The literature comparing macronutrient metabolism in healthy and diabetic subjects is abundant; however, little data exists on how non-diabetic subjects with insulin resistance handle macronutrient. We did two studies to investigate the postprandial responses to macronutrient in healthy, hyperinsulinemic and type 2 diabetic (T2DM) subjects. In the first study, twenty-five healthy, non-diabetic subjects [9 with fasting serum insulin (FSI) <40pmol/L; 8 with 40 ≤ FSI < 70pmol/L; and 8 with FSI ≥ 70 pmol/L] were fed eleven test meals (50g oral glucose with 0-30g doses of canola oil or whey protein) after an overnight fast. There were no significant FSI × fat (p=0.19) or FSI × protein (p=0.08) interaction effects on glucose response, suggesting that the effects of fat or protein on glycemia were independent of FSI of the subjects. In addition, the changes in relative glucose response per gram of fat (r = -0.05, p = 0.82) or protein (r = 0.08, p = 0.70) were not related to FSI of the subjects. In the second study, Healthy (FSI < 40pmol/L), Hyperinsulinemic (FSI ≥ 40pmol/L), and T2DM were fed five foods with 50g available carbohydrate. Among the subject-groups, the Glycemic Index (GI) values were not significantly different for each food, and the mean (±SEM) GI values of all foods were not significantly different (p>0.05). However, the mean (±SEM) Insulinemic Index of the foods was higher in T2DM (100±7, n=10) than those of Healthy (78±5, n=9) and Hyperinsulinemic subjects (70±5, n=12) (p=0.05). The Insulinemic Index was inversely associated with insulin sensitivity (r=-0.66, p<0.0001), positively related to fasting- and postprandial-glucose (both r=0.68, p<0.0001) and hepatic insulin extraction (r=0.62, p=0.0002). The oral-glucose data were pooled from the two studies to investigate whether there was any relationship between GLP-1 and insulin sensitivity, β-cell function and hepatic insulin extraction. No significant correlation was observed (p>0.05). The results suggest that the glucose-lowering effect of fat and protein is not affected by insulin sensitivity. GI is independent of the metabolic status of the subjects; however, unlike GI, Insulinemic Index is influenced by the metabolic status of the subjects, and thus may have limited clinical utility.

The literature comparing macronutrient metabolism in healthy and diabetic subjects is abundant; however, little data exists on how non-diabetic subjects with insulin resistance handle macronutrient. We did two studies to investigate the postprandial responses to macronutrient in healthy, hyperinsulinemic and type 2 diabetic (T2DM) subjects. In the first study, twenty-five healthy, non-diabetic subjects [9 with fasting serum insulin (FSI) <40pmol/L; 8 with 40 ≤ FSI < 70pmol/L; and 8 with FSI ≥ 70 pmol/L] were fed eleven test meals (50g oral glucose with 0-30g doses of canola oil or whey protein) after an overnight fast. There were no significant FSI × fat (p=0.19) or FSI × protein (p=0.08) interaction effects on glucose response, suggesting that the effects of fat or protein on glycemia were independent of FSI of the subjects. In addition, the changes in relative glucose response per gram of fat (r = -0.05, p = 0.82) or protein (r = 0.08, p = 0.70) were not related to FSI of the subjects. In the second study, Healthy (FSI < 40pmol/L), Hyperinsulinemic (FSI ≥ 40pmol/L), and T2DM were fed five foods with 50g available carbohydrate. Among the subject-groups, the Glycemic Index (GI) values were not significantly different for each food, and the mean (±SEM) GI values of all foods were not significantly different (p>0.05). However, the mean (±SEM) Insulinemic Index of the foods was higher in T2DM (100±7, n=10) than those of Healthy (78±5, n=9) and Hyperinsulinemic subjects (70±5, n=12) (p=0.05). The Insulinemic Index was inversely associated with insulin sensitivity (r=-0.66, p<0.0001), positively related to fasting- and postprandial-glucose (both r=0.68, p<0.0001) and hepatic insulin extraction (r=0.62, p=0.0002). The oral-glucose data were pooled from the two studies to investigate whether there was any relationship between GLP-1 and insulin sensitivity, β-cell function and hepatic insulin extraction. No significant correlation was observed (p>0.05). The results suggest that the glucose-lowering effect of fat and protein is not affected by insulin sensitivity. GI is independent of the metabolic status of the subjects; however, unlike GI, Insulinemic Index is influenced by the metabolic status of the subjects, and thus may have limited clinical utility.