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Journal ArticleDOI

The insulinotropic effect of GIP is impaired in patients with chronic pancreatitis and secondary diabetes mellitus as compared to patients with chronic pancreatitis and normal glucose tolerance.

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TLDR
The lack of GIP amplification of the late insulin response to iv glucose develops alongside the deterioration of glucose tolerance in patients with CP, suggesting that the same may be true for the loss of the GIP effect in Patients with type 2 diabetes mellitus.
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This article is published in Regulatory Peptides.The article was published on 2007-12-01. It has received 55 citations till now. The article focuses on the topics: Incretin & Type 2 Diabetes Mellitus.

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Citations
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Four weeks of near-normalisation of blood glucose improves the insulin response to glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes.

TL;DR: Near-normalisation of blood glucose for 4 weeks improves beta cell responsiveness to both GLP-1 and GIP by a factor of three to four, and no effect was found on betacell responsiveness to glucose alone.
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The Sustained Effects of a Dual GIP/GLP-1 Receptor Agonist, NNC0090-2746, in Patients with Type 2 Diabetes.

TL;DR: Patients with type 2 diabetes inadequately controlled with metformin received NNC0090-2746, a fatty-acylated dual agonist possessing in vitro balanced GIPR and GLP-1R agonism significantly improved glycemic control and reduced body weight compared with placebo.
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Impaired incretin effect and fasting hyperglucagonaemia characterizing type 2 diabetic subjects are early signs of dysmetabolism in obesity

TL;DR: People with type 2 diabetes mellitus are characterized by reduced incretin effect and inappropriate glucagon levels, and α and β‐cell responses to oral glucose tolerance test and isoglycaemic intravenous glucose infusion in lean and obese persons with T2DM or normal glucose tolerance (NGT) are evaluated to elucidate the impact of obesity.
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GIP does not potentiate the antidiabetic effects of GLP-1 in hyperglycemic patients with type 2 diabetes.

TL;DR: GIP is unable to further amplify the insulinotropic and glucose-lowering effects of GLP-1 in type 2 diabetes, and the suppression of glucagon elicited by GLp-1 was antagonized by the addition of GIP.
References
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Journal ArticleDOI

Homeostasis model assessment : insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man

TL;DR: The correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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International Union of Pharmacology: Approaches to the Nomenclature of Voltage-Gated Ion Channels

TL;DR: This issue of Pharmacological Reviews includes a new venture in the collaboration between the International Union of Pharmacology (IUPHAR) and the American Society for Pharmacology and Experimental Therapeutics (ASPET), in that a new classification of voltage-gated ion channels is outlined.
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Reduced incretin effect in type 2 (non-insulin-dependent) diabetes.

TL;DR: Integrated incremental immunoreactive insulin and connecting peptide responses to an oral glucose load and an “isoglycaemic” intravenous glucose infusion, respectively, were measured in 14 Type 2 diabetic patients and 8 age- and weight-matched metabolically healthy control subjects.
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Tissue and Plasma Concentrations of Amidated and Glycine-Extended Glucagon-Like Peptide I in Humans

TL;DR: Both amidated and glycine-extended GLP-I molecules are produced in the small intestine and in the pancreas in humans and both are measurable in fasting plasma.
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Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses

TL;DR: A discrepancy between the estimates of the incretin effect derived from peripheral venous insulin responses, and C-peptide responses or calculated insulin secretion rates, exists, which suggests that elimination kinetics of insulin differ between oral and iv glucose administration.
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