We thank Horowitz et al. (1) for their comments on our article (2) on the effect of orlistat on postprandial glucose, insulin, and incretin levels. They raise criticisms regarding the increase in postprandial GLP-1 levels, asserting that it is a result of fat digestion rather than the fat content of the meal. They also state that to draw more definitive conclusions, more frequent blood sampling over a longer period of time is required rather than a single sample at 60 min after the mixed meal. Ours was an observatory pilot study that tested the effect of this drug on postprandial incretin levels. Putative mechanisms of action will be addressed in further studies in which we will take these criticisms into account. Horowitz et al. also state that orlistat would be expected to worsen postprandial hyperglycemia since this drug accelerates gastric emptying. Apart from our study, orlistat was previously shown to ameliorate postprandial blood glucose levels in long-term studies (3).

1.
Horowitz M, Feinle-Bisset C, Jones K, Nauck M: Orlistat augments postprandial increases in glucagon-like peptide-1 in obese type 2 diabetic patients (Letter).
Diabetes Care
27
:
2770
,
2004
2.
Damci T, Yalin S, Balci H, Osar Z, Korugan U, Ozyazar M, Ilkova H: Orlistat augments postprandial increasesin glucagon-like peptide 1 in obese type 2 diabetic patients.
Diabetes Care
27
:
1077
–1080,
2004
3.
Holander PA, Elbein SC, Hirsch IB, Kelley D, McGill J, Taylor T: Role of orlistat in the treatment of obese patients with type 2 diabetes: a 1-year randomized double-blind study.
Diabetes Care
21
:
1288
–1294,
1998

T.D. is an advisory board member for Aventis and has received honoraria from Roche, Aventis, and Pfizer. H.I. is an advisory board member for Aventis and has received honoraria from Roche, Novo Nordisk, Pfizer, and GlaxoSmithKline.