GLP-1 defects in diabetes

Charlotte Janus; Nicolai Jacob Wewer Albrechtsen; Jens Juul Holst

doi:10.14496/dia.0104336116.6

GLP-1 defects in diabetes

Charlotte Janus, Nicolai Jacob Wewer Albrechtsen, Jens Juul Holst

Abstract

Glucagon-like peptide-1 (GLP-1) is secreted from the intestinal L-cells upon nutrient stimulation and regulates glucose levels by stimulating secretion of insulin (insulinotropic effects) in a glucose-dependent manner (the incretin effect). The incretin effect is severely impaired in subjects with type 2 diabetes (T2D) but the underlying mechanisms are still incompletely understood. In subjects with impaired glucose tolerance (IGT) and T2D, reduced levels of circulating GLP-1 have been observed in cross-sectional studies. Regardless of other changes, a reduced GLP-1 secretion must result in a reduced insulinotropic stimulus to the β-cells and may therefore contribute to the decreased incretin effect in T2D. Also, the role of the reduced incretin effect for development of T2D is unclear, although several studies have indicated that the loss is an early event in the development from minimal glucose disturbances to frank diabetes. Therefore, further studies are required. Ideally, longitudinal studies of predisposed subjects (i.e. obesity, first-degree relatives, post gestational diabetes) followed until diagnosis of T2D would be necessary for elucidating if, indeed, impaired GLP-1 secretion predisposes and contributes to the development of T2D. If so, this may have important clinical consequences suggesting that early intervention with incretin-based therapies might prolong the time to overt T2D development. In the following section we will focus on the GLP-1 defects in T2D.

Original language	English
Publication date	2 Feb 2015
DOIs	https://doi.org/10.14496/dia.0104336116.6
Publication status	Published - 2 Feb 2015

Keywords

Faculty of Health and Medical Sciences

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.14496/dia.0104336116.6

Cite this

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title = "GLP-1 defects in diabetes",

abstract = "Glucagon-like peptide-1 (GLP-1) is secreted from the intestinal L-cells upon nutrient stimulation and regulates glucose levels by stimulating secretion of insulin (insulinotropic effects) in a glucose-dependent manner (the incretin effect). The incretin effect is severely impaired in subjects with type 2 diabetes (T2D) but the underlying mechanisms are still incompletely understood. In subjects with impaired glucose tolerance (IGT) and T2D, reduced levels of circulating GLP-1 have been observed in cross-sectional studies. Regardless of other changes, a reduced GLP-1 secretion must result in a reduced insulinotropic stimulus to the β-cells and may therefore contribute to the decreased incretin effect in T2D. Also, the role of the reduced incretin effect for development of T2D is unclear, although several studies have indicated that the loss is an early event in the development from minimal glucose disturbances to frank diabetes. Therefore, further studies are required. Ideally, longitudinal studies of predisposed subjects (i.e. obesity, first-degree relatives, post gestational diabetes) followed until diagnosis of T2D would be necessary for elucidating if, indeed, impaired GLP-1 secretion predisposes and contributes to the development of T2D. If so, this may have important clinical consequences suggesting that early intervention with incretin-based therapies might prolong the time to overt T2D development. In the following section we will focus on the GLP-1 defects in T2D.",

keywords = "Faculty of Health and Medical Sciences, GLP-1, Diabetes",

author = "Charlotte Janus and Albrechtsen, {Nicolai Jacob Wewer} and Holst, {Jens Juul}",

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AU - Janus, Charlotte

AU - Albrechtsen, Nicolai Jacob Wewer

AU - Holst, Jens Juul

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Y1 - 2015/2/2

N2 - Glucagon-like peptide-1 (GLP-1) is secreted from the intestinal L-cells upon nutrient stimulation and regulates glucose levels by stimulating secretion of insulin (insulinotropic effects) in a glucose-dependent manner (the incretin effect). The incretin effect is severely impaired in subjects with type 2 diabetes (T2D) but the underlying mechanisms are still incompletely understood. In subjects with impaired glucose tolerance (IGT) and T2D, reduced levels of circulating GLP-1 have been observed in cross-sectional studies. Regardless of other changes, a reduced GLP-1 secretion must result in a reduced insulinotropic stimulus to the β-cells and may therefore contribute to the decreased incretin effect in T2D. Also, the role of the reduced incretin effect for development of T2D is unclear, although several studies have indicated that the loss is an early event in the development from minimal glucose disturbances to frank diabetes. Therefore, further studies are required. Ideally, longitudinal studies of predisposed subjects (i.e. obesity, first-degree relatives, post gestational diabetes) followed until diagnosis of T2D would be necessary for elucidating if, indeed, impaired GLP-1 secretion predisposes and contributes to the development of T2D. If so, this may have important clinical consequences suggesting that early intervention with incretin-based therapies might prolong the time to overt T2D development. In the following section we will focus on the GLP-1 defects in T2D.

AB - Glucagon-like peptide-1 (GLP-1) is secreted from the intestinal L-cells upon nutrient stimulation and regulates glucose levels by stimulating secretion of insulin (insulinotropic effects) in a glucose-dependent manner (the incretin effect). The incretin effect is severely impaired in subjects with type 2 diabetes (T2D) but the underlying mechanisms are still incompletely understood. In subjects with impaired glucose tolerance (IGT) and T2D, reduced levels of circulating GLP-1 have been observed in cross-sectional studies. Regardless of other changes, a reduced GLP-1 secretion must result in a reduced insulinotropic stimulus to the β-cells and may therefore contribute to the decreased incretin effect in T2D. Also, the role of the reduced incretin effect for development of T2D is unclear, although several studies have indicated that the loss is an early event in the development from minimal glucose disturbances to frank diabetes. Therefore, further studies are required. Ideally, longitudinal studies of predisposed subjects (i.e. obesity, first-degree relatives, post gestational diabetes) followed until diagnosis of T2D would be necessary for elucidating if, indeed, impaired GLP-1 secretion predisposes and contributes to the development of T2D. If so, this may have important clinical consequences suggesting that early intervention with incretin-based therapies might prolong the time to overt T2D development. In the following section we will focus on the GLP-1 defects in T2D.

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KW - GLP-1

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M3 - Net publication - Internet publication

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