From: Glucose prediction by analysis of exhaled metabolites – a systematic review
VOC | Mechanism(s) | Pathway(s) |
---|---|---|
2-pentyl nitrate [22] | Generated through pathways involving organic peroxy radical (RO2▪) with NO or NO2. Could be modulated by acute changes in systematic oxidative status [22]. | |
Derived from acetoacetate and is produced by synthesis and degradation of ketone bodies and is therefore related to blood glucose levels [32]. | Glycolysis/Pyruvate metabolism | |
Cabon monoxide [27] | Possibly due to activation of HO by glucose, and the positive modulation of CO non insulin secretion [27]. | |
Not produced by mammalian cells. Likely due to alcoholic fermentation of glucose by gut bacteria and yeast [32]. | Glycolysis/Gluconeogenesis | |
Inhaled and partly metabolized by liver, then exhaled at lower concentration. Rapid-onset hyperglycemia likely suppressed hepatic metabolism causing peaks in exhaled air [20]. | ||
M/P-xylene [20] | Inhaled and partly metabolized by liver, then exhaled at lower concentration. Rapid-onset hyperglycemia likely suppressed hepatic metabolism causing peaks in exhaled air [20]. | |
Methanol [22] | Reflects gut flora activity and therefore responsive to glycemic fluctuations [22]. | |
A small fraction of superoxide ion (O2▪−), a byproduct of oxidative reactions, reacts with nitric oxide which in turn can react with methanol to eventually form an isomer of Methyl nitrate [39]. | ||
O-xylene [20] | Inhaled and partly metabolized by liver, then exhaled at lower concentration. Rapid-onset hyperglycemia likely suppressed hepatic metabolism causing peaks in exhaled air [20]. | |
Propane [22] | Reflects gut flora activity and therefore responsive to glycemic fluctuations [22]. | N-4 fatty acid Peroxidation Protein oxidation |