CARBOHYDRATE METABOLISM IN HYPOTHERMIC RATS AND HAMSTERS

1962 ◽  
Vol 40 (10) ◽  
pp. 1427-1438 ◽  
Author(s):  
J. M. Maur ◽  
D. M. McComiskey ◽  
J. W. Haynes ◽  
J. R. Beaton
Keyword(s):  
Lactic Acid ◽  
Pyruvic Acid ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Intraperitoneal Administration ◽  
Liver Glycogen ◽  
Progressive Increase ◽  
Glycogen Level ◽  
Apparent Decrease ◽  
Fasted Rats

Unanesthetized female animals were cooled without artifical ventilation in cylindrical screen cages under ice until the desired rectal temperature was attained. When fasted rats are cooled 15 minutes after the intraperitoneal administration of either glucose or sodium pyruvate, there is an impaired utilization of the glucose but not of the pyruvate. Rate of decrease of liver glycogen formed from administered glucose was not affected. The elevated level of blood lactic acid typical of hypothermic rats was further elevated by administration of pyruvate but not of glucose, suggesting increased production of lactic acid via pyruvic acid. Glucose utilization patterns of hamsters (hibernators) and rats (non-hibernators) were similar during hypothermia. In non-fasted rats rendered hypothermic there is a progressive increase in blood level of glucose accompanied by an initial decrease in liver glycogen level. Subsequent to this decrease in liver glycogen level, there is a marked increase in the plasma level of ketone bodies. It is concluded that although in hypothermia there is an impairment in glucose utilization, this probably represents decreased oxidative metabolism of carbohydrate, there being no apparent decrease in the formation of lactic acid via pyruvic acid. From the results of experiments with insulin- and alloxan-treated rats, it is concluded that metabolic alterations of hypothermia in rats may be modified in degree but are not eliminated by a prior state of diabetes or by prior administration of insulin.

CARBOHYDRATE METABOLISM IN HYPOTHERMIC RATS AND HAMSTERS

1962 ◽  
Vol 40 (1) ◽  
pp. 1427-1438
Author(s):  
J. M. Maur ◽  
D. M. McComiskey ◽  
J. W. Haynes ◽  
J. R. Beaton
Keyword(s):  
Lactic Acid ◽  
Pyruvic Acid ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Intraperitoneal Administration ◽  
Liver Glycogen ◽  
Progressive Increase ◽  
Glycogen Level ◽  
Apparent Decrease ◽  
Fasted Rats

Unanesthetized female animals were cooled without artifical ventilation in cylindrical screen cages under ice until the desired rectal temperature was attained. When fasted rats are cooled 15 minutes after the intraperitoneal administration of either glucose or sodium pyruvate, there is an impaired utilization of the glucose but not of the pyruvate. Rate of decrease of liver glycogen formed from administered glucose was not affected. The elevated level of blood lactic acid typical of hypothermic rats was further elevated by administration of pyruvate but not of glucose, suggesting increased production of lactic acid via pyruvic acid. Glucose utilization patterns of hamsters (hibernators) and rats (non-hibernators) were similar during hypothermia. In non-fasted rats rendered hypothermic there is a progressive increase in blood level of glucose accompanied by an initial decrease in liver glycogen level. Subsequent to this decrease in liver glycogen level, there is a marked increase in the plasma level of ketone bodies. It is concluded that although in hypothermia there is an impairment in glucose utilization, this probably represents decreased oxidative metabolism of carbohydrate, there being no apparent decrease in the formation of lactic acid via pyruvic acid. From the results of experiments with insulin- and alloxan-treated rats, it is concluded that metabolic alterations of hypothermia in rats may be modified in degree but are not eliminated by a prior state of diabetes or by prior administration of insulin.

STUDIES ON THE EFFECT OF VITAMIN B6 DEPRIVATION ON CARBOHYDRATE METABOLISM IN THE RAT

1954 ◽  
Vol 32 (6) ◽  
pp. 684-688 ◽  
Author(s):  
J. R. Beaton ◽  
M. E. Goodwin
Keyword(s):  
Lactic Acid ◽  
Carbohydrate Metabolism ◽  
Pyruvic Acid ◽  
Vitamin B6 ◽  
Liver Glycogen ◽  
Blood Levels ◽  
Vitamin B ◽  
Abnormal Metabolism

The results of in vivo and in vitro studies on carbohydrate metabolism in the vitamin-B6-deprived rat are reported. All comparisons were made with pair-fed control animals. Within five days of vitamin B6 restriction, rats have significantly lowered fasting levels of blood sugar and liver glycogen. These abnormalities are more marked after 21 days of deprivation and are accompanied by significantly lowered fasting blood levels of pyruvic acid and lactic acid. The activity of lactic acid dehydrogenase, one enzyme involved in carbohydrate metabolism, was measured in vitro and found to be significantly depressed in the vitamin-B6-deprived rat. The conclusion is drawn that an abnormal metabolism of carbohydrate occurs in rats deprived of vitamin B6. This abnormality is evident early in the deprivation period.

STUDIES ON THE EFFECT OF VITAMIN B6 DEPRIVATION ON CARBOHYDRATE METABOLISM IN THE RAT

1954 ◽  
Vol 32 (1) ◽  
pp. 684-688
Author(s):  
J. R. Beaton ◽  
M. E. Goodwin
Keyword(s):  
Lactic Acid ◽  
Carbohydrate Metabolism ◽  
Pyruvic Acid ◽  
Vitamin B6 ◽  
Liver Glycogen ◽  
Blood Levels ◽  
Vitamin B ◽  
Abnormal Metabolism

The results of in vivo and in vitro studies on carbohydrate metabolism in the vitamin-B6-deprived rat are reported. All comparisons were made with pair-fed control animals. Within five days of vitamin B6 restriction, rats have significantly lowered fasting levels of blood sugar and liver glycogen. These abnormalities are more marked after 21 days of deprivation and are accompanied by significantly lowered fasting blood levels of pyruvic acid and lactic acid. The activity of lactic acid dehydrogenase, one enzyme involved in carbohydrate metabolism, was measured in vitro and found to be significantly depressed in the vitamin-B6-deprived rat. The conclusion is drawn that an abnormal metabolism of carbohydrate occurs in rats deprived of vitamin B6. This abnormality is evident early in the deprivation period.

scholarly journals Glucose metabolism in the newborn rat. Temporal studies in vivo

1973 ◽  
Vol 132 (4) ◽  
pp. 739-752 ◽  
Author(s):  
Keith Snell ◽  
Deryck G. Walker
Keyword(s):  
Intraperitoneal Injection ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Post Partum ◽  
Specific Radioactivity ◽  
Liver Glycogen ◽  
Uterine Environment ◽  
Lactate Formation ◽  
Lactate Utilization

1. The concentrations of plasma d-glucose, l-lactate, free fatty acids and ketone bodies and of liver glycogen were measured in caesarian-delivered newborn rats at time-intervals up to 4h after delivery. Glucose and lactate concentrations decreased markedly during the first hours after delivery, but there was a delay of 60–90min before significant glycogen mobilization occurred. 2. The specific radioactivity of plasma d-glucose was measured as a function of time for up to 75min after the intraperitoneal injection of d-[6-14C]glucose and d-[6-3H]glucose into caesarian-delivered rats at 0, 1 and 2h after delivery. Calculations revealed that there was an appreciable rate of glucose formation at all ages studied, but immediately after delivery this was exceeded by the rate of glucose utilization. Around 2h post partum the rate of glucose utilization decreased dramatically and this coincided with a reversal of the immediately postnatal hypoglycaemia. 3. The specific radioactivity of plasma l-lactate and the incorporation of 14C into plasma d-glucose and liver glycogen was measured as a function of time after the intraperitoneal injection of l-[U-14C]lactate into rats immediately after delivery. The logarithm of the specific radioactivity of plasma l-[U-14C]lactate decreased linearly with time for at least 60min after injection and the calculated rate of lactate utilization exceeded the rate of lactate formation. 4. 14C incorporation into plasma d-glucose was maximal from 30–60min after injection of l-[U-14C]lactate and the amount incorporated at 60min was 23% of that present in plasma lactate. Although 14C was also incorporated into liver glycogen the amount was always less than 3% of that present in plasma glucose. 5. The results are discussed in relationship to the adaptation of the newly born rat to the extra-uterine environment and the possible involvement of gluconeogenesis at this time before feeding is established.

Hyperglycemic effect of glucosamine

1962 ◽  
Vol 203 (2) ◽  
pp. 243-247 ◽  
Author(s):  
Roland A. Coulson ◽  
Thomas Hernandez
Keyword(s):  
Lactic Acid ◽  
Glucose Level ◽  
Plasma Glucose ◽  
Filtration Rate ◽  
Plasma Glucose Level ◽  
Glucose Utilization ◽  
Liver Glycogen ◽  
Severe Diabetes ◽  
Small Doses ◽  
Hyperglycemic Effect

The injection of large amounts of glucosamine into either alligators or rats increased the plasma glucose level to a height as great as that found in severe diabetes. Galactosamine and N-acetylglucosamine were inactive in this respect. Since glucosamine was not found to increase plasma lactic acid in either the alligator or rat or to decrease liver glycogen in the rat, it did not appear to function as a glycogenolytic agent. The injection of glucose combined with amounts of glucosamine which were too small to cause hyperglycemia in either animal led to the development of a very much more marked hyperglycemia than when glucose alone was injected. The evidence indicated that glucosamine inhibited glucose utilization and hence it could be considered to be diabetogenic. Neither glucosamine nor galactosamine were utilized for energy to any great extent and both were excreted in the urine of the two species as rapidly as thiosulfate, an inert compound known to be eliminated at renal filtration rate. Glucosamine and galactosamine in very small doses constricted the pupils of the eyes of the alligator. This miotic response and the glucosamine-induced hyperglycemia were decreased by insulin injections. Insulin hastened the disappearance of glucosamine from the plasma of the alligator.

The Protective Efficacy of Ethanolic Leaves Extract of Citronella Gras (Cymbopogon nardus) on Glucose Metabolism Alteration Induced By Mercury in Rats

2017 ◽  
Vol 9 (03) ◽  
Author(s):  
Fransisca Diana Alexandra ◽  
Dian Mutiasari ◽  
Trilianty Lestarisa ◽  
Eko Suhartono
Keyword(s):  
Glucose Metabolism ◽  
Protective Effect ◽  
Plant Extract ◽  
Protective Efficacy ◽  
Liver Weight ◽  
Liver Glycogen ◽  
Liver Cells ◽  
Glycogen Level ◽  
Group I ◽  
Citronella Grass

The present study was undertaken to investigate the protective effect of ethanolic citronella grass (C. nardus) leaves extract against mercury (Hg) induced glucose metabolism alteration in rats. Four groups of rats were selected, with 6 rats for each group. Animals of group I was received a 1 ppm of Hg only. Animals of groups II, III, and IV received a combination of 1 ppm Hg and plant extract in different dose (1650, 2520, and 3360 mg/ml). The experiment lasted for 4 weeks. The various parameters studied included liver weight, liver glucose, glycogen, and malondialdehyde (MDA) level in all groups after treatment. The results of this present studies showed that the Hg-induced glucose metabolism alteration in rats which can be seen from the increase of liver glucose and the decreasing of liver glycogen levels. The results also showed that the Hginduced glucose metabolism alteration through its activities in the trigger the liver cells damage which can be seen from the decreasing of liver weight and the increase of liver MDA level. The ethanolic of C. nardus leaves extract shows a protective effect to maintain all parameters into a better a condition which can be seen from the significant increase in liver weight and liver glycogen level, and the significant decrease in liver glucose and MDA levels. The present study indicated that the ethanolic C. nardus leaves extract showed a potential protective effect on glucose metabolism alteration induced by Hg

Metabolic effects of oral fructose in the liver of fasted rats

1984 ◽  
Vol 247 (4) ◽  
pp. E505-E512 ◽  
Author(s):  
C. B. Niewoehner ◽  
D. P. Gilboe ◽  
G. A. Nuttall ◽  
F. Q. Nuttall
Keyword(s):  
Uric Acid ◽  
Portal Vein ◽  
Hepatic Vein ◽  
Glycogen Synthase ◽  
Control Level ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Metabolic Effects ◽  
Serum Triglycerides ◽  
Fasted Rats

Twenty-four-hour-fasted rats were given fructose (4 g/kg) by gavage. Fructose absorption and the portal vein, aorta, and hepatic vein plasma fructose, glucose, lactate, and insulin concentrations as well as liver fructose and fructose 1-P, glucose, glucose 6-P, UDPglucose, lactate, pyruvate, ATP, ADP, AMP, inorganic phosphate (Pi), cAMP, and Mg2+, and glycogen synthase I and phosphorylase alpha were measured at 10, 20, 30, 40, 60 and 120 min after gavage. Liver and muscle glycogen and serum uric acid and triglycerides also were measured. Fifty-nine percent of the fructose was absorbed in 2 h. There were modest increases in plasma and hepatic fructose, glucose, and lactate and in plasma insulin. Concentrations in the portal vein, aorta, and hepatic vein plasma indicate rapid removal of fructose and lactate by the liver and a modest increase in production of glucose. The source of the increase in plasma lactate is uncertain. Hepatic glucose 6-P increased twofold; UDPglucose rose transiently and then decreased below the control level. Fructose 1-P increased linearly to a concentration of 3.3 mumol/g wet wt by 120 min. There was no change in ATP, ADP, AMP, cAMP, Pi, or Mg2+. Serum triglycerides and uric acid were unchanged. Glycogen synthase was activated by 20 min without a change in phosphorylase alpha. This occurred with a fructose dose that did not significantly increase either the liver glucose or fructose concentrations. Liver glycogen increased linearly after 20 min, and glycogen storage was equal in liver (38.4%) and muscle (36.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

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