A BST RA CT The oxidation and turnover of plasma glycerol has been studied in lean and obese, fed and starving man by means of a long-term infusion of glycerol-"4C, and the participation of glycerol in gluconeogenesis has been determined.Under none of the experimental conditions did glycerol contribute more than 10% of the total respiratory C02. Glycerol turnover in fed lean subjects was 106 mmoles/min. Glycerol levels and turnover were higher in the obese subjects and with all subjects after starvation. There was a direct correlation between plasma levels and turnover values for which a regression equation was derived: y = 1556 x + 33.1, when y= turnover in micromoles per minute and x = glycerol level in micromoles per milliliter.Whereas a. direct relation was established between glycerol and FFA levels, the FFA/glycerol turnover ratio was 4.7: 1 in the lean group indicating incomplete hydrolysis of adipose tissue triglycerides.

A B S T R A C T The metabolism of acetone was studied in lean and obese humans during starvation ketosis. Acetone concentrations in plasma, urine, and breath; and rates of endogenous production, elimination in breath and urine, and in vivo metabolism were determined. There was a direct relationship between plasma acetone turnover (20-77 ,Umol/m2 per min) and concenitration (0.19-1.68 mM). Breath and urinary excretion of acetone accounted for a 2-30% of the endogenous production rate, and in vivo metabolism accounted for the remainder. Plasma acetone oxidation accounted for -60% of the production rate in 3-d fasted subjects and about 25% of the production rate in 21-d fasted subjects. About 1-2% ofthe total CO2 production was derived from plasma acetone oxidation and was not related to the plasma concentration or production rate. Radioactivity from [14C]acetone was not detected in plasma free fatty acids, acetoacetate, ,-hydroxybutyrate, or other anionic compounds, but was present in plasma glucose, lipids, and proteins. If glucose synthesis from acetone is possible in humans, this process could account for 11% of the glucose production rate and 59% of the acetone production rate in 21-d fasted subjects. During maximum acetonemia, acetone productioni from acetoacetate could account for 37% of the anticipated acetoacetate production, which implies that a significant fraction of the latter compound does not undergo immediate terminal oxidation.

A B S T R A C T Rates of plasma acetoacetate and total ketone-body production and oxidation to C02 were determined by an isotope tracer technique in eight obese subjects undergoing progressive starvation. After a brief fast and under conditions of mild ketonemia and minimal ketonuria, rates of acetoacetate and total ketone-body production and oxidation were directly related to the increasing plasma concentration. After a longer fast and with severer ketonemia, acetoacetate and total ketone-body production and oxidation rates were higher but became constant and unrelated to the plasma concentrations. The maximum rates of total ketone-body production and oxidation were about 150 g/24 h and 129 g/24 h, respectively.Although an increased ketone-body production was the primary factor responsible for the hyperketonemia, an imbalance between production and removal of the ketone bodies cannot be excluded. Such an imbalance could account, at least in part, for the developing hyperketonemia and for the lack of relationship between production rates and plasma concentrations.

With the method described here, samples can be assayed at the rate of 40/h, with increased reproducibility. As described, the method covers an analytical range of 1 to 7 g/liter, but it can be readily adapted to measure different ranges of concentration in other protein preparations.

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