scholarly journals Glucose Oxidation by Normal and Virus-Infected Mice

1956 ◽  
Vol 184 (2) ◽  
pp. 356-358 ◽  
Author(s):  
Benjamin V. Siegel ◽  
Ann M. Hughes
Keyword(s):  
Glucose Metabolism ◽  
Glucose Oxidation ◽  
Apparent Effect ◽  
Diseased Animal ◽  
Poliomyelitis Virus ◽  
Viral Multiplication

The oxidation of uniformly labeled C14-glucose by normal mice and mice infected with strain MEF1 poliomyelitis virus was determined in an apparatus designed to measure respiratory radioactivity excretion. The respiration of normal and virus-infected mice was found to be essentially the same over a 10-day period of infection, although the production of virus in the diseased animal during this time was considerable. It is concluded that the rate and extent of viral multiplication in poliomyelitis is without apparent effect on the rate and extent of glucose metabolism by the infected intact host.

Effects of hypoglycemia and diabetes on fuel metabolism by rat brain microvessels

1988 ◽  
Vol 254 (3) ◽  
pp. E272-E278
Author(s):  
A. L. McCall ◽  
I. Sussman ◽  
K. Tornheim ◽  
R. Cordero ◽  
N. B. Ruderman
Keyword(s):  
Glucose Metabolism ◽  
Glucose Oxidation ◽  
Cerebral Microvessels ◽  
Fuel Metabolism ◽  
Brain Microvessels ◽  
Cerebral Microvasculature ◽  
Streptozotocin Induced Diabetes ◽  
Consistent Increase ◽  
Beta Hydroxybutyrate ◽  
Cerebral Microvessel

Glucose and beta-hydroxybutyrate metabolism were compared in isolated cerebral microvessels from chronically diabetic and hypoglycemic rats. As noted previously, glucose oxidation and conversion to lactate are diminished in rats with streptozotocin-induced diabetes. The decrease in glucose metabolism did not result from selective damage to diabetic vessels during isolation, since the ATP level and the ATP/ADP ratio were similar to those of nondiabetic rats, and O2 consumption was increased. In addition, cerebral microvessel oxidation of beta-hydroxybutyrate was enhanced by diabetes. By contrast, microvessels from rats made chronically hypoglycemic by insulinoma engrafting 30 days earlier had a more than twofold increase in glucose oxidation and conversion to lactate, whereas their oxidation of beta-hydroxybutyrate was diminished by 50%. Unlike the insulinoma rats, no consistent increase in glucose metabolism was observed in microvessels from rats made hypoglycemic either by acute insulin administration or by a 4-day infusion of insulin. These results indicate that diabetes, and under some circumstances chronic hypoglycemia, markedly alters fuel metabolism in the cerebral microvasculature.

Truncal vagotomy does not affect postabsorptive glucose metabolism in humans

1995 ◽  
Vol 79 (1) ◽  
pp. 97-101 ◽  
Author(s):  
E. P. Corssmit ◽  
J. J. Van Lanschot ◽  
J. A. Romijn ◽  
E. Endert ◽  
H. P. Sauerwein
Keyword(s):  
Glucose Metabolism ◽  
Glucose Oxidation ◽  
Plasma Concentrations ◽  
Glucose Production ◽  
Radical Resection ◽  
Truncal Vagotomy ◽  
Glucose Turnover ◽  
Short Term ◽  
Serum Free Fatty Acid ◽  
Glucoregulatory Hormones

To evaluate the effects of hepatic vagal denervation on the adaptation of glucose metabolism to short-term starvation (i.e., < 24 h), glucose metabolism was studied after 16 and again after 22 h of fasting in postsurgical patients with truncal vagotomy (n = 9; radical resection of esophageal carcinoma) and without truncal vagotomy (n = 5; partial resection of the large bowel for carcinoma). Glucose metabolism was studied 3–7.5 mo postoperatively by [3–3H]glucose turnover and by indirect calorimetry. Basal glucose production, plasma glucose concentration, glucose oxidation, serum free fatty acid concentration, and fat oxidation were not different between groups; neither were plasma concentrations of glucoregulatory hormones. The adaptation to prolongation of the fast by 6 h was not different for any of these parameters between both groups. In conclusion, truncal vagotomy does not affect the adaptation of glucose metabolism to the postabsorptive state (16–22 h of fasting).

Dichloroacetate improves cardiac efficiency after ischemia independent of changes in mitochondrial proton leak

2001 ◽  
Vol 280 (4) ◽  
pp. H1762-H1769 ◽  
Author(s):  
Masayuki Taniguchi ◽  
Craig Wilson ◽  
Charlene A. Hunter ◽  
Daniel J. Pehowich ◽  
Alexander S. Clanachan ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Glucose Metabolism ◽  
Pyruvate Dehydrogenase ◽  
Mitochondrial Membrane ◽  
Glucose Oxidation ◽  
Proton Leak ◽  
Cardiac Efficiency ◽  
Cardiac Work ◽  
Atp Production ◽  
Rat Hearts

Dichloroacetate (DCA) is a pyruvate dehydrogenase activator that increases cardiac efficiency during reperfusion of ischemic hearts. We determined whether DCA increases efficiency of mitochondrial ATP production by measuring proton leak in mitochondria from isolated working rat hearts subjected to 30 min of ischemia and 60 min of reperfusion. In untreated hearts, cardiac work and efficiency decreased during reperfusion to 26% and 40% of preischemic values, respectively. Membrane potential was significantly lower in mitochondria from reperfused (175.6 ± 2.2 mV) versus aerobic (185.8 ± 3.1 mV) hearts. DCA (1 mM added at reperfusion) improved recovery of cardiac work (1.9-fold) and efficiency (1.5-fold) but had no effect on mitochondrial membrane potential (170.6 ± 2.9 mV). At the maximal attainable membrane potential, O2consumption (nmol O2 · mg−1 · min−1) did not differ between untreated or DCA-treated hearts (128.3 ± 7.5 and 120.6 ± 7.6, respectively) but was significantly greater than aerobic hearts (76.6 ± 7.6). During reperfusion, DCA increased glucose oxidation 2.5-fold and decreased H+production from glucose metabolism to 53% of untreated hearts. Because H+ production decreases cardiac efficiency, we suggest that DCA increases cardiac efficiency during reperfusion of ischemic hearts by increasing the efficiency of ATP use and not by increasing the efficiency of ATP production.

Epinephrine increases ATP production in hearts by preferentially increasing glucose metabolism

1994 ◽  
Vol 267 (5) ◽  
pp. H1862-H1871 ◽  
Author(s):  
R. L. Collins-Nakai ◽  
D. Noseworthy ◽  
G. D. Lopaschuk
Keyword(s):  
Fatty Acid ◽  
Glucose Metabolism ◽  
Fatty Acid Oxidation ◽  
Glucose Oxidation ◽  
Contractile Function ◽  
Pyruvate Dehydrogenase Complex ◽  
Active Form ◽  
Acid Oxidation ◽  
Complex Activity ◽  
Atp Production

Although epinephrine is widely used clinically, its effect on myocardial energy substrate preference in the intact heart has yet to be clearly defined. We determined the effects of epinephrine on glucose and fatty acid metabolism in isolated working rat hearts perfused with 11 mM glucose, 0.4 mM palmitate, and 100 muU/ml insulin at an 11.5-mmHg left atrial preload and a 60-mmHg aortic afterload. Glycolysis and glucose oxidation were measured in hearts perfused with [5–3H]glucose and [U-14C]glucose, whereas fatty acid oxidation was measured in hearts perfused with [1–14C]palmitate. Addition of 1 microM epinephrine resulted in a 53% increase in the heart rate-developed pressure product. Glycolysis increased dramatically following addition of epinephrine (a 272% increase), as did glucose oxidation (a 410% increase). In contrast, fatty acid oxidation increased by only 10%. Epinephrine treatment did not increase the amount of oxygen required to produce an equivalent amount of ATP; however, epinephrine did increase the uncoupling between glycolysis and glucose oxidation in these fatty acid-perfused hearts, resulting in a significant increase in H+ production from glucose metabolism. Overall ATP production in epinephrine-treated hearts increased 59%. The contribution of glucose (glycolysis and glucose oxidation) to ATP production increased from 13 to 36%, which was accompanied by a reciprocal decrease in the contribution of fatty acid oxidation to ATP production from 83 to 63%. The increase in glucose oxidation was accompanied by a significant increase in pyruvate dehydrogenase complex activity in the active form. We conclude that the increase in ATP required for contractile function following epinephrine treatment occurs through a preferential increase in glucose use.

Enzymatic and 14C-mannitol studies of the Aspergillus mannitol metabolism

1970 ◽  
Vol 16 (5) ◽  
pp. 363-367 ◽  
Author(s):  
Wei Hwa Lee
Keyword(s):  
Glucose Metabolism ◽  
Carbon Source ◽  
Metabolic Rate ◽  
Sole Carbon Source ◽  
Glucose Oxidation ◽  
Sole Source ◽  
Aspergillus Species ◽  
Mannitol Metabolism

Aspergillus species (UC4177) accumulated mannitol from glucose substrate and it also used mannitol as the sole carbon source. Experiment with radioactive mannitol showed that the accumulation of mannitol and the oxidation of mannitol to CO2 proceeded simultaneously. The presence of glucose in the medium did not inhibit mannitol oxidation. Mannitol was oxidized at about 25% of the metabolic rate of glucose. The rate of mannitol oxidation and several of the enzymes directly involved in mannitol metabolism were unaffected by using glucose or mannitol as the sole source of carbon. Nine enzymes of glucose metabolism were tested and none appeared to limit the rate of glucose oxidation. Aspergillus phosphofructokinase was not inhibited by 2.4 mM ATP or 10 mM citrate. Possible enzymatic defects favoring mannitol accumulation were not found.

Glucose metabolism in rat hypothalamus

1981 ◽  
Vol 98 (4) ◽  
pp. 481-487 ◽  
Author(s):  
Pentti Lautala ◽  
Julio M. Martin
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transport ◽  
Glucose Concentration ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Rat Hypothalamus ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Phenazine Methosulphate

Abstract. In vitro glucose oxidation and glucose transport in the rat medial (MH) and lateral (LH) hypothalamic areas was measured. Glucose oxidation was calculated from the conversion of [U-14C]glucose to 14C02 and glucose transport from 14C02 produced from [114C]glucose in the presence of phenazine methosulphate and NaF. Increasing glucose in the medium from 1 him to 20 mm enhanced glucose oxidation two-fold in MH and 40% in LH. Addition of insulin, 100 (iU/ml, to the medium decreased glucose oxidation 30% both in MH and LH at both 4 mm and 20 mm glucose. Fasting did not affect glucose oxidation in either of these hypothalamic areas. Glucose transport was not affected by insulin, but was increased significantly when glucose was raised from 0.25 mm to 1.0 mm. Fasting also increased glucose transport in both hypothalamic areas. In conclusion, extracellular glucose concentration seems to be the major regulator of glucose utilization by the rat hypothalamus. Insulin, rather than increasing, seems to decrease glucose oxidation while having no effect on glucose transport.

Glucose metabolism during fasting through human pregnancy: comparison of tracer method with respiratory calorimetry

1993 ◽  
Vol 265 (3) ◽  
pp. E351-E356 ◽  
Author(s):  
B. Assel ◽  
K. Rossi ◽  
S. Kalhan
Keyword(s):  
Body Weight ◽  
Glucose Metabolism ◽  
Glucose Oxidation ◽  
Respiratory Exchange Ratio ◽  
Late Pregnancy ◽  
Open Circuit ◽  
Glucose Turnover ◽  
Tracer Method ◽  
Third Trimester ◽  
Maternal Glucose

Glucose turnover and glucose oxidation were quantified in six normal pregnant women serially throughout pregnancy, using [U-13C]glucose tracer in combination with open-circuit indirect respiratory calorimetry. Five normal nonpregnant women were studied for comparison. With advancing gestation and increase in maternal body weight, there was a proportionate increase in the rate of appearance (Ra) of glucose so that Ra expressed per kilogram body weight did not change from the first to third trimester. The tracer measured rate of glucose oxidation expressed per kilogram body weight also did not change significantly throughout pregnancy. Oxygen consumption (VO2) in pregnant subjects did not differ from that in nonpregnant subjects. However, the respiratory exchange ratio (RER) increased significantly during pregnancy (0.88 +/- 0.53 3rd trimester and 0.76 +/- 0.50 nonpregnant, P < 0.01). The estimated contribution of carbohydrate to VO2 measured by respiratory calorimetry was greater than that measured by the tracer method. This discrepancy became wider as the respiratory quotient increased in late pregnancy. These data suggest that maternal glucose metabolism adjusts throughout pregnancy to meet the increased demands of the conceptus. The discrepancy between tracer method and respiratory calorimetry was probably due to the contribution of (fetal) lipogenesis and (maternal) gluconeogenesis to RER.

Basal plasma insulin levels exert a qualitative but not quantitative effect on glucose-mediated glucose uptake

1995 ◽  
Vol 268 (6) ◽  
pp. E1089-E1095 ◽  
Author(s):  
S. Del Prato ◽  
A. Riccio ◽  
S. Vigili de Kreutzenberg ◽  
M. Dorella ◽  
A. Tiengo ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Oxidation ◽  
Critical Role ◽  
Glucose Disposal ◽  
Insulin Levels ◽  
Hyperglycemic Clamp ◽  
Basal Plasma ◽  
Plasma Insulin Levels ◽  
Total Body

We assessed the effect of hyperglycemia on glucose uptake in the presence of normal basal insulin levels or somatostatin-induced hypoinsulinemia in seven normal volunteers during a 200-min hyperglycemic clamp (+ 9 mmol/l) carried out with [3-3H]glucose and indirect calorimetry. Hyperglycemia increased glucose uptake to 22.4 +/- 2.6 and 21.3 +/- 1.6 mumol.kg-1.min-1 with and without insulin replacement, respectively. Normoinsulinemia increased glucose oxidation (delta = + 4.5 +/- 0.6 mumol.kg-1.min-1) and nonoxidative glucose metabolism (delta = + 5.2 +/- 1.7 mumol.kg-1.min-1), whereas with insulinopenia, glucose oxidation did not change (delta = -0.3 +/- 0.6 mumol.kg-1.min-1), and nonoxidative glucose metabolism increased (delta = + 48.7 +/- 0.8 mumol.kg-1.min-1). Nonoxidative glucose metabolism was higher during insulinopenic (13.5 +/- 1.8 mumol.kg-1.min-1) than normoinsulinemic hyperglycemia (9.8 +/- 2.7 mumol.kg-1.min-1; P < 0.01). Plasma FFA concentration and lipid oxidation were higher with insulinopenia. Blood lactate and alanine concentrations were greater with normoinsulinemia. In conclusion: 1) hyperglycemia promotes glucose uptake by stimulating both nonoxidative and oxidative glucose disposal; 2) the ability of hyperglycemia to enhance total body glucose uptake is similar with and without normoinsulinemia; 3) although acute insulinopenia does not impair the ability of hyperglycemia to stimulate glucose uptake, it plays a critical role in determining the intracellular metabolic fate of glucose taken up in response to hyperglycemia.

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