pigs suffering from gangrenous intestinal obstruction were recorded in regard to control values (P less than 0.001). An additional experiment was conducted by using carbontetrachloride (CT) to determine whether or not the shortening of survival related to liver glycogen content in animals with strangulation obstruction. The mean tissue glycogen content in the sham-operated group was 816.2 +/- 13.3 micrograms/g, w. wt., whereas in the CT-treated group it was 73.5 +/- 11.0 micrograms/g w. wt. This difference is highly significant (P less than 0.001). The mean survival was 54.4 +/- 5.8 h and 21.9 +/- 5.5 h in animals with gangrenous intestinal obstruction before and after CT treatment, respectively. These results suggested that the liver glycogen depletion was a significant factor in decreasing the survival time of guinea pigs with strangulation obstruction.

Animals↗