Acetone in Diabetic Ketoacidosis

Sulway, M.J.; Malins, J. M.

doi:10.1016/s0140-6736(70)90218-7

Cited by 156 publications

(90 citation statements)

References 27 publications

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“…The Our data show that acetone was present in plasma, urine, and breath of the fasting human in whom appreciable concentrations and rates of endogenous production and use were observed. The concentration of plasma acetone in some subjects was equal to or greater than that of plasma AcAc and also in the range of values recently reported in ketotic diabetic patients (22).…”

Section: Introductionsupporting

confidence: 80%

Plasma Acetone Metabolism in the Fasting Human

Reichard¹,

Haff²,

Skutches³

et al. 1979

J. Clin. Invest.

147

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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.

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Section: Introductionsupporting

confidence: 80%

Plasma Acetone Metabolism in the Fasting Human

Reichard¹,

Haff²,

Skutches³

et al. 1979

J. Clin. Invest.

147

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show abstract

“…Recent investigations have usually reported a direct linear correlation between blood glucose and exhaled acetone concentration. [27][28][29][30] However, some subjects can exhibit a inversely correlation. 31 Galasetti et al 32 have reported investigation results on 10 healthy volunteers during an oral glucose tolerance test.…”

mentioning

confidence: 99%

A Negative Correlation Between Blood Glucose and Acetone Measured in Healthy and Type 1 Diabetes Mellitus Patient Breath

Rydosz

2015

J Diabetes Sci Technol

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Background: Exhaled acetone analysis has long been recognized as a supplementary tool for diagnosis and monitoring diabetes, especially type 1 diabetes. It is essential, therefore to determine the relationship between exhaled acetone concentration and glucose in blood. Usually, a direct linear correlation between this both compounds has been expected. However, in some cases we can observe a reverse correlation. When blood glucose was increasing, breath acetone declined. Methods: The breath analysis as a supplementary tool for diagnosing and monitoring diabetes makes sense only in case of utilization of portable analyzers. This need has created a market for gas sensors. However, commercially available acetone gas sensors are developed for measuring samples at several tens part per million. The exhaled acetone concentration was measured using commercial acetone gas sensor (TGS 822, 823 Figaro, Arlington Heights, IL, USA Inc) with micropreconcentrator in low temperature cofired ceramics. The reference analyzer–mass spectrometry (HPR-20 QIC, Hiden Analytical, Warrington, UK) was used. Results: Twenty-two healthy volunteers with no history of any respiratory disease participated in the research, as did 31 patients diagnosed with type 1 diabetes. Respectively, 3 healthy volunteer and 5 type 1 diabetes mellitus subjects with reverse trend were selected. The linear fitting coefficient various from 0.1139 to 0.9573. Therefore, it is necessary to determine the correlation between blood glucose concentrations and under different conditions, for example, insulin levels, as well as correlate the results with clinical tests, for example, Hb1Ac. Conclusions: It is well known that the concentration of acetone is strongly influenced by diet, insulin treatment, and so on. Therefore, much more complex analysis with long-term measurements are required. Thus, presented results should be regarded as tentative, and validation studies with the analysis of clinical test and in a large number of patients, including control groups, need to be carried out.

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“…Like several anticonvulsant drugs, acetone has sedative and narcotic properties at high concentrations [10,11].…”

Section: Role Of Acetone In the Anticonvulsant Effect Of The Ketogenimentioning

confidence: 99%

Combination treatment of epilepsy with ketogenic diet and concurrent pharmacological inhibition of cytochrome P450 2E1

Palmer

2013

Medical Hypotheses

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While most epileptic patients respond to treatment with existing antiepileptic drugs, there remains a considerable number of patients in whom these drugs do not suffice. Such patients, particularly children, are often treated using the ketogenic diet. This diet imposes a strict limit on carbohydrates; while providing for adequate protein, most of the calories are supplied as triacylglycerol, much of which is metabolized to ketone bodies.Animal experiments have provided evidence that the anticonvulsant effect of the ketogenic diet is mediated by acetone and correlates with acetone levels. Acetone can be converted in vivo to glucose via acetol and pyruvate; the initial conversion to acetol is catalyzed by cytochrome P450 2E1 (CYP2E1). When CYP2E1 knockout mice are subjected to starvation to induce ketogenesis, they develop blood acetone levels much higher than those observed in wild-type mice. Similarly, pharmacological inhibition of CYP2E1 significantly increases blood acetone levels in rat and man.Taken together, these observations suggest that pharmacological inhibition of CYP2E1 has the potential to significantly increase the antiepileptic effect of the ketogenic diet. With patients that respond insufficiently to the diet alone, increased acetone levels may improve response. With patients who respond sufficiently to the diet, CYP2E1 inhibitors might allow relaxation of the fairly severe diet regimen and so improve compliance and quality of life.An existing inhibitor of CYP2E1 is the drug disulfiram. This drug also inhibits the enzyme aldehyde dehydrogenase, which functions in alcohol degradation, and in this capacity has long been used in the treatment of alcohol addiction. Disulfiram inhibits CYP2E1 at conventional therapeutic dosages and increases blood acetone levels in humans and animals. It should therefore be a viable candidate for the proposed drug/diet combination treatment.2

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Acetone in Diabetic Ketoacidosis

Cited by 156 publications

References 27 publications

Plasma Acetone Metabolism in the Fasting Human

Plasma Acetone Metabolism in the Fasting Human

A Negative Correlation Between Blood Glucose and Acetone Measured in Healthy and Type 1 Diabetes Mellitus Patient Breath

Combination treatment of epilepsy with ketogenic diet and concurrent pharmacological inhibition of cytochrome P450 2E1

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