Growth Hormone DeficiencyNCT03878992
Effects of Growth Hormone and IGF-1 on Anabolic Signals and Stem Cell Recruitment in Human Skeletal Muscle
A study testing Genotropin miniquick 0.5 mg, injection in people with Growth Hormone Deficiency and Growth Hormone Treatment, run by University of Aarhus at 1 site in Denmark.
Trial summary
12 adult hypopituitary patients with newly diagnosed Growth hormone (GH)-deficiency will be studied two times. The first examinations will be performed shortly after time of diagnose before initiation of exogenous GH treatment, where each subject will receive a single intravenous bolus of 0.5 mg GH. Read more about this study
- Who is it for?
- Ages 18 to 100 yearsHealthy volunteers can take part
- Conditions the study is for
- Growth Hormone Deficiency, Growth Hormone Treatment
- What is being tested?
- Genotropin miniquick 0.5 mg, injection
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 12 participants
- Where
- 1 siteDenmark
- Study dates
- 30 Apr 2019to 31 Dec 2021
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 100 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Newly diagnosed adult onset growth hormone deficiency
Who cannot join
- Documentation of Growth hormone deficiency for less than three months
- Pregnancy
Trial locations and contacts
1 site in 1 country.
Denmark1 site, 1 recruiting
- Recruiting
Department of Endcrinology
Aarhus N, 8200
Jens Otto L Jørgensen, MD, DMSc, +45 78462015, joj@clin.au.dk
Niels Jessen, MD, Phd, +45 28596352, niels.jessen@biomed.au.dk
About this study
12 adult hypopituitary patients with newly diagnosed Growth hormone (GH)-deficiency will be studied two times. The first examinations will be performed shortly after time of diagnose before initiation of exogenous GH treatment, where each subject will receive a single intravenous bolus of 0.5 mg GH. The examination day will be repeated after prolonged GH replacement therapy (>3 month after treatment initiation).
Read the detailed description
The overarching aim of this project is to investigate the mechanisms underlying loss of muscle mass in adults (sarcopenia) and the therapeutic potential of growth hormone (GH). The underlying hypothesis is that absence of GH and subsequent reduced insulin-like growth factor I (IGF-I) will impair normal proliferation of skeletal muscle stem cells and this is associated with metabolic dysfunction.
GH is an important regulator of substrate metabolism and muscle mass. GH treatment reduces overall fat mass (FM) through lipolytic actions in adipose tissues and decreased adipose tissue triacylglycerol (TAG) synthesis. In skeletal muscle, exogenous GH administration production shifts substrate metabolism from glucose to lipid oxidation. In addition, GH mediates protein anabolic actions by production of IGF-I during sufficient nutrient supply and maintained insulin secretion. Circulating IGF-I is primarily produced in the liver, but animal studies suggest that locally produced autocrine and paracrine IGF-I is sufficient to maintain normal growth.
GH deficiency (GHD) is a rare disorder characterized by the inadequate secretion of GH from the anterior pituitary gland and requires treatment with exogenous GH administration. Cell culture studies demonstrates that GH elicits insulin-like effects in cells deprived of GH. GH exerts its biological effects through binding to site 1 and 2 on the extracellular domain of a preformed GHR dimer. GHR activation initiates auto-phosphorylation of the receptor-associated Janus Kinase 2 (JAK2), which subsequently induces GHR cross-phosphorylation. The insulin-like effects are mediated by tyrosine phosphorylation of downstream targets including insulin receptor substrate-1 (IRS-1) and IRS-2. During physiological conditions, this signaling pathway is inhibited by the actions of a class of proteins known as suppressors of cytokine signaling (SOCSs).
GHD in adults can be acquired as a result of trauma, infection, radiation therapy, or tumor growth within the brain. It is characterized by a number of variable symptoms including reduced energy levels, altered body composition and reduced muscle strength. Satellite cells (SCs), the skeletal muscle stem cells, are essential for muscle regeneration in genetic or autoimmune muscle diseases as well as after ischemic, chemical or mechanical trauma to the myofibers. Furthermore, SCs are the primary source to supply new myonuclei to growing myofibers during non-traumatic mechanical overload. In rats, GH-administration increases number of SCs in cross-sections of muscle fibres22, and fibre type composition in skeletal muscle is altered in animals with GHD. Together these findings indicate an importance of GH and IGF-I stimulation for muscle regeneration.
- Being tested
- Genotropin miniquick 0.5 mg, injection
- Keywords
- Growth hormone, Satellite cells, Metabolism, insulin-like effects
- Medical subject headings
- Dwarfism, Pituitary
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Genotropin miniquick 0.5 mg, injectionDrug
Also called Muscle biopsy, fat biopsy, blood tests, pletysmography
GH will be given as an injection. Muscle biopsy will be obtained from m. vests laterals of the dominant leg. Fat biopsies will be obtained from subcutaneous abdominal fat. Tracers will be given as a bolus followed by continuous infusion for 6 hours. For palmitate tracer the infusion will be for only 1,5 hours followed by a one hour break and then another 1 hour infusion. Blood tests will be drawn from a venous catheter placed on the dorsal side of the hand.
| Study group | Role | What they receive |
|---|---|---|
| GHD | Other | GHD patients will be studied two times - one time before initiation of GH replacement therapy and one time following three months of GH replacement therapy. The two trial days are identical Receives: Drug: Genotropin miniquick 0.5 mg, injection |
What is being measured
The primary outcome is the main question the study is designed to answer.
Phosphorylation of Akt in muscle biopsies
Muscle biopsies will be analysed for phosphorylation of Akt
Measured: Analyses will be performed through study completion, an expected average of 1.5 years
Secondary outcomes (7)
Satellite cell count
The number of Satellite cells per muscle fiber will be analysed on muscle cross sections from muscle biopsies
Measured: Analyses will be performed through study completion, an expected average of 1.5 year
Satellite cell proliferation and differentiation in cell culture
Analyses of satellite cells ability to proliferate and differentiate will be performed on cell culture following fluorescent activated cell sorting. Comparison will be between first and second visit.
Measured: Analyses will be performed through study completion, an expected average of 1.5 year
Strength of muscle
assessed by isokinetic/dynamic measurements using a dynamometer
Measured: Analyses will be performed through study completion, an expected average of 1.5 year
Muscle mass
Qualified by DXA scan
Measured: Analyses will be performed through study completion, an expected average of 1.5 year
Glucose turnover rate
Evaluated through blood samples
Measured: Analyses will be performed through study completion, an expected average of 1.5 year
Fatty acid turn over rate
evaluated through blood samples
Measured: Analyses will be performed through study completion, an expected average of 1.5 year
Urea turnover rate
evaluated by blood samples and urin collection
Measured: Analyses will be performed through study completion, an expected average of 1.5 year
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted18 Mar 2019
- Study start30 Apr 2019
- Primary completion1 Mar 2021 (estimated)
- Study completion31 Dec 2021 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (12)Papers the sponsor has linked to this study.
- Other trials for Growth Hormone DeficiencyStudies of the same condition, open and under way.
- More trials run by University of AarhusThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Intervention model
- Sequential
- Model description
- All participants will be studies two times - one time before initiation of GH replacement therapy and one time following three months of GH replacement therapy. The two times are identical. The trial day includes infusion of tracers (glucose, tyrosine, phenylalanine, urea, palmitate), muscle biopsies, subcutaneous fat biopsies, an intravenous bolus of 0.5 mg GH, indirect calorimetry, plethysmography, blood samples, strength test, DXA scan and spectroscopy of liver and muscle.
- Masking
- None (open label)
- Enrolment
- 12 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Aarhus
- Sponsor type
- University, hospital or other
- Collaborators
- Aarhus University Hospital
- Responsible party
- Sponsor
- Investigators
- Jens Otto Jørgensen, Professor, Study chair, Aarhus University Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03878992
- Sponsor's protocol ID
- GHDSCs
- Status last verified
- Feb 2019
- First submitted
- 7 Mar 2019
- Last updated
- 26 Sep 2019
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No: There is no specific plan to share IPD at the moment. If this should be of interest it will only happen after approval from the local ethics committee
Publications
Zurlo F, Larson K, Bogardus C, Ravussin E. Skeletal muscle metabolism is a major determinant of resting energy expenditure. J Clin Invest. 1990 Nov;86(5):1423-7. doi: 10.1172/JCI114857.
PubMed 2243122DeFronzo RA, Jacot E, Jequier E, Maeder E, Wahren J, Felber JP. The effect of insulin on the disposal of intravenous glucose. Results from indirect calorimetry and hepatic and femoral venous catheterization. Diabetes. 1981 Dec;30(12):1000-7. doi: 10.2337/diab.30.12.1000. No abstract available.
PubMed 7030826Nellemann B, Vendelbo MH, Nielsen TS, Bak AM, Hogild M, Pedersen SB, Bienso RS, Pilegaard H, Moller N, Jessen N, Jorgensen JO. Growth hormone-induced insulin resistance in human subjects involves reduced pyruvate dehydrogenase activity. Acta Physiol (Oxf). 2014 Feb;210(2):392-402. doi: 10.1111/apha.12183. Epub 2013 Nov 22.
PubMed 24148194Salomon F, Cuneo RC, Hesp R, Sonksen PH. The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency. N Engl J Med. 1989 Dec 28;321(26):1797-803. doi: 10.1056/NEJM198912283212605.
PubMed 2687691Rosenbaum M, Gertner JM, Leibel RL. Effects of systemic growth hormone (GH) administration on regional adipose tissue distribution and metabolism in GH-deficient children. J Clin Endocrinol Metab. 1989 Dec;69(6):1274-81. doi: 10.1210/jcem-69-6-1274.
PubMed 2685009Pochini L, Oppedisano F, Indiveri C. Reconstitution into liposomes and functional characterization of the carnitine transporter from renal cell plasma membrane. Biochim Biophys Acta. 2004 Feb 10;1661(1):78-86. doi: 10.1016/j.bbamem.2003.12.001.
PubMed 14967477Ridderstrale M. Signaling mechanism for the insulin-like effects of growth hormone--another example of a classical hormonal negative feedback loop. Curr Drug Targets Immune Endocr Metabol Disord. 2005 Mar;5(1):79-92. doi: 10.2174/1568008053174787.
PubMed 15777207Vahl N, Jorgensen JO, Jurik AG, Christiansen JS. Abdominal adiposity and physical fitness are major determinants of the age associated decline in stimulated GH secretion in healthy adults. J Clin Endocrinol Metab. 1996 Jun;81(6):2209-15. doi: 10.1210/jcem.81.6.8964853.
PubMed 8964853Vahl N, Jorgensen JO, Skjaerbaek C, Veldhuis JD, Orskov H, Christiansen JS. Abdominal adiposity rather than age and sex predicts mass and regularity of GH secretion in healthy adults. Am J Physiol. 1997 Jun;272(6 Pt 1):E1108-16. doi: 10.1152/ajpendo.1997.272.6.E1108.
PubMed 9227458Rasmussen MH, Hvidberg A, Juul A, Main KM, Gotfredsen A, Skakkebaek NE, Hilsted J, Skakkebae NE. Massive weight loss restores 24-hour growth hormone release profiles and serum insulin-like growth factor-I levels in obese subjects. J Clin Endocrinol Metab. 1995 Apr;80(4):1407-15. doi: 10.1210/jcem.80.4.7536210.
PubMed 7536210Meinhardt UJ, Ho KK. Modulation of growth hormone action by sex steroids. Clin Endocrinol (Oxf). 2006 Oct;65(4):413-22. doi: 10.1111/j.1365-2265.2006.02676.x.
PubMed 16984231Ullman M, Oldfors A. Effects of growth hormone on skeletal muscle. I. Studies on normal adult rats. Acta Physiol Scand. 1989 Apr;135(4):531-6. doi: 10.1111/j.1748-1716.1989.tb08612.x.
PubMed 2735197
Study at a glance
From the registry record, last updated by the sponsor on 26 Sep 2019. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effects of Growth Hormone and IGF-1 on Anabolic Signals and Stem Cell Recruitment in Human Skeletal Muscle
- ClinicalTrials.gov ID
- NCT03878992
- Acronym / sponsor ID
- GHDSCs
- Keywords
- Growth hormone, Satellite cells, Metabolism, insulin-like effects
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 12 participants (estimated)
- Lead sponsor
- University of AarhusUniversity, hospital or other
- Collaborators
- Aarhus University Hospital
- Study start
- 30 Apr 2019 (actual)
- Primary completion
- 1 Mar 2021 (estimated)
- Study completion
- 31 Dec 2021 (estimated)
- First posted
- 18 Mar 2019 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
12 adult hypopituitary patients with newly diagnosed Growth hormone (GH)-deficiency will be studied two times. The first examinations will be performed shortly after time of diagnose before initiation of exogenous GH treatment, where each subject will receive a single intravenous bolus of 0.5 mg GH. The examination day will be repeated after prolonged GH replacement therapy (>3 month after treatment initiation).
Detailed description
The overarching aim of this project is to investigate the mechanisms underlying loss of muscle mass in adults (sarcopenia) and the therapeutic potential of growth hormone (GH). The underlying hypothesis is that absence of GH and subsequent reduced insulin-like growth factor I (IGF-I) will impair normal proliferation of skeletal muscle stem cells and this is associated with metabolic dysfunction.
GH is an important regulator of substrate metabolism and muscle mass. GH treatment reduces overall fat mass (FM) through lipolytic actions in adipose tissues and decreased adipose tissue triacylglycerol (TAG) synthesis. In skeletal muscle, exogenous GH administration production shifts substrate metabolism from glucose to lipid oxidation. In addition, GH mediates protein anabolic actions by production of IGF-I during sufficient nutrient supply and maintained insulin secretion. Circulating IGF-I is primarily produced in the liver, but animal studies suggest that locally produced autocrine and paracrine IGF-I is sufficient to maintain normal growth.
GH deficiency (GHD) is a rare disorder characterized by the inadequate secretion of GH from the anterior pituitary gland and requires treatment with exogenous GH administration. Cell culture studies demonstrates that GH elicits insulin-like effects in cells deprived of GH. GH exerts its biological effects through binding to site 1 and 2 on the extracellular domain of a preformed GHR dimer. GHR activation initiates auto-phosphorylation of the receptor-associated Janus Kinase 2 (JAK2), which subsequently induces GHR cross-phosphorylation. The insulin-like effects are mediated by tyrosine phosphorylation of downstream targets including insulin receptor substrate-1 (IRS-1) and IRS-2. During physiological conditions, this signaling pathway is inhibited by the actions of a class of proteins known as suppressors of cytokine signaling (SOCSs).
GHD in adults can be acquired as a result of trauma, infection, radiation therapy, or tumor growth within the brain. It is characterized by a number of variable symptoms including reduced energy levels, altered body composition and reduced muscle strength. Satellite cells (SCs), the skeletal muscle stem cells, are essential for muscle regeneration in genetic or autoimmune muscle diseases as well as after ischemic, chemical or mechanical trauma to the myofibers. Furthermore, SCs are the primary source to supply new myonuclei to growing myofibers during non-traumatic mechanical overload. In rats, GH-administration increases number of SCs in cross-sections of muscle fibres22, and fibre type composition in skeletal muscle is altered in animals with GHD. Together these findings indicate an importance of GH and IGF-I stimulation for muscle regeneration.
Study design
- Primary purpose
- Basic science
- Intervention model
- Sequential
- Masking
- None (open label)
- Number of arms
- 1
- Model description
- All participants will be studies two times - one time before initiation of GH replacement therapy and one time following three months of GH replacement therapy. The two times are identical. The trial day includes infusion of tracers (glucose, tyrosine, phenylalanine, urea, palmitate), muscle biopsies, subcutaneous fat biopsies, an intravenous bolus of 0.5 mg GH, indirect calorimetry, plethysmography, blood samples, strength test, DXA scan and spectroscopy of liver and muscle.
| Arm | Type | Receives |
|---|---|---|
| GHD | Other | Drug: Genotropin miniquick 0.5 mg, injectionGHD patients will be studied two times - one time before initiation of GH replacement therapy and one time following three months of GH replacement therapy. The two trial days are identical |
Who may qualify
- Ages
- 18 to 100 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (1 listed)
- Newly diagnosed adult onset growth hormone deficiency
Key exclusion criteria (2 listed)
- Documentation of Growth hormone deficiency for less than three months
- Pregnancy
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Genotropin miniquick 0.5 mg, injectionAlso: Muscle biopsy, fat biopsy, blood tests, pletysmographyGH will be given as an injection. Muscle biopsy will be obtained from m. vests laterals of the dominant leg. Fat biopsies will be obtained from subcutaneous abdominal fat. Tracers will be given as a bolus followed by continuous infusion for 6 hours. For palmitate tracer the infusion will be for only 1,5 hours followed by a one hour break and then another 1 hour infusion. Blood tests will be drawn from a venous catheter placed on the dorsal side of the hand. | Drug | GHD |
Primary outcome
Phosphorylation of Akt in muscle biopsies
Time frame: Analyses will be performed through study completion, an expected average of 1.5 years
Muscle biopsies will be analysed for phosphorylation of Akt
7 secondary outcomes
Satellite cell count
Time frame: Analyses will be performed through study completion, an expected average of 1.5 year
Satellite cell proliferation and differentiation in cell culture
Time frame: Analyses will be performed through study completion, an expected average of 1.5 year
Strength of muscle
Time frame: Analyses will be performed through study completion, an expected average of 1.5 year
Muscle mass
Time frame: Analyses will be performed through study completion, an expected average of 1.5 year
Glucose turnover rate
Time frame: Analyses will be performed through study completion, an expected average of 1.5 year
Fatty acid turn over rate
Time frame: Analyses will be performed through study completion, an expected average of 1.5 year
Urea turnover rate
Time frame: Analyses will be performed through study completion, an expected average of 1.5 year
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 26 Sep 2019.
- Background: PubMed 2243122Zurlo F, Larson K, Bogardus C, Ravussin E. Skeletal muscle metabolism is a major determinant of resting energy expenditure. J Clin Invest. 1990 Nov;86(5):1423-7. doi: 10.1172/JCI114857.
- Background: PubMed 7030826DeFronzo RA, Jacot E, Jequier E, Maeder E, Wahren J, Felber JP. The effect of insulin on the disposal of intravenous glucose. Results from indirect calorimetry and hepatic and femoral venous catheterization. Diabetes. 1981 Dec;30(12):1000-7. doi: 10.2337/diab.30.12.1000. No abstract available.
- Background: PubMed 24148194Nellemann B, Vendelbo MH, Nielsen TS, Bak AM, Hogild M, Pedersen SB, Bienso RS, Pilegaard H, Moller N, Jessen N, Jorgensen JO. Growth hormone-induced insulin resistance in human subjects involves reduced pyruvate dehydrogenase activity. Acta Physiol (Oxf). 2014 Feb;210(2):392-402. doi: 10.1111/apha.12183. Epub 2013 Nov 22.
- Background: PubMed 2687691Salomon F, Cuneo RC, Hesp R, Sonksen PH. The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency. N Engl J Med. 1989 Dec 28;321(26):1797-803. doi: 10.1056/NEJM198912283212605.
- Background: PubMed 2685009Rosenbaum M, Gertner JM, Leibel RL. Effects of systemic growth hormone (GH) administration on regional adipose tissue distribution and metabolism in GH-deficient children. J Clin Endocrinol Metab. 1989 Dec;69(6):1274-81. doi: 10.1210/jcem-69-6-1274.
- Background: PubMed 14967477Pochini L, Oppedisano F, Indiveri C. Reconstitution into liposomes and functional characterization of the carnitine transporter from renal cell plasma membrane. Biochim Biophys Acta. 2004 Feb 10;1661(1):78-86. doi: 10.1016/j.bbamem.2003.12.001.
- Background: PubMed 15777207Ridderstrale M. Signaling mechanism for the insulin-like effects of growth hormone--another example of a classical hormonal negative feedback loop. Curr Drug Targets Immune Endocr Metabol Disord. 2005 Mar;5(1):79-92. doi: 10.2174/1568008053174787.
- Background: PubMed 8964853Vahl N, Jorgensen JO, Jurik AG, Christiansen JS. Abdominal adiposity and physical fitness are major determinants of the age associated decline in stimulated GH secretion in healthy adults. J Clin Endocrinol Metab. 1996 Jun;81(6):2209-15. doi: 10.1210/jcem.81.6.8964853.
- Background: PubMed 9227458Vahl N, Jorgensen JO, Skjaerbaek C, Veldhuis JD, Orskov H, Christiansen JS. Abdominal adiposity rather than age and sex predicts mass and regularity of GH secretion in healthy adults. Am J Physiol. 1997 Jun;272(6 Pt 1):E1108-16. doi: 10.1152/ajpendo.1997.272.6.E1108.
- Background: PubMed 7536210Rasmussen MH, Hvidberg A, Juul A, Main KM, Gotfredsen A, Skakkebaek NE, Hilsted J, Skakkebae NE. Massive weight loss restores 24-hour growth hormone release profiles and serum insulin-like growth factor-I levels in obese subjects. J Clin Endocrinol Metab. 1995 Apr;80(4):1407-15. doi: 10.1210/jcem.80.4.7536210.
- Background: PubMed 16984231Meinhardt UJ, Ho KK. Modulation of growth hormone action by sex steroids. Clin Endocrinol (Oxf). 2006 Oct;65(4):413-22. doi: 10.1111/j.1365-2265.2006.02676.x.
- Background: PubMed 2735197Ullman M, Oldfors A. Effects of growth hormone on skeletal muscle. I. Studies on normal adult rats. Acta Physiol Scand. 1989 Apr;135(4):531-6. doi: 10.1111/j.1748-1716.1989.tb08612.x.
- Individual participant dataSharing planned: No. There is no specific plan to share IPD at the moment. If this should be of interest it will only happen after approval from the local ethics committee
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Jens Otto Jørgensen, Professor study chair
Aarhus University Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Genotropin miniquick 0.5 mg, injection in people with Growth Hormone Deficiency and Growth Hormone Treatment, run by University of Aarhus at 1 site in Denmark.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 2 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 26 Sep 2019. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Denmark. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Tine B Billeskov, PhD student (+4560169141, tine@clin.au.dk), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Phosphorylation of Akt in muscle biopsies (time frame: Analyses will be performed through study completion, an expected average of 1.5 years). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03878992, which also lists 12 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 26 Sep 2019.