Eating disorders: A role for dipeptidyl peptidase IV in nutritional control

Citation
M. Hildebrandt et al., Eating disorders: A role for dipeptidyl peptidase IV in nutritional control, NUTRITION, 17(6), 2001, pp. 451-454
Citations number
29
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
NUTRITION
ISSN journal
08999007 → ACNP
Volume
17
Issue
6
Year of publication
2001
Pages
451 - 454
Database
ISI
SICI code
0899-9007(200106)17:6<451:EDARFD>2.0.ZU;2-A
Abstract
Dipeptidyl peptidase IV (DPP IV), a serine protease with broad tissue distr ibution and known activity in serum, has been postulated to modulate nutrit ion control by modification or inactivation of peptide hormones operating i n the enteroinsular axis. We hypothesized that changes of DPP IV activity i n serum are related to the nutrition status of patients with eating disorde rs. Serum DPP IV activity was measured in 52 patients (28 with anorexia ner vosa and 24 with bulimia nervosa) in four consecutive weekly analyses. Simu ltaneously, the number of CD26 (DPP IV)-positive peripheral blood lymphocyt es was counted. The same analyses were carried out in 28 healthy female vol unteers. In week 1 and throughout the observation period, DPP IV activity i n the sera of patients with anorexia nervosa and, to a lesser extent, those with bulimia nervosa was elevated in comparison to that of healthy control s (week 1: means = 92.8 U/L for anorexia-nervosa patients and 893 Un for bu limia-nervosa patients versus 74.7 Un for healthy control subjects, P = 0.0 14; weeks 1-4. 91.8 U/L for anorexia-nervosa patients and 86.2 U/L for buli mia-nervosa patients versus 77.6 U/L for healthy controls, P < 0.001). We a ssume that the increase in DPP IV serum activity will increase the turnover of distinct peptide hormones with known effects on nutrition control and s usceptibility to degradation by DPP IV. The potential impact of an increase in DPP IV activity in serum on satiety and nutrition control contributes t o previously reported implications for immune function. (C) Elsevier Scienc e Inc. 2001.