期刊
DIABETES OBESITY & METABOLISM
卷 13, 期 4, 页码 378-381出版社
WILEY
DOI: 10.1111/j.1463-1326.2011.01358.x
关键词
dipeptidyl peptidase inhibitor; GLP-1; gastric bypass; weight loss
资金
- American Diabetes Association [CR-7-05 CR-18]
- NIH [R01-DK67561]
- GCRC [1 UL1 RR024156-02]
- National Institute of Mental Health [MH-48858]
- Swedish Research Council [6834]
- [ORCDK-26687]
- [DERCDK-63068-05]
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.
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