Substrate Metabolism, Growth Hormone Signaling (GH), and Insulin Sensitivity During GH and Ketone Bodies Infusion

Status

Completed

Phases

Study type

Interventional

Source

ClinicalTrials.gov

Registry ID

NCT02655263

Enrollment

Registered

2016-01-14

Start date

2016-01-31

Completion date

2017-10-31

Last updated

2017-11-01

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Healthy

Brief summary

Background: Humans naturally produce ketone bodies under daily living conditions. The main ketone bodies are two functioning acids, beta-hydroxybutyric acid (3-OHB) and acetoacetate, and the pH-neutral, but odorous, acetone. In the fed state, level of 3-OHB is suppressed to an almost unmeasurable level while, in the fasted state, it rises to 0.1-0.5 millimoles (mM). Main regulation of ketone synthesis is the abundance of sugars and resulting adaptations in insulin secretion. Thus, ketone bodies are formed when sugar is not readily available and insulin is suppressed. This picture is, to a certain degree, seen in acute inflammatory states and, indeed, during starvation, where level of 3-OHB increases to 5-8 mM. Hypothesis: 1. Ketone bodies changes the insulin sensitivity and substrate metabolism in human subjects 2. Ketone bodies changes the GH signaling in muscle and adipose tissue Aim: The investigators wish to provide knowledge on changes in metabolites and shift in signaling pathways and insulin sensitivity during GH infusion and concomitant ketone bodies infusion among healthy subjects.

Interventions

DRUGSomatropin

Somatropin infusion (Genotropin®)

OTHERKetone bodies

ketone bodies infusion

Study design

Allocation

RANDOMIZED

Intervention model

CROSSOVER

Primary purpose

BASIC_SCIENCE

Masking

SINGLE (Subject)

Eligibility

Sex/Gender

MALE

Age

20 Years to 50 Years

Healthy volunteers

Yes

Inclusion criteria

* healthy men * written consent * body mass index (BMI) 18.5 - 25 * age 20-50 years

Exclusion criteria

* any kind of disease * regular medication

Design outcomes

Primary

Measure	Time frame	Description
Insulin and growth hormone signaling, expressed as CHANGE in phosphorylation of intracellular target proteins in muscle- and fat-tissue.	Muscle and fat biopsies obtained at t1= 9.00 am (60 min) and t2=12.30 am (270 min) on each study day after 0, 4 and 8 weeks (interval of 4 weeks between each of the three study days	Change in phosphorylation of target proteins using Western Blotting (WB)

Secondary

Measure	Time frame	Description
Glucose metabolism	Change in glucose metabolism using glucose tracer from t=0 min - 360 min on each study day after 0, 4 and 8 weeks (interval of 4 weeks between each of the three study days.	Change in glucose metabolism assessed by tracer kinetics on every study day.
Insulin and growth hormone signaling, expressed as CHANGE in messenger ribonucleic acid (mRNA) expression of target genes in muscle- and fat-tissue.	Muscle and fat biopsies obtained at t1= 9.00 am (60 min) and t2=12.30 am (270 min) on each study day after 0, 4 and 8 weeks (interval of 4 weeks between each of the three study days.	Change in mRNA expression of target genes using Polymerase Chain Reaction (PCR).
Investigation of the balance in the autonomic nervous system	Measurement of heart rate variability at t1=10.30 am(150 min) and 12.30 am (270 min) on each study day after 0, 4 and 8 weeks (interval of 4 weeks between each of the three study days.	Heart rate variability (the study of beat-to-beat fluctuations in heart rate).

Countries

Denmark

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026