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Gastric bypass surgery, but not caloric restriction, decreases dipeptidyl peptidase‐4 activity in obese patients with type 2 diabetes
Author(s) -
Alam M. L.,
Van der Schueren B. J.,
Ahren B.,
Wang G. C.,
Swerdlow N. J.,
Arias S.,
Bose M.,
Gorroochurn P.,
Teixeira J.,
McGinty J.,
Laferrère B.
Publication year - 2011
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2011.01358.x
Subject(s) - incretin , medicine , endocrinology , dipeptidyl peptidase , type 2 diabetes , glucagon like peptide 1 , dipeptidyl peptidase 4 , diabetes mellitus , weight loss , gastric inhibitory polypeptide , insulin , gastric bypass , obesity , chemistry , glucagon , enzyme , biochemistry
The mechanism by which incretins and their effect on insulin secretion increase markedly following gastric bypass (GBP) surgery is not fully elucidated. We hypothesized that a decrease in the activity of dipeptidyl peptidase‐4 (DPP‐4), the enzyme which inactivates incretins, may explain the rise in incretin levels post‐GBP. Fasting plasma DPP‐4 activity was measured after 10‐kg equivalent weight loss by GBP (n = 16) or by caloric restriction (CR,n = 14) in obese patients with type 2 diabetes. DPP‐4 activity decreased after GBP by 11.6% (p = 0.01), but not after CR. The increased peak glucagon‐like peptide‐1 (GLP‐1) and glucose‐dependent insulinotropic polypeptide (GIP) response to oral glucose after GBP did not correlate with DPP‐4 activity. The decrease in fasting plasma DPP‐4 activity after GBP occurred by a mechanism independent of weight loss and did not relate to change in incretin concentrations. Whether the change in DPP‐4 activity contributes to improved diabetes control after GBP remains therefore to be determined.