scholarly journals Gluconeogenesis in the cow. The effects of a glucocorticoid on hepatic intermediary metabolism

1970 ◽  
Vol 116 (5) ◽  
pp. 865-874 ◽  
Author(s):  
G. D. Baird ◽  
R. J. Heitzman
Keyword(s):  
Blood Glucose ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Tyrosine Aminotransferase ◽  
Aspartate Transaminase ◽  
Blood Concentrations ◽  
Lactating Cows ◽  
Glycolytic Intermediates ◽  
Blood Glucose Concentrations ◽  
Parallel Measurements

1. The hepatic concentrations of the ketone bodies and of metabolites and activities of enzymes involved in gluconeogenesis were measured in healthy lactating and non-lactating cows 48h after administration of Voren, an ester of dexamethasone, and compared with those found in control animals given saline. Parallel measurements were also made of the blood concentrations of several of the metabolites. 2. Blood glucose concentrations were raised in the Voren-treated animals, whereas blood ketone body and free fatty acid concentrations were unaltered. Similarly there was no change in the hepatic concentrations of the ketone bodies. 3. Significant increases were found in the hepatic concentrations of citrate, 2-oxo-glutarate and malate in both groups of animals given Voren. 4. The hepatic concentrations of those glycolytic intermediates that were measured either decreased or did not change after Voren treatment. 5. The enzymes aspartate transaminase and fructose 1,6-diphosphatase were unchanged in activity after Voren administration, whereas phosphopyruvate carboxylase (EC 4.1.1.32) activity was depressed in the lactating group. However, glucose 6-phosphatase, tryptophan oxygenase and tyrosine aminotransferase increased in activity. 6. In several cases those hepatic metabolites that increased in concentration after Voren administration were present in lower concentration in normal lactating cows than in normal non-lactating cows. The same applied mutatis mutandis to those metabolites that were decreased by Voren. 7. These findings are discussed in relation to the use of glucocorticoids in the treatment of bovine ketosis.

scholarly journals Metabolic interactions of dichloroacetate and insulin in experimental diabetic ketoacidosis. Studies on whole animals and after functional hepatectomy

1975 ◽  
Vol 146 (2) ◽  
pp. 447-456 ◽  
Author(s):  
P J Backshear ◽  
P A H Holloway ◽  
K G M M Alberti
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Blood Lactate ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Blood Concentrations ◽  
Metabolic Interactions ◽  
Lactate And Pyruvate ◽  
Body Production ◽  
Body Concentration

1. The infusion of sodium dichloroacetate into rats with severe diabetic ketoacidosis over 4h caused a 2mM decrease in blood glucose, and small falls in blood lactate and pyruvate concentrations. Similar findings had been reported in normal rats (Blackshear et al., 1974). In contrast there was a marked decrease in blood ketone-body concentration in the diabetic ketoacidotic rats after dichloroacetate treatment. 2. The infusion of insulin alone rapidly decreased blood glucose and ketone bodies, but caused an increase in blood lactate and pyruvate. 3. Dichloroacetate did not affect the response to insulin of blood glucose and ketone bodies, but abolished the increase of lactate and pyruvate seen after insulin infusion. 4. Neither insulin nor dichloroacetate stimulated glucose disappearance after functional hepatectomy, but both agents decreased the accumulation in blood of lactate, pyruvate and alanine. 5. Dichloroacetate inhibited 3-hydroxybutyrate uptake by the extra-splachnic tissues; insulin reversed this effect. Ketone-body production must have decreased, as hepatic ketone-body content was unchanged by dicholoracetate yet blood concentrations decreased. 6. It was concluded that: (a) dichloroacetate had qualitatively similar effects on glucose metabolism in severely ketotic rats to those observed in non-diabetic starved animals; (b) insulin and dichloroacetate both separately and together, decreased the net release of lactate, pyruvate and alanine from the extra-splachnic tissues, possibly through a similar mechanism; (c) insulin reversed the inhibition of 3-hydroxybutyrate uptake caused by dichloroacetate; (d) dichloroacetate inhibited ketone-body production in severe ketoacidosis.

scholarly journals Ketone-body metabolism in tumour-bearing rats

1986 ◽  
Vol 233 (2) ◽  
pp. 485-491 ◽  
Author(s):  
A M Rofe ◽  
R Bais ◽  
R A Conyers
Keyword(s):  
Blood Glucose ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Hepatic Glycogen ◽  
Turnover Rates ◽  
Total Blood ◽  
Normal Tissues ◽  
Tumour Bearing ◽  
And Control

During starvation for 72 h, tumour-bearing rats showed accelerated ketonaemia and marked ketonuria. Total blood [ketone bodies] were 8.53 mM and 3.34 mM in tumour-bearing and control (non-tumour-bearing) rats respectively (P less than 0.001). The [3-hydroxybutyrate]/[acetoacetate] ratio was 1.3 in the tumour-bearing rats, compared with 3.2 in the controls at 72 h (P less than 0.001). Blood [glucose] and hepatic [glycogen] were lower at the start of starvation in tumour-bearing rats, whereas plasma [non-esterified fatty acids] were not increased above those in the control rats during starvation. After functional hepatectomy, blood [acetoacetate], but not [3-hydroxybutyrate], decreased rapidly in tumour-bearing rats, whereas both ketone bodies decreased, and at a slower rate, in the control rats. Blood [glucose] decreased more rapidly in the hepatectomized control rats. Hepatocytes prepared from 72 h-starved tumour-bearing and control rats showed similar rates of ketogenesis from palmitate, and the distribution of [1-14C] palmitate between oxidation (ketone bodies and CO2) and esterification was also unaffected by tumour-bearing, as was the rate of gluconeogenesis from lactate. The carcinoma itself showed rapid rates of glycolysis and a poor ability to metabolize ketone bodies in vitro. The results are consistent with the peripheral, normal, tissues in tumour-bearing rats having increased ketone-body and decreased glucose metabolic turnover rates.

EFFECTS OF POSTFEEDING INTERVAL ON BLOOD CONSTITUENTS RELATED TO ENERGY METABOLISM IN NONPREGNANT ANGUS AND HEREFORD HEIFERS

1973 ◽  
Vol 53 (4) ◽  
pp. 641-646 ◽  
Author(s):  
D. M. BOWDEN
Keyword(s):  
Blood Glucose ◽  
Plasma Nefa ◽  
Blood Concentrations ◽  
Nonesterified Fatty Acids ◽  
Blood Constituents ◽  
Initial Sampling ◽  
Glucose Plasma ◽  
Blood Glucose Concentrations ◽  
Subcutaneous Adipose ◽  
Angus Heifers

Ten Angus heifers and 10 Hereford heifers were fasted for 48 h to study changes in blood glucose, plasma nonesterified fatty acids (NEFA), and plasma ketone concentrations and their relationships to prefast feeding levels and breed. Prior to fasting, five heifers of each breed were fed for 140 days on one of two rations, which produced significantly different average rates of gain (0.16 vs. 0.47 kg/day) and average depths of subcutaneous adipose tissue (5.0 vs. 10.3 mm). Blood was sampled at 1, 24, and 48 h postfeeding. Blood glucose concentrations were higher (P < 0.01) at 24 h postfeeding but did not change from 24 to 48 h postfeeding. Plasma NEFA concentrations increased during the 48-h fast. Plasma ketones were lower (P < 0.01) at 24 h postfeeding but at 48 h were higher (P < 0.01) than at 1 h postfeeding. Packed cell volume (PCV) increased during 24 and 48 h of fasting. Blood concentrations of glucose, NEFA, and ketones at either 24 or 48 h of fasting were not influenced by prefast feeding level. Angus heifers had higher (P < 0.05) blood glucose and higher (P < 0.05) PCV than Hereford heifers. Correlations between the blood constituents at the three sampling times were generally low. Only the correlations of plasma NEFA with ketone concentrations at 24 h postfeeding (.55) and glucose with PCV at the initial sampling (−.52) reached significance (P < 0.05).

scholarly journals Effects of food deprivation on ketonaemia, ketogenesis and hepatic intermediary metabolism in the non-lactating dairy cow

1979 ◽  
Vol 178 (1) ◽  
pp. 35-44 ◽  
Author(s):  
G D Baird ◽  
R J Heitzman ◽  
I M Reid ◽  
H W Symonds ◽  
M A Lomax
Keyword(s):  
Dairy Cows ◽  
Food Deprivation ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Tricarboxylic Acid Cycle ◽  
Energy Charge ◽  
Fold Increase ◽  
Lactating Cows ◽  
A Value ◽  
Lactating Dairy Cows

1. The aim of this work was to investigate why non-lactating dairy cows are less susceptible to the development of ketonaemia during food deprivation than are dairy cows in early lactation. 2. The first experiment (Expt. A) consisted of determining the effect of 6 days of food deprivation on the concentrations of ketone bodies, and of metabolites related to the regulation of ketogenesis, in jugular blood and liver of non-lactating cows. 3. During the food deprivation, blood ketone-body concentrations rose significantly, but to a value that was only 16% of that achieved in lactating cows deprived of food for 6 days [Baird, Heitzman & Hibbitt (1972) Biochem. J. 128, 1311–1318]. 4. In the liver, food deprivation caused: a rise in ketone-body concentrations; a fall in the concentration of glycogen and of various intermediates of the Embden-Meyerhof pathway and the tricarboxylic acid cycle; an increase in cytoplasmic reduction; a decrease in the [total NAD+]/[total NADH] ratio; a decrease in energy charge. These changes were all qualitatively similar to those previously observed in the livers of the food-deprived lactating cows. 5. There appeared therefore to be a discrepancy in the food-deprived non-lactating cows between the absence of marked ketonaemia and the occurrence of metabolic changes within the liver suggesting increased hepatic ketogenesis. This discrepancy was partially resolved in Expt. B by the observation in two catheterized non-lactating cows that, although there was a 2-fold increase in hepatic ketogenesis during 6 days of food deprivation, ketogenesis from the splanchnic bed as a whole (i.e. gut and liver combined) declined slightly owing to cessation of gut ketogenesis.

scholarly journals Turnover rates of ketone bodies in normal, starved and alloxan-diabetic rats

1968 ◽  
Vol 110 (4) ◽  
pp. 655-661 ◽  
Author(s):  
Margaret W. Bates ◽  
H. A. Krebs ◽  
D. H. Williamson
Keyword(s):  
Ketone Body ◽  
Alloxan Diabetes ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Turnover Rates ◽  
Blood Concentrations ◽  
Order Of Magnitude ◽  
The Mean ◽  
Body Production ◽  
Body Concentration

1. Rates of appearance and disappearance of total ketone bodies were determined in normal, starved and alloxan-diabetic rats by measuring specific radioactivities and concentrations of blood acetoacetate and 3-hydroxybutyrate at different times after injection of 3-hydroxy[14C]butyrate. 2. The mean rates of appearance were 1·7, 4·2 and 10·9μmoles/min./100g. body wt. respectively for normal, starved and alloxan-diabetic rats. The rates of disappearance were of the same order of magnitude as the rates of appearance. 3. There was a direct correlation between the rates of appearance and disappearance and the blood concentrations of the ketone bodies. 4. The results indicate that in the rat increased ketone-body production is paralleled by increased ketone-body utilization and that the raised ketone-body concentration in the blood in starvation and alloxan-diabetes is due to a slight imbalance between the rates of production and utilization. 5. The findings are discussed in relation to the concept that ketone bodies can serve as fuels of respiration when the supply of carbohydrate is limited.

CONCENTRATION OF CERTAIN BLOOD METABOLITES IN OBESE PREGNANT AND NON-PREGNANT EWES

1969 ◽  
Vol 49 (1) ◽  
pp. 91-95 ◽  
Author(s):  
J. P. Ross ◽  
W. D. Kitts
Keyword(s):  
Lactic Acid ◽  
Fatty Acid ◽  
Blood Glucose ◽  
Volatile Fatty Acid ◽  
Ketone Bodies ◽  
Total Volatile ◽  
Blood Concentrations ◽  
The Mean ◽  
Mean Blood Glucose ◽  
Total Volatile Fatty Acid

A total of 14 obese pregnant and non-pregnant ewes were compared for blood glucose, ketone bodies, lactic acid and total volatile fatty acid concentrations. A method of blood sampling which successfully eliminated the effect of excitement on the metabolites studied was devised. The mean values and standard errors for the metabolites of pregnant and non-pregnant ewes, respectively, were glucose 57 ± 4.2 mg/100 ml and 63 ± 4.2 mg/100 ml, ketone bodies 3.2 ± 0.75 mg/100 ml and 2.3 ± 0.75 mg/100 ml, lactic acid 18 ± 2.9 mg/100 ml and 19 ± 2.9 mg/100 ml, and total volatile fatty acid 1.96 ± 0.28 meq/liter and 1.58 ± 028 meq/liter. The mean blood glucose concentration was lower (P < 0.10) for the pregnant ewes than for the non-pregnant ewes, but there were no significant differences between pregnant and non-pregnant ewes for blood concentrations of ketone bodies, lactic acid and total volatile fatty acid. The mean blood glucose values for both the pregnant and non-pregnant ewes were higher than earlier values reported in the literature.

Cerebral carbohydrate and energy metabolism during hypoglycemia in newborn dogs

1981 ◽  
Vol 240 (3) ◽  
pp. R192-R199 ◽  
Author(s):  
R. C. Vannucci ◽  
E. E. Nardis ◽  
S. J. Vannucci ◽  
P. A. Campbell
Keyword(s):  
Blood Glucose ◽  
Glucose Consumption ◽  
Regular Insulin ◽  
High Energy ◽  
Glycolytic Flux ◽  
Glucose Levels ◽  
Glycolytic Intermediates ◽  
Withdrawal Reflexes ◽  
Lactate Levels ◽  
Blood Glucose Concentrations

The metabolic responses of the perinatal brain to hypoglycemia were studied in newborn dogs. Hypoglycemia, induced by the intravenous injection of regular insulin (0.2-0.3 U/g body wt), resulted in final blood glucose concentrations ranging from 0.1 to 1.5 mmol/l; blood lactate levels were little changed from normoglycemic values. Righting, sucking, and nociceptive withdrawal reflexes were progressively lost during the course of hypoglycemia. Slowing of the electroencephalogram was apparent at or below 1.5 mmol/l blood glucose and advanced to paroxysmal discharges and convulsive activity as glucose approached 0.5 mmol/l. In lightly anesthetized, paralyzed, and artificially ventilated puppies, blood glucose concentrations approximating 1.0 mmol/l were associated with a 91% reduction in cerebral glucose; the concentrations of other glycolytic intermediates (glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-diphosphate, pyruvate, lactate) were unchanged from control. Further declines in blood glucose resulted in cerebral glucose levels below 0.1 mmol/kg as well as in partial depletions of all measured glycolytic intermediates including lactate. These changes reflect reduced cerebral glucose consumption and glycolytic flux. Despite the alterations in carbohydrate metabolism, both lactate/pyruvate ratios and high-energy phosphate reserves (phosphocreatine, ATP, ADP) in brain were well preserved even at the extreme of hypoglycemia. The present data, coupled with previous findings of enhanced lactic acid entry into and consumption by newborn dog brain, suggest that this metabolite serves as an important, if not the predominant, substitute fuel for cerebral oxidative metabolism during perinatal hypoglycemia.

Blood Lactate and Ketone Body Concentrations in Salicylate Intoxication

1986 ◽  
Vol 5 (6) ◽  
pp. 363-366 ◽  
Author(s):  
P.D. Bartels ◽  
H. Lund-Jacobsen
Keyword(s):  
Blood Lactate ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Metabolic Disturbances ◽  
Blood Concentrations ◽  
Salicylate Poisoning ◽  
Treatment Centre ◽  
Salicylate Intoxication ◽  
Acid Base Disturbance ◽  
Base Disturbance

1 Blood concentrations of lactate, ketone bodies and non-esterified (free) fatty acids were measured in 45 adult patients on admission to the poisoning treatment centre, with salicylate and mixed salicylate-sedative/ethanol poisoning. 2 Nine patients had blood lactate concentrations above 2 mmol/l and six patients had ketone-body concentrations greater than 1 mmol/l. 3 Eight of the nine patients with hyperlactacidaemia had mixed salicylate/ethanol or sedative poisoning, whereas four of the six patients with hyperketonaemia had pure salicylate poisoning. 4 No direct correlation was found between the presence of these metabolic disturbances and the severity of poisoning. 5 Since only one patient was found with organic acid concentration in the blood exceeding 5 mmol/l, it is concluded that concomitant endogenous acidosis rarely contributes to the acid-base disturbance seen in salicylate poisoning in adults.

Early effects of ‘total’ pancreatectomy on fat metabolism in the rat

1958 ◽  
Vol 196 (1) ◽  
pp. 125-131 ◽  
Author(s):  
Sidney S. Chernick ◽  
Robert O. Scow
Keyword(s):  
Blood Glucose ◽  
Ketone Bodies ◽  
Total Pancreatectomy ◽  
Total Lipids ◽  
Blood Concentrations ◽  
Insulin Effect ◽  
Resistance To Insulin ◽  
Early Effects ◽  
Blood Ketone Bodies ◽  
First Time

Within 2 hours after ‘total’ pancreatectomy in fasting rats blood concentrations of glucose, ketone bodies and total lipids were significantly elevated. Blood ketone bodies and total lipids increased before the blood glucose reached diabetic levels. The increase in blood lipids was due largely to triglycerides and was accompanied by accumulation of fat in the liver and kidneys. When depleted of body fat prior to surgery, pancreatectomized rats did not develop ketosis, hyperlipemia or fatty liver and kidneys. Repeated injections of insulin started immediately after pancreatectomy prevented development of diabetes. When insulin was given for the first time 1 day after pancreatectomy, blood glucose, ketone bodies and fats were lowered to normal fasting levels within 3 hours; 2 days after pancreatectomy, blood glucose and fats were reduced to normal levels whereas the ketonemia, although somewhat decreased, remained high. The rapid changes in blood ketone bodies are interpreted as evidence of a direct insulin action on liver. The decreased insulin effect on ketonemia in rats deprived of insulin for 2 days may indicate development of hepatic resistance to insulin.

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