Growth Hormone, IGF-1 and Medical Treatment in Acromegaly: Are There Effects on Gut Hormone Physiology and Postprandial Substrate Metabolism?

Status

Completed

Phase

Phase not stated

Enrollment

21 participants (actual)

Sponsor

University Hospital, Ghent · Other

Design

Not stated

Countries

1 country

Belgium

Start

1 Jun 2014

Primary completion

31 Aug 2017

Completion

31 Aug 2017

First posted

2 Jun 2014 (estimated)

Last update posted

29 Dec 2022

Conditions

Acromegaly

Acromegaly is a rare hormonal disorder leading to increased morbidity and mortality. In the vast majority of cases, a pituitary somatotroph cell adenoma causes excess growth hormone (GH) secretion, leading to hepatic insulin-like-growth factor 1 (IGF-1) hypersecretion. Both the disease as well as its treatment with long-acting somatostatin analogs (LA-SMSA) and/or pegvisomant affect glucose and lipid metabolism, possibly contributing to increased cardiovascular risk. In this pilot study, the investigators want to explore insulin sensitivity, postprandial gut hormone response, lipid handling and adipocytokine profile in the following 4 groups: * controlled acromegalic patients on LA-SMSA (group 1) * controlled acromegalic patients on combination treatment of LA-SMSA and pegvisomant (group 2) * acromegalic patients without need for medical therapy after surgery (group 3) * healthy control subjects (group 4) Furthermore, a longitudinal exploration will be performed in uncontrolled acromegalic patients (i.e. patients with serum IGF-1 levels above age-specific thresholds and/or symptoms due to active acromegaly (excessive sweating , arthralgia)) on LA-SMSA monotherapy (group 5). In this group, insulin sensitivity, postprandial gut hormone response, lipid handling and adipocytokine profile will be explored before introducing pegvisomant and three months after normalisation of IGF-1 levels. The investigators hypothesize that lipid and glucose handling will be less efficient in the controlled acromegalic patients on LA-SMSA than in controlled patients on combination therapy or after surgery, and that there will be no difference in substrate metabolism between healthy controls and controlled acromegalic patients on combination treatment or after surgery. Further, they hypothesize that introducing pegvisomant in uncontrolled acromegalic patients will improve their postprandial lipid and glucose handling.

• Other

  Controlled on LA-SMSA

  Patients with controlled acromegaly on long-acting somatostatin analogs

• Other

  Controlled on LA-SMSA and pegvisomant

  Patients with controlled acromegaly on long-acting somatostatin analogs and pegvisomant

• Other

  Controlled after surgery

  Controlled acromegaly patients without need for medical therapy after surgery

• Other

  Healhy controls

  Healthy volunteers

• Other

  Uncontrolled on LA-SMSA

  Patients with uncontrolled acromegaly (i.e. with serum IGF-1 levels above age-specific thresholds and/or symptoms due to active acromegaly (e.g. excessive sweating, arthralgia)) on LA-SMSA monotherapy in maximal dosage

1. change in insulin sensitivity

   Time frame · before start of pegvisomant and 3 months after normalisation of IGF-1 after start of pegvisomant in group 5

   Registry description

   Glucose disposal rate during last half hour of hyperinsulinemic-euglycemic clamp procedure, corrected for lean body mass (in µmol/min/kgLBM)

2. insulin sensitivity

   Time frame · At enrollment in groups 1-4

   Registry description

   Glucose disposal rate during last half hour of hyperinsulinemic-euglycemic clamp procedure, corrected for lean body mass (in µmol/min/kgLBM)