Table 1.
Compound | Possible Source/Relevance for Diabetes and Metabolism |
---|---|
Aerosolized glucose | Elevated in EBC during experimental hyperglycemia[104] |
Aromatic compounds (ethylbenzene, o/m/p- xylene, toluene) | Partly metabolized by hepatic enzymes (cytochrome P450 system); rapid-onset hyperglycemia likely suppresses hepatic metabolism of the gases[16, 80] |
Alkyl nitrates (2-, 3-pentyl nitrate, methyl nitrate) | By-product of the interaction of oxidative radicals and NO[105] Methyl nitrate correlated with plasma glucose in diabetic patients[106] |
Carbon dioxide | Direct oxidative by-product of energy substrates |
Carbon monoxide | Marker of oxidative stress (that can be caused by hyperglycemia)[107] Difference in the 13CO excretion were found between diabetic and healthy subjects following a labeled oral glucose tolerance test[108] |
Ethane and pentane | Oxidation of ω3 and ω6 fatty acids[91] |
Ethanol and methanol | Bacterial fermentation of glucose in intestines and subsequent movement into the portal circulation[79, 109] |
Ketones (acetone, 2-pentanone) | Increases in diabetic ketoacidosis, fasting, and high-fat/ketogenic diets[9, 79, 82, 101] Suppressed with insulin-mediated suppression of lipolysis[83, 110] Acetone correlates with blood glucose and hemoglobin A1c in T1DM [98] but not in T2DM patients[99, 100]; exhaled at ~1/330 of plasma acetone concentrations [98]; follows a diurnal pattern [98]; elevated in men [100] |
Isoprene | Cholesterol synthesis (from acetyl-CoA via the melavonic acid pathway) [81] |
Propane | generated by n-4 fatty acid (18:3) peroxidation[111] or protein oxidation of branched-chain amino acids or production by colonic bacteria[24] |
Propionic and butanoic acids | Elevated in EBC following sucrose ingestion[88] |