- ►diabetesjournals.org CF Deacon, P Danielsen, L Klarskov, M Olesen, JJ … - Diabetes, 2001 - Am Diabetes Assoc Glucose-dependent insulinotropic peptide (GIP) is known to be degraded by dipeptidyl peptidase
IV (DPP IV), forming an inactive metabolite, but the extent of the enzyme's role in regulating the
biological activity of GIP in vivo is still largely unknown. In nonfasted anesthetized pigs ... Cited by 88 - Related articles - BL Direct - All 6 versions
- ►endocrinology-journals.org [PDF] CF Deacon, S Wamberg, P Bie, TE Hughes, … - Journal of …, 2002 - Soc Endocrinology The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic
polypeptide (GIP) are degraded by dipeptidyl peptidase IV (DPP IV), thereby losing insulinotropic
activity. DPP IV inhibition reduces exogenous GLP-1 degradation, but the extent of ... Cited by 63 - Related articles - BL Direct - All 3 versions
CF Deacon, TE Hughes, JJ Holst - DIABETES-NEW YORK-, 1998 - Am Diabetes Assoc Glucagon-like peptide 1 (GLP-1) has been proposed as a new therapeutic agent in the management
of diabetes because of its glucose-dependent stimulation of insulin secretion, but this is limited
by its rapid degradation in vivo by dipeptidyl peptidase IV (DPP IV). In nonfasted ... Cited by 193 - Related articles - BL Direct - All 8 versions
- ►endocrinology-journals.org [PDF] FP O'Harte, MH Mooney, CM Kelly, PR … - Journal of Endocrinology, 2000 - Soc Endocrinology Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular
axis which is rapidly inactivated by the exopeptidase dipeptidyl peptidase (DPP) IV. The present
study has examined the ability of Tyr1-glucitol GIP to be protected from plasma ... Cited by 42 - Related articles - BL Direct - All 10 versions
SA Hinke, RW Gelling, RA Pederson, S Manhart, C … - Diabetes, 2002 - Am Diabetes Assoc The therapeutic potential of glucose-dependent insulinotropic polypeptide (GIP) for improving
glycemic control has largely gone unstudied. A series of synthetic GIP peptides modified at the
NH 2 -terminus were screened in vitro for resistance to dipeptidyl peptidase IV (DP IV) ... Cited by 57 - Related articles - BL Direct - All 6 versions
- ►pasteur.ac.ir [PDF] B Ahrén, JJ Holst, H Mårtensson, B Balkan - European journal of pharmacology, 2000 - Elsevier We explored whether inhibition of the enzyme dipeptidyl peptidase IV (DPP IV) increases endogenous
levels of glucagon-like peptide-1 (GLP-1) and improves glucose tolerance and insulin secretion
in mice. Glucose (150 mg) was administered through a gastric gavage with or without the ... Cited by 133 - Related articles - All 5 versions
- ►endojournals.org CF Deacon, MA Nauck, J Meier, K Hucking, JJ … - Journal of Clinical …, 2000 - Endocrine Soc Gastric inhibitory polypeptide (GIP) is susceptible to degradation, but only recently has dipeptidyl
peptidase IV been identified as the enzyme responsible. Most RIAs recognize both intact
GIP-(1–42) and the noninsulinotropic N-terminally truncated metabolite, GIP-(3–42), ... Cited by 174 - Related articles - BL Direct - All 4 versions
B Balkan, L Kwasnik, R Miserendino, JJ Holst, X Li - Diabetologia, 1999 - Springer Control of prandial plasma concentrations of sub- strates, particularly glucose, is aided by
incretins. In- cretins are hormones released by the digestive tract in response to ingested nutrients
[1]. The role of in- cretins is to sensitize beta cells to stimulation by glu- Cited by 158 - Related articles - BL Direct - All 3 versions
JA Pospisilik, SG Stafford, HU Demuth, R Brownsey, W … - Diabetes, 2002 - Am Diabetes Assoc The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide
1 (GLP-1) are responsible for >50% of nutrient-stimulated insulin secretion. After being released
into the circulation, GIP and GLP-1 are rapidly inactivated by the circulating enzyme ... Cited by 135 - Related articles - BL Direct - All 6 versions
B Sudre, P Broqua, RB White, D Ashworth, DM Evans, … - Diabetes, 2002 - Am Diabetes Assoc Acute suppression of dipeptidyl peptidase IV (DPP-IV) activity improves glucose tolerance in
the Zucker fatty rat, a rodent model of impaired glucose tolerance, through stabilization of
glucagon-like peptide (GLP)-1. This study describes the effects of a new and potent ... Cited by 106 - Related articles - BL Direct - All 5 versions
