GLP-1 defects in diabetes

Research output: Other contributionNet publication - Internet publicationResearchpeer-review

Standard

GLP-1 defects in diabetes. / Janus, Charlotte; Albrechtsen, Nicolai Jacob Wewer; Holst, Jens Juul.

2015, .

Research output: Other contributionNet publication - Internet publicationResearchpeer-review

Harvard

Janus, C, Albrechtsen, NJW & Holst, JJ 2015, GLP-1 defects in diabetes.. https://doi.org/10.14496/dia.0104336116.6

APA

Janus, C., Albrechtsen, N. J. W., & Holst, J. J. (2015, Feb 2). GLP-1 defects in diabetes. https://doi.org/10.14496/dia.0104336116.6

Vancouver

Janus C, Albrechtsen NJW, Holst JJ. GLP-1 defects in diabetes. 2015. https://doi.org/10.14496/dia.0104336116.6

Author

Janus, Charlotte ; Albrechtsen, Nicolai Jacob Wewer ; Holst, Jens Juul. / GLP-1 defects in diabetes. 2015.

Bibtex

@misc{ad71305600fa44a28890f6bac8573893,
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 = "The Faculty of Health and Medical Sciences, GLP-1, Diabetes",
author = "Charlotte Janus and Albrechtsen, {Nicolai Jacob Wewer} and Holst, {Jens Juul}",
note = "Senest {\ae}ndret: 05/02/2015",
year = "2015",
month = "2",
day = "2",
doi = "10.14496/dia.0104336116.6",
language = "English",
type = "Other",

}

RIS

TY - ICOMM

T1 - GLP-1 defects in diabetes

AU - Janus, Charlotte

AU - Albrechtsen, Nicolai Jacob Wewer

AU - Holst, Jens Juul

N1 - Senest ændret: 05/02/2015

PY - 2015/2/2

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.

KW - The Faculty of Health and Medical Sciences

KW - GLP-1

KW - Diabetes

U2 - 10.14496/dia.0104336116.6

DO - 10.14496/dia.0104336116.6

M3 - Net publication - Internet publication

ER -

ID: 130765205