Search PubMed⌕ Search

Biomedical subjects

G Hetenyi

Publications and source records attributed to G Hetenyi.

At least 37 records · Page 2Linked to original sources
PubMed1983

Correction for metabolic exchange in the calculation of the rate of gluconeogenesis in rats.

The degree by which the rate of gluconeogenesis is underestimated when calculated from the transfer of 14C atoms from circulating precursors to plasma glucose was estimated from the ratio of the specific activity of plasma glucose and blood acetoacetate during the infusion of [2-14C]acetate in rats fasted for 3 days. The specific activity of blood acetoacetate was taken to be equal to that of its only precursor, the acetyl C atoms of hepatocellular AcCoA. These latter are assumed not to be available for the net synthesis of glucose and may be incorporated into the molecule by "metabolic exchange" in the hepatic oxalo-acetate pool only. By this approach 25% of the C atoms of plasma glucose have been estimated to arise from AcCoA. Multiplication by a correction factor H = 1.33 +/- 0.03 is being suggested to compensate for the metabolic exchange of 14C for 12C atoms when the rate of gluconeogenesis is calculated from the transfer of 14C atoms from labeled precursors to glucose.

Animals↗
PubMed1982

Calculation of the rate of gluconeogenesis from the incorporation of 14C atoms from labelled bicarbonate or acetate.

The rate of gluconeogenesis in vivo may be estimated by the incorporation of 14C atoms from a labelled precursor into plasma glucose or by introducing 14C atoms into the pathway of gluconeogenesis at known stages by metabolites which in themselves do not contribute to the net synthesis of glucose (e.g., bicarbonate or acetate). The purpose of the investigation was to examine some of the assumptions involved in the calculation of gluconeogenic flux by the second approach. [2-14C]acetate or NaH14CO3 was infused to dogs, and the specific activity (SA) of glucose, bicarbonate CO2, urea, and lactate in the plasma was followed. The incorporation of 14C atoms from [2-14C]acetate into glucose allows the calculation of the degree of underestimation of glucose formation due to "metabolic exchange" in the hepatic oxaloacetate pool. The possible error introduced into this calculation by the incorporation of 14C atoms from 14CO2 (a product of acetate oxidation) was found to be negligible, but the heavy labelling of plasma lactate may possibly affect the estimate of metabolic exchange. It is proposed that in the calculation of the rate of gluconeogenesis from infused NaHCO3 the SA of hepatocellular and not of plasma bicarbonate CO2 should be related to that of plasma glucose. This latter is expected to equal the SA of plasma urea, since the sole precursor of its C atom is hepatocellular CO2. The rate of gluconeogenesis estimated from the SA(glucose)/SA(urea) ratio and a previously estimated correction factor for metabolic exchange was 51% of the glucose production in the postabsorptive state. The nearly identical SA(urea)/SA(CO2) ratios, irrespective of the tracer infused, indicated that plasma CO2 is a major precursor of urea C and that a large fraction of injected acetate is oxidized by extrahepatic tissues.

Acetates↗
PubMed1982

Correction for the metabolic exchange of 14C for 12C atoms in the pathway of gluconeogenesis in vivo.

Methods designed for estimation of the synthesis of plasma glucose are based on the transfer of 14C atoms from a selected precursor (substrate) such as lactate or alanine. This approach was shown to lead to an underestimation of the true synthesis of glucose because of the metabolic exchange of 14C atoms for 12C atoms in the hepatic oxaloacetate pool. From the incorporation of 14C atoms from intravenously infused [2-14C]acetate into plasma glucose, the extent of the metabolic exchange has been estimated. In normal dogs, metabolic exchange leads to an underestimation of plasma glucose synthesis from plasma lactate or alanine by a factor of 2.2 +/- 0.07, i.e., by 55%. In insulin-deprived diabetic dogs, the factor was found to be 1.8 +/- 0.05. In long-term fasted dogs, the factor may be higher than in the postabsorptive state, whereas treatment with methylprednisolone has no effect. The assumptions and sources of possible errors in the estimation of the extent of metabolic exchange are reviewed.

Alanine↗
PubMed1981

Effect of cooling on the glucoregulation of anaesthetized and non-anaesthetized newborn dogs.

UNLABELLED: When newborn dogs 2-14 days of age, anaesthetized with Nembutal, were cooled to 30 degrees C body core temperature, their rate of CO2 production (QCO2) decreased as predicted by van't Hoff's law, but the rates of hepatic glucose production and overall glucose utilization were decreased to a lesser degree, indicating an increase in the percentage contribution of plasma glucose to the overall energy turnover. In different litters of pups cooled to 32 degrees C, QCO2 and the rate of glucose production and utilization were decreased as predicted by van't Hoff's law. The metabolic clearance rate of glucose was decreased by cooling in all pups. These changes were wholly or partially reversible upon rewarming. Because of the approximate parallelity in the changes in the rates of production and utilization of glucose, no consistent change in blood glucose was observed during cooling. When non-anaesthetized pups less than 6 days old were exposed to cold until their core temperature was decreased to 32 degrees C QCO2 increased transiently during cooling. A small and transient elevation in plasma glucose concentration was observed due to a small increase in hepatic glucose production. Older pups fell into two categories: those which were able to maintain their body temperature by increasing their metabolic rate did not react with any change in their rates of glucose production and utilization. On the other hand pups which, during cooling, failed to raise their metabolic rate became hyperglycaemic because of an increased rate of glucose production and a decrease in glucose clearance. IN CONCLUSION: in anaesthetized pups QCO2 and the rates of hepatic glucose production and utilization follow approximately van't Hoff's law, indicating the absence of significant regulatory responses. Non-anaesthetized pups, if they are able to maintain their body temperature during cooling by an increase of their metabolic rate, show no significant changes in glucose production and utilization. Hyperglycaemia developed only in those pups which failed to increase their metabolic rate and consequently became severely hypothermic. In no case did hypothermia lead to hypoglycaemia.

Aging↗
PubMed1980

Transfer of carbon atoms among circulating glucose, alanine, and lactate in pancreatectomized dogs.

The rates of transfer of carbon atoms (mg C . kg body wt-1 . min-1) among plasma glucose, alanine, and lactate have been calculated in pancreatectomized dogs from the tracer concentration versus time curves in the plasma after an intravenous injection of either [2,3-3H]- and [U-14C]alanine or [3-3H]- and [U-14C]glucose. The calculations were based on an integrated kinetic model derived earlier from experimental data. In comparison to normal dogs, in insulin-deprived pancreatectomized dogs, the rate of turnover of glucose (mg C . kg-1 . min-1) is increased about twofold, but the turnover rates of lactate and alanine are not changed significantly. About twice as much carbon is transferred from lactate to glucose, whereas the transfer of carbon from alanine is increased by 47%. Carbon transfer to glucose from unidentified sources is also doubled. In conclusion, in the pancreatectomized dog, gluconeogenesis is increased not by an increased production of alanine and lactate but by an increased diversion of their carbon atoms to glucose at the expense of other pathways.

Alanine↗
PubMed1979

Correction factor for the estimation of plasma glucose synthesis from the transfer of 14C-atoms from labelled substrate in vivo: A preliminary report.

Based on a previously designed method for the estimation of the contribution of C-atoms by acetylcoenzyme A to the hepatic oxaloacetate pool, the loss of 14C-atoms on their way from a precursor to plasma glucose due to 'metabolic exchange' was estimated in normal and diabetic dogs and in normal rats. Due to this loss of 14C-atoms, the rates of gluconeogenesis when calculated from the transfer of 14C-atoms from precursors (other than glycerol) are underestimated by a factor of 2.2 +/- 0.07 in normal, 1.8 +/- 0.05 in diabetic dogs, and by 1.55 +/- 0.04 in normal rats.

Acetyl Coenzyme A↗
PubMed1977

The turnover and conversion to glucose of alanine in newborn and grown dogs.

The extent of transfer of carbon atoms from alanine to glucose was examined in pups and grown dogs. [U-14C]Alanine and [2-3H]glucose were injected intravenously and by using the SAAM-26 program a compartmental model was formulated from the tracer data to quantify the kinetics of the alanine- and glucose-carbon system. A 3-compartment model was necessary to describe the alanine-carbon kinetics. Strict identification of these compartments with physiological counterparts was not possible. The overall transport (turnover) rate of alanine-C was found not to change significantly with age when calculated on the basis of body weight. Carbon atoms from alanine reach glucose by three identifiable pathways of different speed. The kinetics suggest that the different pathways are at least in part due to differences in the metabolism of the three carbon atoms of alanine. In pups less than 11 days of age 45-49% of the carbon atoms leaving the alanine subsystem enter glucose; in adults it was 70%. In young pups 18-19% of glucose-C utilized was derived from alanine-C, whereas in adults, 62%. Accordingly a smaller percentage of carbon atoms utilized as alanine appears in glucose and a smaller percentage of glucose-C is derived from alanine in pups than in grown dogs.

Age Factors↗
PubMed1976

Effects of age and fasting on gluconeogenesis from glycerol in dogs.

The extent of gluconeogenesis from glycerol was examined in pups and adult dogs. With use of the SAAM-26 program, a four compartment model was formulated from tracer data to calculate the kinetics of the glycerol:glucose system. In the postabsorptive state gluconeogenesis from glycerol declines with age: 13.8% of glucose carbon originated from glycerol in 0- to 4-day-old pups, 6% in adults. Approximately 50% of glycerol carbon is converted to glucose carbon independent of age. During fasting, a) the percentage of glucose carbon arising from glycerol carbon increased to 13.3% and 10.3% in adult dogs and pups 5-19 days old, respectively, in younger pups it declined to 3.4%; b) glycerol production increased in adults, but decreased in the youngest pups; c) glucose production and utilization decreased at all ages, and a smaller percentage of glycerol carbon was converted to glucose carbon, especially in the youngest pups. Thus in neonates fasting decreases gluconeogenesis from glycerol.

Aging↗
PubMed1976

Plasma glucagon in pups, decreased by fasting, unaffected by somatostatin or hypoglycemia.

In pups less than 4 days old, the mean basal plasma immunoreactive glucagon (IRG) level was about 3 times higher than in adult dogs. This high level decreased with age, and in pups older than 12 days the mean plasma IRG level did not differ from that in adults. Insulin-induced hypoglycemia did not raise plasma IRG concentration in young pups. Fasting decreased plasma IRG in young, but not in older pups. This decrease is consistent with the decrease in gluconeogenesis and in contrast to the metabolic adjustments observed in the adult organism. In pups less than 7 days old, both the pancreas and gastric mucosa contained considerably more IRG than the normal value reported for adult dogs. Gastroduodenal IRG was immunologically indistinguishable from pancreatic glucagon. In pups, somatostatin did not decrease the plasma concentration of either IRG or immunoreactive insulin (IRI) and caused no change in plasma glucose or in the rates of glucose production and utilization calculated from experiments with tracers. The experiments indicate that in pups the pancreatic and gastric alpha-cells are unresponsive to stimuli normally effective in grown dogs.

Age Factors↗