On the physiology of GIP and GLP-1
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On the physiology of GIP and GLP-1. / Holst, Jens Juul.
In: Hormone and Metabolic Research. Supplement, Vol. 36, No. 11-12, 19.01.2005, p. 747-54.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - On the physiology of GIP and GLP-1
AU - Holst, Jens Juul
PY - 2005/1/19
Y1 - 2005/1/19
N2 - Recent studies have indicated that GIP and GLP-1 are about as important as each other in the incretin effect, being released rapidly after meals and being active already at fasting glucose levels. Although the density of GLP-1 producing cells is higher distally, GlP-1 is normally secreted by jejunal L-cells, explaining the rapid onset of secretion. Moreover, many endocrine cells in the small intestine appear to produce both GIP and GLP-1. Both are metabolized rapidly by the dipeptidyl peptidase IV enzyme, but unlike GIP, about 90 % of GLP-1 is degraded before it reaches the systemic circulation. Apparently, before it is degraded, GLP-1 activates sensory afferents in the gastrointestinal mucosa with cell bodies in the nodose ganglion, signaling onwards to the brain stem and the hypothalamus. A similar mechanism seems to be involved in GLP-1's effect on gastrointestinal motility and secretion, and perhaps its actions on appetite and food intake, all of which may be even more physiologically important than its effects on the beta cells. Cardiovascular and neuroprotective actions of GLP-1 have also recently been reported. Regarding GIP, several lines of evidence suggest that GIP, in addition to its incretin effects, may affect lipid metabolism and promote lipid storage.
AB - Recent studies have indicated that GIP and GLP-1 are about as important as each other in the incretin effect, being released rapidly after meals and being active already at fasting glucose levels. Although the density of GLP-1 producing cells is higher distally, GlP-1 is normally secreted by jejunal L-cells, explaining the rapid onset of secretion. Moreover, many endocrine cells in the small intestine appear to produce both GIP and GLP-1. Both are metabolized rapidly by the dipeptidyl peptidase IV enzyme, but unlike GIP, about 90 % of GLP-1 is degraded before it reaches the systemic circulation. Apparently, before it is degraded, GLP-1 activates sensory afferents in the gastrointestinal mucosa with cell bodies in the nodose ganglion, signaling onwards to the brain stem and the hypothalamus. A similar mechanism seems to be involved in GLP-1's effect on gastrointestinal motility and secretion, and perhaps its actions on appetite and food intake, all of which may be even more physiologically important than its effects on the beta cells. Cardiovascular and neuroprotective actions of GLP-1 have also recently been reported. Regarding GIP, several lines of evidence suggest that GIP, in addition to its incretin effects, may affect lipid metabolism and promote lipid storage.
KW - Animals
KW - Appetite
KW - Cardiovascular System
KW - Gastric Inhibitory Polypeptide
KW - Gastrointestinal Motility
KW - Glucagon
KW - Glucagon-Like Peptide 1
KW - Humans
KW - Intestine, Small
KW - Jejunum
KW - Mice
KW - Mice, Knockout
KW - Neurosecretory Systems
KW - Peptide Fragments
KW - Protein Precursors
U2 - 10.1055/s-2004-826158
DO - 10.1055/s-2004-826158
M3 - Journal article
C2 - 15655703
VL - 36
SP - 747
EP - 754
JO - Hormone and Metabolic Research. Supplement
JF - Hormone and Metabolic Research. Supplement
SN - 0170-5903
IS - 11-12
ER -
ID: 132053985