|
Anorexia
|
0.330 |
Biomarker
|
disease |
CTD_human |
Furthermore, the GIP receptor antagonist Pro3GIP dose-dependently attenuated both GIP- and T-2 toxin-induced anorectic responses.
|
29689362 |
2018 |
|
Anorexia
|
0.330 |
Biomarker
|
disease |
BEFREE |
To summarize, these findings suggest that both GIP and PYY<sub>3-36</sub> might be critical mediators of anorexia induction by T-2 toxin.
|
29689362 |
2018 |
|
Anorexia
|
0.330 |
Biomarker
|
disease |
CTD_human |
Role of Glucagon-Like Peptide-1 and Gastric Inhibitory Peptide in Anorexia Induction Following Oral Exposure to the Trichothecene Mycotoxin Deoxynivalenol (Vomitoxin).
|
28633506 |
2017 |
|
Anorexia
|
0.330 |
Biomarker
|
disease |
BEFREE |
In contrast, the GIP receptor antagonist Pro3GIP induced a dose-dependent attenuation of both GIP- and DON-induced anorexia.
|
28633506 |
2017 |
|
Anorexia
|
0.330 |
Biomarker
|
disease |
BEFREE |
Together, these findings suggest that PYY3-36 and GIP play a role in T-2-, HT-2-, DAS-, and NEO-induced anorexia.
|
28666375 |
2017 |
|
Anorexia
|
0.330 |
Biomarker
|
disease |
CTD_human |
Role of Peptide YY3-36 and Glucose-Dependent Insulinotropic Polypeptide in Anorexia Induction by Trichothecences T-2 Toxin, HT-2 Toxin, Diacetoxyscirpenol, and Neosolaniol.
|
28666375 |
2017 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
Among the gastrointestinal hormones, the incretins: glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 have attracted interest because of their importance for the development and therapy of type 2 diabetes and obesity.
|
31815785 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
Initial interest in the therapeutic use of GIP was dampened by evidence that its insulinotropic activity was reduced in type 2 diabetes and by reports that it increased glucagon secretion and adipose deposition in non-diabetic individuals.
|
31756366 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
In line with this, the insulinotropic effects of GIP and GLP-1 are impaired in patients with type 2 diabetes, even when administered in supraphysiological doses.
|
31693916 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
AlteredExpression
|
disease |
BEFREE |
However, GIP stimulates glucagon secretion even at hyperglycemia in people with T2D, suggesting that inappropriate GIPR activity in α-cells contributes to the pathogenesis of T2D.
|
31785304 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
Recent studies with a GIP receptor antagonist suitable for human studies have confirmed these concepts regarding the actions of endogenous GIP and point to potential beneficial metabolic effects of GIP receptor antagonists rather than agonist in the treatment of obesity and type 2 diabetes.
|
31838219 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
DPP-4 inhibitors reduce degradation of GIP, and although the insulinotropic effects of GIP are impaired in patients with T2D, they can be at least partially restored if glycaemic control is improved.
|
31706956 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
In various models, GIP has effects on glucagon secretion, bone and lipid homeostasis, but whether these effects contribute substantially to the pathophysiology of type 2 diabetes is at present controversial.
|
31682875 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
This review will discuss the physiological effects of GIP on fat metabolism in human adipose and other non-adipose tissues such as liver, pancreas, skeletal muscle and heart, describe where the actions of GIP may contribute to the pathophysiology of obesity, T2D and NAFLD and finally describe the therapeutic implications of GIP antagonism and agonism in these conditions.
|
31759125 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
A synthetic monomeric peptide triple receptor agonist, termed "Triagonist" that incorporates glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon (Gcg) actions, was previously developed to improve upon metabolic and glucose regulatory benefits of single and dual receptor agonists in rodent models of diet-induced obesity and type 2 diabetes.
|
31730763 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
In this review, we summarize the known aspects of the effects of GIP on beta and other islet cells and discuss the most recent developments on GIP-based therapeutic agents for the improvement of beta cell function in T2D patients.
|
31751656 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
Lastly, we discuss how dysmetabolic conditions such as obesity and type 2 diabetes may shift the actions of GIP in an atherogenic direction, and we provide a perspective on the therapeutic potential of GIP receptor agonism and antagonism in cardiovascular diseases.
|
31689454 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
These results show PPARγ agonists regulate GIP-R expression through PPRE in human adipocytes, but suggests this mechanism is not important for regulation of the insulinotropic effect of GIP in subjects with T2DM.
|
31757794 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.300 |
Biomarker
|
disease |
BEFREE |
Rapid tachyphylaxis in response to continuous exposure to slightly supraphysiological concentrations of GIP does not explain the reduced insulinotropic response to GIP infusions in patients with type 2 diabetes or their first-degree relatives.
|
31669136 |
2020 |
|
Obesity
|
0.300 |
GeneticVariation
|
disease |
BEFREE |
Nonetheless, interrogation of the GIP/GIPR axis on cardiac function in humans will involve the systemic actions of the GIPR within the myocardium and other systems (e.g. adipose tissue, vasculature), which will influence the long-term future of GIPR modification for the treatment of obesity/T2DM.
|
31812593 |
2020 |
|
Obesity
|
0.300 |
Biomarker
|
disease |
BEFREE |
GIP analogues and the treatment of obesity-diabetes.
|
31756366 |
2020 |
|
Obesity
|
0.300 |
Biomarker
|
disease |
BEFREE |
This review will discuss the physiological effects of GIP on fat metabolism in human adipose and other non-adipose tissues such as liver, pancreas, skeletal muscle and heart, describe where the actions of GIP may contribute to the pathophysiology of obesity, T2D and NAFLD and finally describe the therapeutic implications of GIP antagonism and agonism in these conditions.
|
31759125 |
2020 |
|
Obesity
|
0.300 |
Biomarker
|
disease |
BEFREE |
Lastly, we discuss how dysmetabolic conditions such as obesity and type 2 diabetes may shift the actions of GIP in an atherogenic direction, and we provide a perspective on the therapeutic potential of GIP receptor agonism and antagonism in cardiovascular diseases.
|
31689454 |
2020 |
|
Obesity
|
0.300 |
Biomarker
|
disease |
BEFREE |
Recent studies with a GIP receptor antagonist suitable for human studies have confirmed these concepts regarding the actions of endogenous GIP and point to potential beneficial metabolic effects of GIP receptor antagonists rather than agonist in the treatment of obesity and type 2 diabetes.
|
31838219 |
2020 |
|
Obesity
|
0.300 |
GeneticVariation
|
disease |
BEFREE |
This, together with reports on GIP antagonists that may protect against obesity, has revived the interest on the GIP/GIPR axis as a potential anti-diabetic pathway.
|
31751656 |
2020 |