The method of successive measured injections of tracer using uniformly labeled C-14-glucose as tracer was applied to determine the pool size, apparent distribution space and the rates of endogenous glucose production and utilization in the fasting state and at twenty to 110 minutes after the intravenous injection of a 0.3 gm./kg. glucose load in six nondiabetic and sixteen diabetic subjects.
The amount of intermixing glucose (“pool”) and the endogenous glucose production in the fasting state were higher in diabetics than in normals. The rate of glucose production decreased after the intravenous injection of the glucose in normals and nonketotic diabetics, but not in three out of four ketotic diabetics.
The average rate of glucose utilization in the fasting state was found to be slightly higher in diabetics than in normals, but it increased to a lesser extent following the injection of glucose. This smaller increase and larger glucose pool are the main causes of decreased glucose tolerance in diabetics.
The exponential slope of the concentration of glucose in the plasma after an intravenous injection of glucose (usually referred to as ‘K’) was not found to be correlated significantly with the rate of glucose utilization.
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.
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