혈액내 beta-OHB 농도(mmol/L)와 호흡내 Acetone 농도(ppm) 사이의 상관관계

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혈액내 β‐hydroxybutyrate의 농도와 

호흡내 Acetone 농도 사이엔 비례하는 상관관계가 있다.

그 비율은 대략 혈액내 β‐hydroxybutyrate 1mmol/L  당 Acetone 10ppm 정도로 간략하게 대치할 수 있음.

Ex) Breath Acetone 수치가 40ppm이면 , 혈액 내 β‐hydroxybutyrate는 약 4mmol/L 라고 간주할 수 있음.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4737348/

Measuring breath acetone for monitoring fat loss: Review

Joseph C. Anderson

Breath Acetone and BOHB

BrAce can be related to ketosis levels via blood BOHB. Multiple studies have reported strong correlations between BrAce and BOHB with an average R 2 = 0.77 [Range: 0.54 to 0.94] 5, 16, 17, 21, 22, 23. To demonstrate this relationship, blood‐breath data from multiple studies were captured and plotted (Figure ​(Figure2)2) 5, 17, 21, 22, 23. The data was fit with an exponential relationship 21. Although data was taken from multiple sources and experimental conditions, the non‐linear relationship between BrAce and BOHB appears to correlate well. BrAce is most sensitive to changes in BOHB between 0 and 1 mM. Note that Figure ​Figure22 is demonstrative; readers are referred to the primary references for further details.

Figure 2

Breath acetone concentration (BrAce) has a non‐linear relationship with blood β‐hydroxybutyrate. Experimental data (open circles) were captured from multiple studies 5, 17, 21, 22, 23 and fit (black line) using an exponential relationship 21. 1 ppm = 39.7 nM (molar basis).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4471925/

Acetone as biomarker for ketosis buildup capability - a study in healthy individuals under combined high fat and starvation diets

Amlendu Prabhakar,#1 Ashley Quach,#1 Haojiong Zhang,1 Mirna Terrera,1 David Jackemeyer,1 Xiaojun Xian,1 Francis Tsow,1 Nongjian Tao,1,3 and Erica S Forzani

1,2

Figure 4 shows correlations of breath acetone levels with blood ketone, urinary ketone, and blood glucose. The very high breath acetone levels collected from all 11 subjects were confirmed with the high blood ketone and urinary ketone levels. In addition, the exponential decay relationship between breath acetone and blood glucose also indicated that blood glucose was depleted as breath acetone was produced.

Figure 4

Correlation of breath acetone levels with blood ketone and urine ketone as well as blood glucose collected from different subjects on their fasting days.

​케토스캔 Mini 제작사에서 제시하는 비율

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6264102/

Guiding Ketogenic Diet with Breath Acetone Sensors

Andreas T. Güntner,1,* Julia F. Kompalla,1 Henning Landis,1 S. Jonathan Theodore,1 Bettina Geidl,2 Noriane A. Sievi,3 Malcolm Kohler,3 Sotiris E. Pratsinis,1 and Philipp A. Gerber2,*

3.4. Monitoring Individual Ketosis through Breath and Blood

As a next step, the individual sensor-measured breath acetone dynamics of the volunteers during the KD were analyzed and compared to a commercial capillary blood BOHB and glucose monitoring system. Figure 3 shows the simultaneously measured profiles for (a) breath acetone, (b) capillary blood BOHB and (c) glucose of five representative volunteers during a 36-h KD. Data of all eleven volunteers are provided in Figure S1. For volunteer #3 (black diamonds), breath acetone almost tripled within the first 12 h, similar to other KD studies where an average increase by a factor of 3.5 was observed [12]. Most interestingly, the strongest increase was observed after 30 h when breath acetone concentrations exceeded 20 ppm, which should reflect advanced ketosis from intensified ketogenesis [9] (Figure 1a, box). This is significantly higher than observed, for instance, during exercise and post-exercise rest where breath acetone levels did not exceed 3 ppm [29]. Remarkably, capillary blood BOHB (Figure 3b) as an established marker for ketosis followed the same dynamic. In specific, nutritional ketosis (0.5–3 mM [54]) is entered after 9 h and mild ketosis (2–7 mM [55]) after 36 h of KD, the latter is needed for an efficient treatment of epilepsy [56]. This indicates that the present breath acetone sensor is suitable to monitor ketosis during KD and, most importantly, it operates non-invasively.

Figure 3

Individual (a) breath acetone levels as determined by the Si-doped WO3 sensor, capillary blood (b) BOHB and (c) glucose concentrations of five representative volunteers during a 36-h KD. Note that volunteer #1 (green circles) had to abort the experiment already after 24 h due to strong nausea. Scatter plot of (d) BOHB and (e) glucose versus acetone concentrations for all eleven volunteers (105 samples) with corresponding Pearson’s (r) and Spearman’s (ρ) correlation coefficients. Dashed lines indicate fitted (power law in d and linear in e) trend lines.

Within the first 12 h, a similar breath acetone trend was observed also for volunteers #5 (red squares), #10 (orange stars) and #11 (blue triangles). However, #5 and #11 differed significantly afterwards. In particular, breath acetone concentrations of both increased strongly already during overnight fasting (t = 12–24 h). On the second day, further increase was observed for volunteer #5 who reached breath acetone concentrations above 60 ppm after 33 h, while they leveled off for #11 at around 30 ppm. These breath acetone trends were in agreement with BOHB (Figure 3b) where volunteer #5 reached highest levels above 3 mM toward the end of the KD. It is also interesting to observe that BOHB increased stronger than the breath acetone levels within the first 12 h for volunteer #11 and especially #5. This may be related to the dynamic equilibrium between BOHB and AcAc (Figure 1a, box) [9]. In summary, the volunteers showed distinctly different ketosis dynamics despite similar KD conditions, as recognized correctly by the sensor.

Finally, it is worth discussing volunteer #1 (Figure 3a, green circles) who showed a distinctly different breath acetone profile. Most notably, this volunteer had already an extraordinary increase in breath acetone at the beginning of the KD reaching about 60 ppm after 12 h. A similar trend within the first 6 h is observed for blood BOHB (Figure 3b), though less distinct from the other volunteers (e.g., #5, red squares) than observed for breath acetone (Figure 3a). Interestingly, BOHB decreases thereafter. Glucose concentrations (Figure 3c, green circles), on the other hand, decreased until t = 6 h and started to increase slightly thereafter coinciding with the drop in BOHB levels. On the second day, this volunteer had to stop the KD due to strong nausea. This is probably caused by ketones activating the chemoreceptor zone in the vomiting center of the brain that is a known reason for nausea and vomiting in ketosis [57]. As a result, this volunteer showed low tolerance to the KD protocol that was reflected in an abnormal breath acetone pattern. In a next step, the present breath acetone sensor could be used to guide this volunteer to an optimized KD protocol (e.g., different nutritional composition) to achieve and maintain a healthy status of ketosis.

Corresponding capillary glucose levels (Figure 3c) of the five volunteers (for all volunteers, see Figure S1c) were consistently below 5.5 mM at the start and during the KD. This suggests that they adhered to the overnight fasting prior to the KD and stayed abstinent from other external carbohydrate sources during the KD (see Figure 1c for protocol). During the KD, glucose levels typically decreased within the first 12 h and leveled off thereafter between 3 and 5 mM probably due to gluconeogenesis to inhibit hypoglycemia [10], as suggested above.

3.5. Correlations between Breath and Blood Parameters

The blood and breath ketone concentrations for all volunteers are shown in Figure 3d. Breath acetone and capillary blood BOHB correlated significantly with Spearman’s rank correlation coefficient ρ of 0.83 (p < 0.001) and Pearson’s correlation coefficient r of 0.78 (p < 0.001), as expected from their similar intra-subject dynamics during KD (Figure 3a vs. Figure 3b) and joint biochemical origin as products of ketogenesis (Figure 1a, box) [9]. When applying a power law fit (dashed line), a degree of determination (R2) of 0.62 is obtained that is well within the range of fasting and dieting experiments (0.54 ≤ R2 ≤ 0.94) [14].

A weaker and inverse correlation was found between breath acetone and capillary blood glucose (r = −0.63, ρ = −0.59, both p < 0.001). This was anticipated from the observed trends during KD (Figure 3a vs. Figure 3c). Ketogenesis is driven by hepatic β-oxidation which increases during fasting when lipolysis increases as no longer suppressed by insulin and by the expression‎ of mitochondrial HMG-CoA synthase which is induced by fasting and downregulated by insulin [11]. Although low insulin and high glucagon levels resulting from low blood glucose serve as an initial trigger for ketogenesis, ketone body levels are rather determined by glucose level-independent effects, such as free fatty acid availability for ketone body production and ketone body consumption by peripheral tissues [58].

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6963753/

Blood Ketone Bodies and Breath Acetone Analysis and Their Correlations in Type 2 Diabetes Mellitus

Valentine Saasa,1,2,* Mervyn Beukes,3 Yolandy Lemmer,4 and Bonex Mwakikunga1,5,*

After successfully determining the plasma concentration of acetoacetate, β-hydroxybutyrate and breath acetone, it was necessary to check the correlation of the blood ketones with breath acetone. The diversity of ketone bodies among 30 diabetes patients appeared at baseline (Figure 5). Significant positive correlations between breath acetone and blood AcAc and between breath acetone and blood β-OHB were observed at baseline (R = 0.897 and R = 0.821). This shows a positive indicator of using acetone as a non-invasive biomarker of diabetes mellitus. There are many hypotheses to explain the relationship. One reason being that acetone is a metabolite produced after enzymatic decarboxylation of AcAc, which is in equilibrium with β-OHB via an enzymatic-controlled process by β-OHB dehydrogenase [9]. Although an exponential relationship between acetone and β-OHB, and acetone and AcAc, were observed, acetone reflected overall ketone metabolite concentrations in diabetic patients. This is due to the fact that acetone presents positive deviations from well-known gas/liquid partition laws, such as Henry’s law or Raoul’s law.

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Figure 5
(a) Correlation between breath acetone and acetoacetate; (b) Correlation between breath acetone and beta-hydroxybutyrates. The correlations were calculated using linear regression.

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