Reappraisal of GIP Pharmacology for Metabolic Diseases
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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Reappraisal of GIP Pharmacology for Metabolic Diseases. / Finan, Brian; Müller, Timo D; Clemmensen, Christoffer; Perez-Tilve, Diego; DiMarchi, Richard D; Tschöp, Matthias H.
I: Trends in Molecular Medicine, Bind 22, Nr. 5, 05.2016, s. 359-76.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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TY - JOUR
T1 - Reappraisal of GIP Pharmacology for Metabolic Diseases
AU - Finan, Brian
AU - Müller, Timo D
AU - Clemmensen, Christoffer
AU - Perez-Tilve, Diego
AU - DiMarchi, Richard D
AU - Tschöp, Matthias H
N1 - Copyright © 2016 Elsevier Ltd. All rights reserved.
PY - 2016/5
Y1 - 2016/5
N2 - Glucagon-like peptide-1 (GLP-1) analogs are considered the best current medicines for type 2 diabetes (T2D) and obesity due to their actions in lowering blood glucose and body weight. Despite similarities to GLP-1, glucose-dependent insulinotropic polypeptide (GIP) has not been extensively pursued as a medical treatment for T2D. This is largely based on observations of diminished responses of GIP to lower blood glucose in select patients, as well as evidence from rodent knockout models implying that GIP promotes obesity. These findings have prompted the belief in some, that inhibiting GIP action might be beneficial for metabolic diseases. However, a growing body of new evidence - including data based on refined genetically modified models and improved pharmacological agents - suggests a paradigm shift on how the GIP system should be manipulated for metabolic benefits.
AB - Glucagon-like peptide-1 (GLP-1) analogs are considered the best current medicines for type 2 diabetes (T2D) and obesity due to their actions in lowering blood glucose and body weight. Despite similarities to GLP-1, glucose-dependent insulinotropic polypeptide (GIP) has not been extensively pursued as a medical treatment for T2D. This is largely based on observations of diminished responses of GIP to lower blood glucose in select patients, as well as evidence from rodent knockout models implying that GIP promotes obesity. These findings have prompted the belief in some, that inhibiting GIP action might be beneficial for metabolic diseases. However, a growing body of new evidence - including data based on refined genetically modified models and improved pharmacological agents - suggests a paradigm shift on how the GIP system should be manipulated for metabolic benefits.
KW - Animals
KW - Blood Glucose
KW - Diabetes Mellitus, Type 2
KW - Gastric Inhibitory Polypeptide
KW - Glucagon-Like Peptide 1
KW - Humans
KW - Insulin
KW - Metabolic Diseases
KW - Mice
KW - Obesity
KW - Receptors, Gastrointestinal Hormone
KW - Journal Article
KW - Review
U2 - 10.1016/j.molmed.2016.03.005
DO - 10.1016/j.molmed.2016.03.005
M3 - Review
C2 - 27038883
VL - 22
SP - 359
EP - 376
JO - Trends in Molecular Medicine
JF - Trends in Molecular Medicine
SN - 1471-4914
IS - 5
ER -
ID: 186640138