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Glycemic, hormone, and appetite responses to monosaccharide ingestion in patients with type 2 diabetes.

To investigate the relative effects of fructose and glucose on blood glucose, plasma insulin and incretin (glucagon-like peptide-1 [GLP-1] and gastric inhibitory peptide [GIP]) concentrations, and acute food intake, 10 (6 men, 4 women) patients with diet-controlled type 2 diabetes (diabetic) (44 to 71 years) and 10 age and body mass index (BMI)-matched (6 men, 4 women) nondiabetic, control subjects with varying degrees of glucose tolerance (nondiabetic), were studied on 3 days. In random order, they drank equienergetic preloads of glucose (75 g) (GLUC), fructose (75 g) (FRUCT) or vehicle (300 mL water with noncaloric flavoring [VEH]) 3 hours before an ad libitum buffet lunch. Mean glucose concentrations were lower after FRUCT than GLUC in both type 2 diabetics (FRUCT v GLUC: 7.5 +/- 0.3 v 10.8 +/- 0.4 mmol/L, P <.001) and nondiabetics (FRUCT v GLUC: 5.9 +/- 0.2 v 7.2 +/- 0.3 mmol/L, P <.05). Mean insulin concentrations were approximately 50% higher after FRUCT in type 2 diabetics than in nondiabetics (diabetics v nondiabetics: 23.1 +/- 0.7 v 15.1 +/- 1.3 microU/mL; P <.0001). Plasma GLP-1 concentrations after fructose were not different between type 2 diabetics and nondiabetics (P >.05). Glucose, but not FRUC, increased GIP concentrations, which were not different between type 2 diabetics and nondiabetics (P >.05). Food intake was suppressed 14% by GLUC (P <.05 v CONT) and 14% by FRUC (P <.05 v CONT), with no difference between the amount of food consumed after GLUC and FRUC treatment in either type 2 diabetics or nondiabetics (P >.05). We have confirmed that oral fructose ingestion produces a lower postprandial blood glucose response than equienergetic glucose and demonstrated that (1) fructose produces greater increases in plasma insulin concentration in type 2 diabetics than nondiabetics, not apparently due to greater plasma incretin concentrations and (2) fructose and glucose have equivalent short-term satiating efficiency in both type 2 diabetics and nondiabetics. We conclude that on the basis of improved glycemic control, but not satiating efficiency, fructose may be useful as a replacement for glucose in the diet of obese patients with type 2 diabetes.