A limitation of the present study is the broad metabolic range of subjects regarding glucose metabolism, which could confound the findings and interpretation of results, but no correlation was found between degree of impaired glucose tolerance (e.g., HOMA2-IR, HbA1c, or fasting glucose) and effect size of reduction in postprandial glucose excursion or insulin secretion, though.A strength of the present study is the measurement of postprandial responses to two subsequent meals, as the response to a second meal can differ from the response to the first meal, as discussed above. The gene discussed is INS; the disease is Impaired glucose tolerance.