Kinetics Of Glucose Metabolism Research Articles

Effects of Body Size on Kinetics of Glucose Metabolism and on Nitrogen Balance in Growing Cattle

Effects of body size on the kinetics of glucose metabolism were examined. In trial 1, steers were fed 6 kg of an 80:20 concentrate:roughage diet daily across a weight range of 226 to 470 kg. In trial 2, steers were fed 4.5 kg of a 45:55 concentrate:roughage diet daily across a weight range of 134 to 390 kg. Glucose irreversible loss averaged 820 ± 32 and 461 ± 13 mg/min for trials 1 and 2 and was not affected by body size. Thus, glucose irreversible loss seems to be regulated by feed intake when intake is above maintenance. Body size had no effect on glucose total entry rate, recycling or pool size. Blood glucose concentration and glucose space decreased at 0.004 mg · ml-1 · kg-1 and 0.002 fractional units body wt · kg-1 as body size increased. Digestible energy and nitrogen balance were measured in trial 2. Digestibility of energy increased at 0.0054 Mcal · d-1 · kg-1 as body size increased. Nitrogen retention averaged 28.2 g · d-1 and was not influenced by body size even though energy intake approached maintenance amounts at the end of the trial. On the basis of urinary nitrogen excretion data, we conclude that the maximum net contribution of amino acid carbon to glucose synthesis was 8% of glucose carbon.

Investigation of Metabolism of Exogenous Glucose at the Early Stage and Onset of Diabetes Mellitus in Otsuka Long-Evans Tokushima Fatty Rats Using [1, 2, 3-13C]Glucose Breath Tests.

This study aimed to evaluate changes in glucose metabolism at the early stage and onset of diabetes in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Specifically, after the oral administration of [1, 2, 3-13C]glucose, the levels of exhaled 13CO2, which most likely originated from pyruvate decarboxylation and tricarboxylic acid, were measured. Eight OLETF rats and eight control rats (Long-Evans Tokushima Otsuka [LETO]) were administered 13C-glucose. Three types of 13C-glucose breath tests were performed thrice in each period at 2-week intervals. [3-13C]glucose results in a 13C isotope at position 1 in the pyruvate molecule, which provides 13CO2. The 13C at carbons 1 and 2 of glucose is converted to 13C at carbons 2 and 1 of acetate, respectively, which produce 13CO2. Based on metabolic differences of the labeled sites, glucose metabolism was evaluated using the results of three breath tests. The increase in 13CO2 excretion in OLETF rats was delayed in all three breath tests compared to that in control rats, suggesting that OLETF rats had a lower glucose metabolism than control rats. In addition, overall glucose metabolism increased with age in both groups. The utilization of [2-13C]glucose was suppressed in OLETF rats at 6–12 weeks of age, but they showed higher [3-13C]glucose oxidation than control rats at 22–25 weeks of age. In the [1-13C]glucose breath test, no significant differences in the area under the curve until 180 minutes (AUC180) were observed between OLETF and LETO rats of any age. Glucose metabolism kinetics were different between the age groups and two groups of rats; however, these differences were not significant based on the overall AUC180 of [1-13C]glucose. We conclude that breath 13CO2 excretion is reduced in OLETF rats at the primary stage of prediabetes, indicating differences in glucose oxidation kinetics between OLETF and LETO rats.

Inhibition effects of ethanol on the kinetics of glucose metabolism by S. cerevisiae: NMR and modelling study

Saccharomyces cerevisiae is an important model to understand the eukaryotic cells control mechanisms. In this Letter, an approach based on in vivo 13C NMR and mathematical modelling was presented to develop a basis for a deeper understanding of eukaryotic responses to environmental stresses. Despite the few metabolites included, the model describes correctly the dynamical behaviour of glucose degradation and ethanol production, providing a qualitative and quantitative description of the response of S. cerevisiae metabolism to stressful concentrations of ethanol. The data and the model highlight that an exogenous stress is able to influence the cellular activity and the ethanol production rate constant.

Glucose metabolism and insulin release in mouse beta HC9 cells, as model for wild-type pancreatic beta-cells.

Glucose metabolism and its relationship with glucose-induced insulin release were studied in beta HC9 and beta TC3 cells to identify and characterize key factors controlling the intermediary metabolism of glucose and glucose-induced insulin release. The beta HC9 cell line, derived from pancreatic islets with beta-cell hyperplasia, is characterized by a normal concentration-dependency curve for glucose-stimulated insulin release, whereas the beta TC3 cell line, derived from pancreatic beta-cell tumors, shows a marked leftward shift of this curve. Maximum velocity and the Michaelis-Menten constant of glucose uptake in beta HC9 and beta TC3 cells were similar, even though GLUT-2 expression in these two cell lines differed. In both cell lines, the kinetic characteristics of glucose usage, glucose oxidation, and glucose-induced oxygen consumption were similar to those of glucose phosphorylation, indicating that the kinetics of glucose metabolism from the glucose phosphorylation step in the cytosol to the mitochondrial process of oxidative phosphorylation are determined by the glucose-phosphorylating enzyme, that is, by glucokinase in beta HC9 cells and by hexokinase in beta TC3 cells. Thus beta HC9 cells provide an opportunity for the quantitative analysis of glucose metabolism, the associated generation of coupling factors, and other essential beta-cell functions involved in glucose sensing and insulin secretion.

Kinetics of glucose metabolism in mothers with intrauterine growth retardation

Data on oral and I.V. glucose tolerance tests in normal pregnant women and pregnancy induced hypertensives (PIH) were subjected to kinetic analysis to obtain plasma zero concentration (CPO), area under the curve (AUC), half life (t 1/2) and metabolic clearance rates (MCR). Since no differences were observed either in the glucose tolerance (both oral and I.V.) or in the various kinetic parameters between the normal women and PIH's, the analysis of data was done in relation to the birth weight of the infant in both these groups. Accordingly, women were divided into 4 groups. 1. Normotensive normal birth weight (NBW), 2. normotensive IUGR, 3. hypertensive NBW, and 4. hypertensive IUGR. It was observed that fasting blood glucose was low in IUGR in N, NBW as well as PIHNBWs. AUC was low with shorter t 1/2 and faster MCR in IUGR as compared to normals both in normotensives and PIHs indicating a rapid elimination of glucose from the plasma with both oral and intravenous GTTs. A mechanism by the maternal tissue to take up higher amount of glucose for maintaining a high concentration gradient across the placenta in IUGR is being suggested.

Kinetics of Glucose Metabolism in Relation to Insulin Concentrations in Patients With Alcoholic Cirrhosis and in Healthy Persons

To characterize the insulin resistance in alcoholic cirrhosis we determined in vivo insulin-glucose disposal dose-response relationships in 6 patients with alcoholic cirrhosis of varying severity and in 6 control subjects, using the glucose-insulin clamp technique. Each subject was infused sequentially with insulin at rates of 0.5, 1.0, 2.0, and 10 mU/min X kg, each rate for 2 h. Euglycemia was maintained by a continuous servo-adjusted glucose infusion. The amount of glucose infused during the last 40 min of each 2-h period, corrected for accumulation in the glucose space, reflects overall net glucose metabolism. The dose-response curves demonstrated saturation kinetics. Lineweaver-Burk plots were consistently convex, rejecting a simple Michaelis-Menten relationship, but were linear when accommodated to allosterism with two active sites. The calculated affinity constant (i.e., the concentration of insulin leading to half-maximum glucose metabolism) of patients with cirrhosis was higher than that of normal controls (104 +/- 30 vs. 32 +/- 3 mU/L, mean +/- SD). In addition the maximum rate of glucose metabolism was significantly lower than that of normals (53 +/- 9 vs. 72 +/- 16 mumol/min X kg). We conclude that, in patients with alcoholic cirrhosis, insulin resistance is caused both by a marked decrease in sensitivity to insulin and a decreased maximum effect of insulin, indicating a combined receptor-postreceptor defect as the underlying cause.

Plasma and Liver Metabolites and Glucose Kinetics as Affected by Prolonged Ketonemia-Glucosuria and Fasting in Steers

For 28 days, four steers received 1,3-butanediol, which causes ketonemia, and phlorizin, which causes glucosuria. Steers also were fasted for 9 days. Effects of treatments on concentrations of metabolites in blood and liver and on kinetics of glucose metabolism were determined. Treatments were: control, control with dietary butanediol plus injected phlorizin, and fasting. Fasting caused hypoinsulinemia and decreased liver glycogen by 60%. Butanediol plus phlorizin and fasting caused 18 and 19% decreases of plasma glucose and 2.5- and 6-fold increases of free fatty acid concentrations in blood plasma. Glucose irreversible loss averaged 371, 541, and 182 g/day during control, butanediol plus phlorizin treatment, and fasting. Butanediol plus phlorizin increased liver ketone body concentrations, caused glucosuria, ketonuria, and ketonemia, but did not affect insulin, glucagon, or growth hormone concentrations in plasma or triglyceride and glycogen contents in liver. Steers given butanediol plus phlorizin did not show all the usual signs of lactation ketosis, but the treatment still offers promise for studying causes and effects of ketosis.

Glucose Kinetics, Plasma Metabolites, and Endocrine Responses During Experimental Ketosis in Steers

Phlorizin and 1,3-butanediol were used to determine effects of glucosuria and ketonemia on concentrations of metabolites in blood plasma and on kinetics of glucose metabolism. Four steers received four treatments (control; control plus dietary 1,3-butanediol; control plus phlorizin injections; and control plus phlorizin and 1,3-butanediol) in a Latin square design. Treatments lasted 14 days. All steers received a 30% grain, 70% forage ration in equal meals every 2h. Metabolite concentrations in blood plasma and urine and glucose kinetics were measured on each of the last 3 days of each treatment period. Phlorizin caused glucosuria; decreased plasma glucose, glucose total entry rate, and glucose recycling; and increased plasma free fatty acids and glucose irreversible loss. Glucose pool size was increased by 1,3-butanediol. Phlorizin plus 1,3-butanediol caused glucosuria and ketonuria; decreased plasma glucose; and increased blood ketone bodies, plasma free fatty acids, glucose irreversible loss, and glucose pool size. Growth hormone, insulin, and glucagon were not affected by treatment. Physiological perturbations in these steers were characteristic of some of those in ketotic cows.

Effects of Diet and Energy Intake on Kinetics of Glucose Metabolism in Steers

To test the hypothesis that glucose utilization in ruminants is related to energy consumption independent of diet composition or energy content, eight Holstein steers (165–230 kg) were fed either a high grain (70% corn, 20% alfalfa, 8.8% soybean meal) or high hay (70% alfalfa, 28% corn) diet. The two diets were fed in quantities that allowed comparisons to be made either isocalorically based on calculated net energy for gain (NEg) or at identical dry matter intakes. The daily ration was divided into 12 equal portions and dispensed every 2 hours by automatic feeders to achieve steady-state conditions with respect to glucose metabolism. After adaptation to the dietary regimen, rates of glucose irreversible loss were measured following a single injection of 500 µCi of [6-3H]glucose. Glucose irreversible loss also was measured after a 7-day fast. Glucose irreversible loss was equal when both diets were fed isocalorically, was larger among steers fed the grain diet when comparisons were made at equal intakes of dry matter, and increased when the intake of either diet was increased. The increase in glucose irreversible loss with increasing energy intake showed a highly significant linear relationship over the range of intakes for both diets. It was concluded that energy intake, in contrast to diet composition, is responsible for the regulation of glucose irreversible loss.

Kinetics of glucose metabolism in sheep.

The kinetics of glucose cycling in 24 ewes bearing twins were studied 1 month before term by bolus injections of [6-3H]- and [U-14C]glucose. The function representing glucose carbon recycling was determined by deconvolution of the [3H]glucose from the [14C]glucose decay curves in plasma by using the SAAM and CONSAM programs, and a model for kinetics of glucose cycling was developed. The [3H]glucose data were fitted by four compartments, and an additional three compartments were required to explain recycling. The results show that labelled carbon was still recycling to plasma 2 days after the injection of tracer. By contrast, a similar analysis on a non-pregnant sheep, with data taken from the literature, showed that no more material was recycled after 1 day. It appears that a larger fraction (20 v. 5%) of the carbon 6 of glucose recycles in pregnant than in non-pregnant sheep. This presumably reflects the metabolism by the feto-placental unit and the increased rate of glucose metabolism during pregnancy.

The effects of hypoglycin on glucose metabolism in the rat. A kinetic study in vivo and [U-14C,2-3H]glucose.

1. The kinetics of glucose metabolism were evaluated in rats deprived of food 15-21 h after the administration of hypoglycaemic doses of hypoglycin (100 mg/kg body wt.) by following changes in the specific radioactivities of 14C and 3H in blood glucose after an intravenous dose of [U-14C,2-3H]glucose [Katz, Rostami & Dunn (1974) Biochem. J. 142, 161-170]. 2. During this time, recycling of glucose through the Cori cycle was virtually abolished, the rate of irreversible disposal of glucose and its total body mass were both decreased by about 70%, whereas there was little effect on the mean transit time for glucose. 3. It was concluded that hypoglycaemia is due to inhibition of gluconeogenesis.

Kinetics of Glucose Metabolism in the Normal Laying Hen

(1967). Kinetics of Glucose Metabolism in the Normal Laying Hen. Acta Agriculturae Scandinavica: Vol. 17, No. 1, pp. 3-12.