Galactose and Hepatic Metabolism in Malnutrition and Sepsis in Man

1978 ◽  
Vol 55 (2) ◽  
pp. 199-204 ◽  
Author(s):  
G. Royle ◽  
M. G. W. Kettlewell ◽  
Vera Ilic ◽  
D. H. Williamson
Keyword(s):  
Blood Glucose ◽  
Metabolic Response ◽  
Ketone Bodies ◽  
Fasting Blood Glucose ◽  
Hepatic Metabolism ◽  
Liver Function Tests ◽  
Lactate And Pyruvate ◽  
Blood Ketone Bodies ◽  
And Function ◽  
Septic Group

1. Hepatic carbohydrate metabolism was studied by an intravenous galactose test in control patients, malnourished non-septic patients, patients with prolonged severe sepsis and patients after recovery from sepsis. 2. Blood galactose half-life was not significantly increased in the septic group despite abnormal liver-function tests, whereas it was approximately doubled in the malnourished patients. 3. The rise in blood glucose after galactose injection was less in both the septic and malnourished groups, as compared with that in the control subjects. 4. Fasting blood glucose, lactate and pyruvate concentrations were similar in all groups, whereas blood ketone bodies were increased in the malnourished and septic groups, and blood alanine was decreased only in the septic group. 5. The changes in hepatic metabolism and function were reversible on recovery from sepsis. 6. It is suggested that alterations in hepatic blood flow and the metabolic fate of galactose within the liver may explain the changes in the metabolic response to galactose observed in malnourished or septic patients.

scholarly journals Measurement of blood acetoacetate and β-hydroxybutyrate in an automatic analyser

2001 ◽  
Vol 23 (3) ◽  
pp. 69-76 ◽  
Author(s):  
Amparo Galán ◽  
Josém. Hernández ◽  
Orlando Jimenez
Keyword(s):  
Ethylenediaminetetraacetic Acid ◽  
Ketone Bodies ◽  
Mitochondrial Diseases ◽  
Turnaround Time ◽  
Sample Volume ◽  
Intermediary Metabolites ◽  
Transport Chain ◽  
Analytical Response ◽  
Lactate And Pyruvate ◽  
Blood Ketone Bodies

g-hydroxybutyrate and acetoacetate as well as lactate and pyruvate are intermediary metabolites normally present in blood. The g-hydroxybutyrate/acetoacetate ratio is an expression of the mitochondrial oxido-reduction state. This ketone body ratio can provide a clue to diagnosis and metabolic status in congenital errors of the electron transport chain and pyruvate metabolism. The standardization of these analytical procedures improves the interpretation of the results helping in the difficult diagnosis of mitochondrial diseases in children. This study describes an adaptation to a Dimension R 2 L (Dade Behring, Newark, Delaware, USA) automatic analyser for a method to measure blood ketone bodies (g-hydroxybutyrate and acetoacetate). The method allows the metabolites to be measured directly in nondeproteinized plasma (fluoride/ethylenediaminetetraacetic acid). This adaptation simplifies the analytical procedure and limits the turnaround time to 20 minutes. With a sample volume of 200 μ l metabolite concentrations ranging from 12 to 1300 μ molL−1of g-hydroxybutyrate and from 10 to 450 μ molL−1of acetoacetate may be measured with a reliable analytical response.

Fetal metabolic response to maternal fasting in the rat.

1977 ◽  
Vol 232 (5) ◽  
pp. E456 ◽  
Author(s):  
J R Girard ◽  
P Ferré ◽  
M Gilbert ◽  
A Kervran ◽  
R Assan ◽  
...  
Keyword(s):  
Phosphoenolpyruvate Carboxykinase ◽  
Metabolic Response ◽  
Specific Activity ◽  
Ketone Bodies ◽  
Fetal Liver ◽  
Hormonal Changes ◽  
Blood Ketone Bodies ◽  
Fetal Response ◽  
Gluconeogenic Substrate

To determine the fetal response to altered maternal fuel supply, the effects of prolonged maternal fasting, begun 24-96 h before term, were examined and compared with values from normally fed term animals. Fetal weight decreased only after 48 h of maternal fasting. Prolonged maternal fasting was associated with low blood glucose, high blood ketone bodies, and decreased gluconeogenic substrate in the fetus. Plasma insulin was decreased, whereas plasma glucagon was increased in the fetus of fasted mothers. Infusion of [2-3H]glucose into the mother to constant specific activity gave a ratio of maternal to fetal glucose activity of 1.0 in fed and 1.56 in fasted mothers. Fetal liver from fasted mothers showed both increase in activity of key gluconeogenic enzymes (glucose-6-phosphatase and phosphoenolpyruvate carboxykinase) and increased conversion in vitro of lactate, alanine, serine, and glycerol in glucose by liver slices. It is inferred that maternal fasting induces fetal substrate alterations and hormonal changes appropriate to premature appearance of hepatic gluconeogenesis. The priority for endogenous fuel provision in this state leads to impaired fetal growth.

Some effects of fasting on rats fed a choline-deficient diet

1960 ◽  
Vol 198 (2) ◽  
pp. 371-374 ◽  
Author(s):  
E. Douglas Rees ◽  
William W. Winternitz ◽  
William F. Lattanzi
Keyword(s):  
Blood Glucose ◽  
Ketone Bodies ◽  
Blood Glucose Concentration ◽  
Liver Glycogen ◽  
Control Group ◽  
Deficient Diet ◽  
Hepatic Fat ◽  
Blood Ketone Bodies ◽  
Deficient Group

The blood ketone body concentrations of fasted and nonfasted rats fed a diet deficient in choline were determined and found to be similar to the concentrations obtained from a control group fed the same diet supplemented with choline. However, the animals on the choline-deficient diet had an 18–20% greater mean liver mass, and this could account for the failure to demonstrate the depressed level of blood ketone bodies which was anticipated on the basis of previous in vitro studies. Other possible explanations of this discrepancy are discussed. Despite a high hepatic fat content, the choline-deficient group had a normal concentration of liver glycogen. The nonfasting blood glucose concentration of the choline-deficient group (91.5 ± 5 mg %) was lower than that of the control group (102 ± 3 mg %). After 24 hours of fasting, the values were 52 ± 3 mg % and 61 ± 5 mg % for the choline-deficient and control group, respectively. The 72-hour fasting values were 43 ± 2 mg %, and 49 ± 2 mg %, respectively. Data showing the effect of diet composition on ketonemia, liver glycogen and blood glucose are presented and are in accord with previous studies.

scholarly journals The effects of inhibition of gluconeogenesis in suckling newborn rats

1977 ◽  
Vol 162 (1) ◽  
pp. 209-212 ◽  
Author(s):  
P Ferre ◽  
J P Pegorier ◽  
J Girard
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Free Fatty Acid ◽  
Ketone Bodies ◽  
Plasma Free Fatty Acid ◽  
High Plasma ◽  
Normal Blood ◽  
Newborn Rats ◽  
High Concentrations ◽  
Blood Ketone Bodies

Inhibition of gluconeogenesis with 3-mercaptopicolinate in suckling newborn rats caused a fall in blood [glucose], but no change in their high plasma [free fatty acid] and blood [ketone bodies]. Active gluconeogenesis seems to be more important than sparing of glucose by high concentrations of fat-derived substrates for the maintenance of normal blood [glucose] in suckling newborn rats.

scholarly journals The effects of inhibition of fatty acid oxidation in suckling newborn rats

1977 ◽  
Vol 166 (3) ◽  
pp. 631-634 ◽  
Author(s):  
J P Pégorier ◽  
P Ferré ◽  
J Girard
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Fatty Acid Oxidation ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Normal Blood ◽  
Acid Oxidation ◽  
Newborn Rats ◽  
Normal Blood Glucose ◽  
Blood Ketone Bodies

Inhibition of fatty acid oxidation with pent-4-enoate in suckling newborn rats caused a fall in blood [glucose] and blood [ketone bodies] and inhibition of gluconeogenesis from lactate. Glucose utilization was not increased in newborn rats injected with pent-4-enoate. Active fatty acid oxidation appears to be essential to support gluconeogenesis and to maintain normal blood [glucose] in suckling newborn rats.

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.

Effects of d-mannoheptulose and d-sedoheptulose on blood glucose and ketone bodies in the rat

1961 ◽  
Vol 201 (6) ◽  
pp. 1073-1077 ◽  
Author(s):  
Ernst Simon ◽  
Robert O. Scow ◽  
Sidney S. Chernick
Keyword(s):  
Blood Glucose ◽  
Blood Concentration ◽  
Ketone Bodies ◽  
Glucose Administration ◽  
Blood Ketone Bodies

The effects of mannoheptulose and its isomer, sedoheptulose, were studied in fasting rats. Mannoheptulose, 400 mg injected subcutaneously, increased blood glucose to 200 mg/100 ml and ketone bodies to 21 mg/100 ml in 1 hr. These effects began to disappear in 2 hr when the blood concentration of mannoheptulose was less than 40 mg/100 ml. Administration of glucose with the heptulose increased the degree of hyperglycemia. Glucose, given alone, lowered the blood ketone bodies in fasting rats; this effect was delayed by mannoheptulose until the concentration of the latter was less than 40 mg/100 ml. Insulin, 1 unit injected subcutaneously, decreased the amounts of glucose and ketone bodies in the blood of fasting rats. Mannoheptulose did not alter the effects of insulin. Mannoheptulose had no effect on blood glucose or ketone bodies in "totally" pancreatectomized rats. The findings suggest that mannoheptulose may act in the pancreas by blocking or suppressing release of insulin. Sedoheptulose did not have any diabetogenic or ketogenic activity; its effect on lowering blood ketone bodies was similar to that after glucose administration.

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.

scholarly journals Azadirachta excelsa Improves Renal Morphology and Function in Streptozotocin Induced-Diabetic Sprague Dawley Rats

2020 ◽  
Vol 17 (12) ◽  
pp. 1307-1320
Author(s):  
Nur Syimal Aain AZMI ◽  
Nooraain HASHIM ◽  
Nurdiana SAMSULRIZAL ◽  
Noor Syaffinaz NOOR ◽  
Mohamad ZIN
Keyword(s):  
Blood Glucose ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
Structure And Function ◽  
Therapeutic Effects ◽  
Sprague Dawley ◽  
Standard Drug ◽  
Sprague Dawley Rats ◽  
Renal Morphology ◽  
And Function

Long term diabetes mellitus (DM) is associated with serious complications such as nephropathy. Previous studies revealed the ability of A. excelsa leaf extract treatment to reduce fasting blood glucose (FBG) in streptozotocin (STZ)-induced diabetic rats. The aim of this study was to determine the effect of A. excelsa extract in delaying the progression of diabetic nephropathy by evaluating the kidney structure and function. The effects were compared with 2 positive controls, which were metformin (standard drug) and quercetin (plant active compound). Induction of diabetic conditions was conducted by the intraperitoneal (IP) injection of STZ (60 mg/kg bwt) in male Sprague Dawley rats. The experimental animals were grouped into: 1) normal control (NC, saline); 2) diabetic control (DC, saline); 3) metformin-treated diabetic rats (DMET, 1000 mg/kg bwt); 4) quercetin-treated diabetic rats (DQ, 40 mg/kg bwt), and 5) A. excelsa-treated diabetic rats (DAE, 250 mg/kg bwt). All treatments were given once daily for 8 weeks through oral gavage. The inter-relation between the changes in the fasting blood glucose and kidney oxidative stress, structure, and function was evaluated. The results showed a significant increase (p < 0.05) of MDA and SOD level and a decrease (p < 0.05) of GPx levels, plus distortion of renal morphology among the DC and DMET groups. Meanwhile, both DQ and DAE groups showed significant reduction (p < 0.05) of MDA levels and elevation (p < 0.05) of SOD and GPx levels. The quercetin and A. excelsa treatments also improved the kidney function parameters and morphological changes of the diabetic rats. These findings indicate that quercetin and A. excelsa possess renal therapeutic effects.

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