Incretin secretion: direct mechanisms
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Incretin secretion: direct mechanisms. / Balk-Møller, Emilie; Holst, Jens Juul; Kuhre, Rune Ehrenreich.
Diapedia: The living textbook of diabetes. European Association for the Study of Diabetes (EASD), 2014. p. 1-3.Research output: Chapter in Book/Report/Conference proceeding › Encyclopedia chapter › Communication
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TY - ENCYC
T1 - Incretin secretion: direct mechanisms
AU - Balk-Møller, Emilie
AU - Holst, Jens Juul
AU - Kuhre, Rune Ehrenreich
PY - 2014/6/12
Y1 - 2014/6/12
N2 - The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted from gastro-intestinal K- and L-cells, respectively, and play an important role in post-prandial blood glucose regulation. They do this by direct stimulation of the pancreatic β-cell, accounting for some 25-70% of postprandial insulin secretion in healthy subjects. In patients with type 2 diabetes (T2D, however, this effect is greatly reduced or lost due to a combination of severely impaired or eliminated insulinotrophic effect of GIP and reduced meal stimulated GLP-1 secretion. This suggests that the therapeutic potential of GIP for the treatment for T2D is limited, whereas GLP-1 based treatments have been on the market since 2005. Research is now pursuing novel approaches to utilize the effects of GLP-1 for T2D treatment. A combinatorial approach by which the activity of the major enzyme responsible for incretin degradation (dipeptidyl peptidase-4) is inhibited (drugs are already on the market) while the secretion of endogenous GLP-1 secretion is stimulated at the same time may prove particularly rewarding. In this section we review current knowledge on the mechanisms for direct activation of GIP and GLP-1 secretion.
AB - The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted from gastro-intestinal K- and L-cells, respectively, and play an important role in post-prandial blood glucose regulation. They do this by direct stimulation of the pancreatic β-cell, accounting for some 25-70% of postprandial insulin secretion in healthy subjects. In patients with type 2 diabetes (T2D, however, this effect is greatly reduced or lost due to a combination of severely impaired or eliminated insulinotrophic effect of GIP and reduced meal stimulated GLP-1 secretion. This suggests that the therapeutic potential of GIP for the treatment for T2D is limited, whereas GLP-1 based treatments have been on the market since 2005. Research is now pursuing novel approaches to utilize the effects of GLP-1 for T2D treatment. A combinatorial approach by which the activity of the major enzyme responsible for incretin degradation (dipeptidyl peptidase-4) is inhibited (drugs are already on the market) while the secretion of endogenous GLP-1 secretion is stimulated at the same time may prove particularly rewarding. In this section we review current knowledge on the mechanisms for direct activation of GIP and GLP-1 secretion.
KW - Faculty of Health and Medical Sciences
KW - GIP
KW - GLP-1
KW - Direct mechanisms of secretion
U2 - 10.14496/dia.5105252812.7
DO - 10.14496/dia.5105252812.7
M3 - Encyclopedia chapter
SP - 1
EP - 3
BT - Diapedia
PB - European Association for the Study of Diabetes (EASD)
ER -
ID: 113811545