Growth Hormone Feedback to Insulin-like Growth Factor-I (IGF-1) and Oral Glucose Tolerance Test (OGTT)

What Was Tested

The trial (not phased) is built around IGF-1 LR3.

Growth hormone (GH) and Insulin-like growth factor-I (IGF-I) secretion are altered in acromegaly and type 2 Diabetes Mellitis (DM).

The secretion of GH is mediated by central hypothalamic hormones (GH Releasing Hormone and somatostatin) as well as peripheral factors providing feedback inhibition (IGF-I and glucose, among others).

The purpose of this study is to compare growth hormone suppression after an oral glucose tolerance test (OGTT) to growth hormone suppression after recombinant human IGF-I (rhIGF-I) administration.

It had three arms (groups): Active Acromegaly (active comparator), Type 2 Diabetes Mellitus(DM) (active comparator) and Heathy Controls (active comparator).

Placebo, oral glucose tolerance test, and subcutaneous administration of recombinant human IGF-1 will be given at visits 2, 3, and 4 respectively. All visits will be performed within a 4 week period.

Placebo, oral glucose tolerance test, and subcutaneous administration of recombinant human IGF-1 will be given at visits 2, 3, and 4 respectively. All visits will be performed within a 4 week period.

Placebo, oral glucose tolerance test, and subcutaneous administration of recombinant human IGF-1 will be given at visits 2, 3, and 4 respectively. All visits will be performed within a 4 week period.

The registry classes the interventions as diagnostic test.

More on the Plan

Acromegaly is characterized by unrestrained growth hormone (GH) secretion and subsequent elevated insulin-like growth factor (IGF)-1 resulting from a benign somatotroph GH-secreting adenoma in the pituitary.

In healthy individuals, the negative feedback loop regulating GH secretion is modulated in part by IGF-1, which inhibits basal GH secretion as well as GH secretion mediated by hypothalamic growth hormone releasing hormone (GHRH).

IGF-1 also suppresses basal and GHRH-induced gene transcription and downregulates GH receptors in the periphery to limit local GH action.

In acromegaly, somatotroph proliferation and transformation may lead to disrupted GH feedback regulation, leading to tonically elevated GH and IGF-1 levels that remain unrestrained.

Who Took Part

Enrollment: 28 actual participants took part.

It was open to people of any sex aged from 18 years with no upper age limit.

Healthy volunteers could join, not only people with the condition.

Examples of who could join: Active acromegaly due to excess GH produced by a pituitary adenoma.

The full record lists 3 inclusion and 24 exclusion criteria; among the exclusions: acromegaly group; for subjects on current therapy the following washout periods may be used:; cabergoline: 4 weeks.

How the Study Was Run

The set-up was non-randomized, parallel-group and single-blind.

Groups ran in parallel: each of the participants stayed in one arm throughout.

Only one side, usually the participants, was kept unaware of whether IGF-1 LR3 was given.

Those kept unaware of assignments: participant.

It started in 2008-12 with completion listed for 2013-08.

It ran at 1 site in United States.

Its stated primary purpose is other.

What Was Measured

Primary outcome: Percentage With Growth Hormone (GH) Suppression to < 0.4 ng/ml (time frame: Before injection and at time 15, 30, 60, 90, 120 and 180 minutes after rhIGF-1 injection on week 4).

It also tracked 3 secondary outcomes, for example Median Insulin Level in Response to Placebo, OGTT, and rhIGF1 Testing and Median Bioactive IGF-1 Area Under the Curve in Response to Placebo, OGTT, and rhIGF1 Testing.

What This Means in Plain Language

Put simply, this is a not phased, non-randomized trial of IGF-1 LR3 in 28 people.

Its size is small, so on its own it can only give an early look.

The trial is marked completed; results are posted on the registry, and this page does not restate them.

More context: the IGF-1 LR3 compound page, all human trials.