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Hyperglucagonemia clinical trials

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NCT ID: NCT05056584 Completed - Clinical trials for Chronic Kidney Diseases

The Role of the Kidneys and Liver in the Elimination of Glucagon

MCR_EndCir
Start date: August 1, 2020
Phase: N/A
Study type: Interventional

The study aims to evaluate the kinetics and effect of glucagon in patients with chronic kidney disease and liver cirrhosis and matched healthy subjects, respectively.

NCT ID: NCT02237053 Completed - Obesity Clinical Trials

Effects of Glucagon Administration on Energy Expenditure

GLEE
Start date: September 2014
Phase: Phase 1
Study type: Interventional

The purpose of this study is to collect data to help researchers better understand the effects of glucagon on the amount of calories burned.

NCT ID: NCT01436734 Completed - Hyperglucagonemia Clinical Trials

Role of Aprotinin in Glucagon Degradation, Measurement by Radioimmunoactive Method (RIA) I125

Start date: July 2011
Phase: N/A
Study type: Interventional

The aim of the study was to investigate the role of the Trasylol in glucagon prevention in degradation using radioimmunoactive method with I125. Additionally different incubation time was introduced in human plasma samples after oral glucose stimulation, also in fasted and hypoglycemia blood samples from patients' type 2 diabetes. Since, the structure and the techniques for the glucagon measurement are well described nowadays.

NCT ID: NCT00862589 Completed - Hyperglycemia Clinical Trials

Glucagon-Like Peptide-1 (GLP-1) Suppression of Alpha Cell Secretion in Type 2 Diabetes Mellitus (T2DM)

Start date: October 2006
Phase: N/A
Study type: Interventional

The incretin hormone glucagon-like peptide-1 (GLP-1) has known insulinotrophic and glucagonostatic properties. However, inpatients with type 2 diabetes mellitus (T2DM)it is shown, that the beta cell sensitivity towards GLP-1 is decreased, when comparing to healthy controls. Further, these patients have decreased GLP-1 response to a meal. The aim of this study is to elucidate if the diabetic hyperglucagonemia, seen in these patients both during fasting and in a postprandial condition, is coursed by a decreased sensitivity to GLP-1 in the diabetic alpha cell. Ten T2DM patients and ten matched healthy control subjects will be examined on two separate days. Day 1: increasing GLP-1 infusions and Day 2: saline. During both days plasma glucose (PG) will be clamped at fasting level (FPG). Patients with T2DM will be submitted til a Day 3, here PG will be normalized over-night by an adjustable insulin infusion, on the following day the GLP-1 infusion of Day 1 will be repeated. The hypothesis is that these patients have decreased alpha cell sensitivity to GLP-1 as is the case with the beta cell sensitivity. This decreased sensitivity, the investigators speculate, contributes the defect suppression og glucagon and thereby to the increased PG levels seen in T2DM. Further the investigators will elucidate if this sensitivity can be increased by normalizing the diabetic PG to a normal FPG level.

NCT ID: NCT00704795 Active, not recruiting - Diabetes Mellitus Clinical Trials

Glucagon Responses During Oral- and iv Glucose in Patients With Type 1 Diabetes

Start date: June 2008
Phase: N/A
Study type: Observational

In order to evaluate the potential role of the gastrointestinal (GI) tract in the postprandial hyperglucagonemia, which characterizes type 1 diabetes mellitus (T1DM) (as well as type 2 diabetes mellitus (T2DM)), we wish to investigate the secretion of glucagon in patients with T1DM without residual beta-cell function during 50-g oral glucose tolerance test (OGTT) and during isoglycemic iv glucose infusion. By evaluating C-peptide negative patients with T1DM we aim to describe the glucagon response to glucose (+/-stimulation of the GI tract) independently of the potentially very important regulation of glucagon secretion by endogenous insulin secretion. A more detailed understanding of the inappropriate glucagon secretion in T1DM is highly needed in order to establish new intervention strategies in the future treatment of the growing numbers of T1DM patients.