An observational study in End-stage Renal Disease, sponsored by Bo Feldt-Rasmussen. Completed at 1 site in Denmark. Open to participants aged 18 Years to 90 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2017-05-22.
Sponsored by Bo Feldt-Rasmussen · Observational
Patients with end-stage renal disease (ESRD) have a high prevalence of impaired glucose metabolism. The pathophysiological cause is uncertain, but disturbances in the secretion, elimination and effect of glucagon, insulin and the two incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), probably play important roles. Our research group has previously found that dialysis patients without type 2 diabetes mellitus (T2DM) have a reduced incretin effect and an inability to suppress glucagon after a meal - two early pathophysiological characteristics of patients with T2DM and normal kidney function.
The aim of the project is to provide a detailed description of the mechanisms underlying the (patho)physiological effects of the incretin hormones in patients with ESRD. We plan to investigate the above mentioned disturbances during fasting and hyperglycaemic conditions using incretin infusions during glucose clamping. Furthermore, stable isotopic tracers will be used to determine the effect of the incretin hormones on the endogenous glucose handling.
We hypothesise that the effects of the incretin hormones in ESRD will be reduced in respect to healthy control subjects.
The effect of the incretin hormones on the endocrine pancreatic function in a uremic environment will be explored during fasting and hyperglycemic conditions in three randomised examination days.
At a preceding screening day, an oral glucose tolerance test (OGTT) and a dual energy x-ray absorptiometry (DXA) scan will be performed to determine glucose tolerance and the distribution of muscle and adipose tissue. The study will be carried out on three separate days differing with respect to the hormones infused: GLP-1, GIP or placebo (saline) which are double blinded. The patients will meet from an overnight fast and an infusion of one of the hormones is initiated. At the same time labeled glucose will be infused to determine the endogenous hepatic glucose production. A glucose infusion is adjusted according to frequent plasma glucose measurements to maintain fasting glucose level. After 2 hours a steady state of the tracer is achieved and a 2 hour hyperglycemic clamp, 3 mmol/l above fasting glucose concentration will be started. The tracer infusions are continued during the hyperglycemia. After the 4 hour clamp an arginine bolus will be administered to measure the ability to increase the secretion of insulin and glucagon.
3,840 studies on the registry are indexed under Kidney Diseases; 500 are open to participants now.
This study's enrollment of 24 is below the median of 192 across 1,033 observational studies indexed under Kidney Diseases.
Browse Kidney Diseases studies →Bo Feldt-Rasmussen is the lead sponsor of 8 studies on the registry; 1 is open to participants now.
Counted across the registry records on this site, refreshed daily.
Inclusion Criteria (End-stage renal disease):
Inclusion Criteria (Healthy controls):
Exclusion Criteria:
Patients with normal glucose tolerance and end-stage renal disease
Other: Eu- and hyperglycemic clamp · Other: Arginine test
Healthy controls with normal kidney function and normal glucose tolerance
Other: Eu- and hyperglycemic clamp · Other: Arginine test
Eu- and hyperglycemic clamp with concomitant infusion of the natural occurring hormones glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) or placebo along with stable glucose isotope infusion to measure the effects of the incretins.
Bolus infusion of the natural occurring amino acid arginine to measure the ability to increase the secretion of insulin and glucagon
The effect of GLP-1 and GIP on insulin response during hyperglycemia between groups
Average plasma insulin concentrations during hyperglycemia
Time frame: Average during the last 2 hours of each examination day. Blood samples are collected at time 122, 124, 126, 130, 210, 225 and 240 minutes
The effect of GLP-1 and GIP on insulin, glucagon and endogenous glucose production during euglycemia
Average plasma insulin and glucagon concentrations as well as glucose rate of appearance during euglycemia.
Time frame: Average during the first 2 hours of each examination day. Blood samples are collected at time 90, 105 and 120 minutes
The effect of GLP-1 and GIP on early and late phase of insulin, glucagon and endogenous glucose production during hyperglycemia
Average plasma insulin and glucagon concentrations as well as glucose rate of appearance during the first 10 minutes and last 30 minutes of hyperglycemia.
Time frame: Averages during the last 2 hours of each examination day. Blood samples are collected at time 122, 124, 126, 130, 210, 225 and 240 minutes
The effect of GLP-1 and GIP on insulin and glucagon response to arginine
Average plasma insulin and glucagon concentrations 10 minutes following arginine bolus at the end of the examination.
Time frame: Average following ariginine bolus. Blood samples are collected at time 242, 244, 246 and 250 minutes
The effect of GLP-1 and GIP on the peripheral glucose handling
Average glucose infusion rate during both euglycemia (the first 2 hours) and hyperglycemia (the last 2 hours).
Time frame: Average during the first 4 hours of each examination day. Blood samples are collected at 5-15 minutes interval from time 0 to time 240 minutes
The effect of GLP-1 and GIP on potassium concentrations during euglycemia
Average plasma potassium concentrations during euglycemia
Time frame: Average during the first 2 hours of each examination day. Blood samples are collected at time 30, 60, 90 and 120 minutes
This study is completed, as verified in May 2017. You cannot join it, but the record below documents what was studied.
Get an email when the registry record changes — status, dates, results — or when someone posts here.
Sign in to followQuestions and observations about this study, from anyone following it. Not medical advice, and not a channel to the study team — their contact details are on the registry record.
Sign in to join the discussion. Reading takes no account; posting does. You choose a display name, and a pseudonym is the default.
Nothing here yet. If you are running this trial, taking part in it, or weighing whether to, this is the place to say so.
Bo Feldt-Rasmussen