Background: The aim of this study was to investigate the relationship between postprandial glycemic levels based on flashmonitoring and the production of intestinal hydrogen (H₂) and methane (CH₄) gases based on the measurement of the amount of these gases in exhaled air. Materials and Methods: We studied 14 subjects with type 2 diabetes mellitus (T2DM) and 14 individuals without diabetes (control) with two food load tests, including two types of dietary fiber (inulin and guar gum), with the simultaneous determination of gases in exhaled air and the assessment of glucose levels. Results: All subjects in the control group had a significant increase in exhaled H₂. OR for increased hydrogen production in patients with T2DM was 0.17 (95% CI 0.031–0.93, p = 0.043). The level of H₂ in exhaled breath after food load in patients with T2DM was lower than in normoglycemic subjects. There was an inverse correlation between maximum glucose rise and maximum H₂ in exhaled air after food load in normoglycemic subjects (r = −0.569, p = 0.034). Patients with T2DM had direct correlations between the level of CH₄ in exhaled air and the parameters of postprandial glycemia in the lactulose test (p < 0.05). Conclusions: The confirmation of a causal relationship between decreased H₂ production, increased intestinal CH₄ production, and more severe postprandial glycemia may identify new therapeutic targets in the correction of postprandial glycemia in patients with T2DM.

The aim of this study was to investigate the relationship between postprandial glycemic levels based on flash-monitoring and the production of intestinal hydrogen (H2) and methane (CH4) gases based on measurement of the amount of these gases in exhaled air. We studied 14 subjects with type 2 diabetes mellitus (T2DM) and 10 individuals without diabetes (control) with 3 food-load tests with simultaneous determination of gases in exhaled air and assessment of glucose levels. In 15.4% of patients with T2DM, there was a non-significant increase in exhaled H2. How-ever, all subjects in the control group had significant increase in exhaled H2. Moreover, the level of H2 in exhaled breathafter food load in patients with T2DM was lower than in normoglycemic subjects. Also, in normoglycemic subjects there was an inverse correlation between maximum glucose rise and maximum H2 in exhaled air after food load. At the same time in patients with T2DM the level of CH4 in exhaled air directly correlated with the parameters of postprandial glycemia in the test with lactulose. Confirmation of a causal relationship between decreased H2 production, increased intestinal CH4 production, and more severe postprandial glycemia may identify new therapeutic targets in the correction of postprandial glycemia in patients with T2DM.