Search PubMed⌕ Search

Biomedical subjects

J Radziuk

Publications and source records attributed to J Radziuk.

62 records · Page 4Linked to original sources
PubMed1978

Experimental validation of measurements of glucose turnover in nonsteady state.

The aim of the present experiments is to validate, in conscious dogs, the tracer infusion methods of measuring nonsteady turnover rates. This was done in nine experiments performed in four normal dogs by infusing isotopically labeled glucose (2-3H, 6-3H, 1-14C) and monitoring the concentrations of both the labeled and unlabeled substances. The validation is based on the observation that a high exogenous infusion of glucose will suppress endogenous glucose production and become the sole source of glucose in the body. By infusing glucose at a high, time-varying rate, calculating its rate of appearance, (Ra) and comparing it to the infused rate, the method can be verified. The calculations were based on: a) a single-compartment model with a modified volume of distribution; b) a two-compartment model; and c) a generalized dispersion model. The absolute values of the areas of the deviations of the calculated from the infused curves were found to be, respectively, 9.5, 8.4, and 7.8 percent of the total area under the infused curve. It was concluded that the tracer infusion method can reliably measure Ra of glucose when it is changing rapidly, and the system is out of steady state.

Animals↗
PubMed1977

Estimating rapid changes in the rates of glucose production from glycogenolysis and recycling through lactate.

In order to obtain independent estimates of changes in the rate of glucose production from glycogenolysis from the glucose carbon recycled throught lactate, previously validated nonsteady tracer methods are used. Changes in glycogenolysis are estimated by calculating the rate of appearance of a label ([6-3H]glucose) uniformly distributed through glycogen and simultaneously the rate of recycling of 14C is measured under nonsteady-state conditions. It is indicated that these results can be extended to the determination of absolute rates of glucose production from glycogen breakdown and gluconeogenetic precursors.

Animals↗
PubMedDate not supplied

Hepatic glucose uptake, gluconeogenesis and the regulation of glycogen synthesis.

Hepatic glycogen is replenished during the absorptive period postprandially. This repletion is prompted partly by an increased hepatic uptake of glucose by the liver, partly by metabolite and hormonal signals in the portal vein, and partly by an increased gluconeogenic flux to glycogen (glyconeogenesis). There is some evidence that the direct formation of glycogen from glucose and that formed by gluconeogenic pathways is linked. This includes: (i) the inhibition of all glycogen synthesis, in vivo, when gluconeogenic flux is blocked by inhibitors; (ii) a dual relationship between glucose concentrations, lactate uptake by the liver and glycogen synthesis (by both pathways) which indicates that glucose sets the maximal rates of glycogen synthesis while lactate uptake determines the actual flux rate to glycogen; (iii) the decrease of both gluconeogenesis and glycogen synthesis by the biguanide, metformin; and (iv) correlations between increased gluconeogenesis and liver glycogen in obese patients and animal models. The degree to which the liver extracts portal glucose is not entirely agreed upon although a preponderance of evidence points to about a 5% extraction rate, following meals, which is dependent on a stimulation of glucokinase. This enzyme may be linked to the expression of other enzymes in the gluconeogenic pathway. Perivenous cells in the liver may induce additional gluconeogenesis in the periportal cells by increasing glycolytically produced lactate. A number of potential mechanisms therefore exist which could link glycogen synthesis from glucose and gluconeogenic substrate.

Animals↗
PubMedDate not supplied

The liver and glycogen metabolism.

It was shown that the liver is not the major site of removal of glucose after a carbohydrate meal in man. Fractional extractions varied from 5 to 10%. Alternative substrates for postprandial hepatic glycogen synthesis were therefore sought. It was demonstrated than, in man, about 60% of hepatic glycogen was formed from gluconeogenetic substrates. Since significant excursions occur only in plasma lactate after glucose loading, this was deemed the most likely substrate under these circumstances. By differential sampling across the liver and the gut in a conscious pig model, it was found that the liver takes up enough lactate (fractional extraction of 40-50%) to account for the gluconeogenetic production of glycogen. Forty percent of this arises from the gut. Muscle (as represented by the forearm in man) does not contribute lactate during glucose loading, suggesting that other tissues such as the skin are of importance. The gluconeogenetic process may be an important site for the obligatory tissue production of lactate.

Animals↗
PubMedDate not supplied

Aldosteronemia in patients with acute renal failure.

In 19 patients with acute renal failure the plasma renin activity and aldosterone were determined in the phase of anuria and oliguria. A highly increased plasma renin activity was found while aldosteronemia was only moderately raised. No significant correlation was demonstrated between plasma renin activity and aldosterone while a negative correlation was found between aldosteronemia and plasma sodium and bicarbonates concentrations. Lack of significant correlation between plasma renin activity and aldosteronemia in cases of acute renal failure suggests that factors other than renin participate in the regulation of aldosterone secretion in these patients.

Acute Kidney Injury↗