Plasma Acetone Metabolism in the Fasting Human (original) (raw)
Research Article Free access | 10.1172/JCI109344
A. C. Haff, C. L. Skutches, P. Paul, C. P. Holroyde, and O. E. Owen
Department of Research, Lankenau Hospital, Philadelphia, Pennsylvania 19151
Department of Medicine and the General Clinical Research Center, Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140
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Department of Research, Lankenau Hospital, Philadelphia, Pennsylvania 19151
Department of Medicine and the General Clinical Research Center, Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140
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Department of Research, Lankenau Hospital, Philadelphia, Pennsylvania 19151
Department of Medicine and the General Clinical Research Center, Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140
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Department of Research, Lankenau Hospital, Philadelphia, Pennsylvania 19151
Department of Medicine and the General Clinical Research Center, Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140
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Department of Research, Lankenau Hospital, Philadelphia, Pennsylvania 19151
Department of Medicine and the General Clinical Research Center, Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140
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Department of Research, Lankenau Hospital, Philadelphia, Pennsylvania 19151
Department of Medicine and the General Clinical Research Center, Temple University Health Sciences Center, Philadelphia, Pennsylvania 19140
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Published April 1, 1979 -More info
Published April 1, 1979 -Version history
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 μmol/m2 per min) and concentration (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% of the 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, β-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 production 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.
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