ObesityaeroghreNCT00486161
Acylated Ghrelin Response to Acute Exercise in Obesity
An observational study of Obesity, run by Istituto Auxologico Italiano at 1 site in Italy.
Trial summary
Ghrelin is a GH-secretagogue gastrointestinal hormone that regulates feeding behavior by interacting directly with hypothalamic centers in concert with other negative and permissive neuromodulators. Read more about this study
- Who is it for?
- Ages 20 to 45 yearsHealthy volunteers can take part
- Conditions the study is for
- Obesity
- How many people
- 16 participants
- Where
- 1 siteItaly
- Study dates
- Mar 2004to Dec 2006
- Phase
- Observational
- 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 20 to 45 years
- All sexes
- Healthy volunteers accepted
- Adult
Who may be able to join
- healthy status
- lean (BMI < 25 kg/m2) and obese subjects (BMI>30 kg/m2)
Who cannot join
- cardiovascular disease
- gastrointestinal disease
- diabetes mellitus
- alcohol consumption (wine or equivalents) > 125 ml Day
- physical inability
Trial locations and contacts
1 site in 1 country.
Italy1 site
IRCCS Istituto Auxologico Italiano, Ospedale San Giuseppe
Piancavallo Di Oggebbio, Verbania, 28921
About this study
Official title: Evaluation of Acylated Ghrelin Response Following Acute Exercise in Relation to Adiposity, Metabolic Homeostasis and Growth Hormone Secretion
Ghrelin is a GH-secretagogue gastrointestinal hormone that regulates feeding behavior by interacting directly with hypothalamic centers in concert with other negative and permissive neuromodulators. Ghrelin is involved in controlling energy balance in the short-term and long-term, and its levels are inversely related to the degree of obesity, insulin-resistance and energy accumulation. Consequently, obesity bears decreased ghrelin levels which increase upon weight loss, energy depletion and long-term exercise programs. Nevertheless, the role of acute exercise on the secretion of the bioactive component of ghrelin is yet unknown in conditions of normal and excessive body weight.
Our study examines acylated and total ghrelin secretion following a cycloergometric exercise test in obese and age- and sex-matched lean subjects to document if ghrelin components change as a function of fat accumulation, insulin homeostasis, growth hormone secretion, non-esterified fatty acid availability and exercise performance. Our study aims at testing the hypothesis that ghrelin components may be regulated by acute exercise, with concentrations at the exercise peak being related to acute metabolic homeostasis. Targetting this purpose may help to clarify ghrelin involvement in acute conditions unrelated to gastrointestinal activities.
Read the detailed description
- Ghrelin is the natural ligand of the hypothalamic GH-secretagogue receptor (GHS-R)-1a (1). Over the time, it has been documented that ghrelin predominantly functions as a central modulator of energy homeostasis via NP-Y and AgRP-containing neurons located in the arcuate nucleus of the hypothalamus (2). It thus promotes the drive to eat and governs long-term energy accumulation; clearly, circulating ghrelin concentrations are related to energy balance based on the following evidences (3):
- ghrelin levels are acutely modulated by food intake and glucose administration
- long-term ghrelin homeostasis reflects adiposity, insulin resistance and chronic exercise
- in fasting and postabsorptive conditions, a negative correlation exists between ghrelin and resting energy expenditure independent of variations in insulin levels, energy intake, body composition or body weight. In summary, circulating ghrelin levels are approximately 30% lower than normal; are inversely related to increasing body fat, leptin and insulin levels; and are far less responsive to post-meal inhibition than in controls (3).
- In the circulation, ghrelin is found as acylated and desacylated peptide. Ser(3)-octanoylation is a prerequisite for ghrelin biological activity (3). Des-octanoyl ghrelin variants have been additionally identified (4,5) and found to exert novel antiapoptotic effects in primary adult and cultured rat cardiomyocytes (6). Using specific immunoassays recognizing active (N-terminus) and total (N- plus C-terminus) ghrelin levels, assessment of circulating ghrelin concentrations helped to further discriminate specific functions of each at the hypothalamic level (7), on insulin sensitivity (8) or after bariatric surgery (9). Also, an association has been documented between obesity and total and acylated ghrelin concentrations, being respectively 30% and 56% lower than normal (10). Our laboratory showed previously that stratification of obese patients by the ratio of measured/predicted resting energy expenditure, allowed to detect a positive relationship between acylated ghrelin levels and the efficiency of energy expenditure (10). Speculatively, this could be interpreted as an obesity-related compensatory mechanism acting to contain the orexigenic signals afferent to the brain.
- Studies on ghrelin responsiveness to cycloergometer exercise, treadmill exercise or long-distance marathons, originally showed no variation of ghrelin secretion (11-13). More recently, significant decrements of ghrelin levels following acute exercise bouts has been observed in elite athletes and their healthy controls, as well as in lean individuals (14, 15). While these findings suggested a link of ghrelin suppression with GH rise on one side and appetite regulation upon exercise on the other, little is known on the metabolic mechanisms regulating ghrelin response to acute exercise in the lean and obese state.
Based on these observations, our comparative study aims at exploring the response of ghrelin components to a standardized maximal exercise test in the lean and obese state, to identify the neuroendocrine and metabolic predictors of ghrelin response in these groups and document if ghrelin components change as a function of fat accumulation, insulin homeostasis, growth hormone secretion, non-esterified fatty acid availability and exercise performance.
- Conditions
- Obesity
- Keywords
- Obesity, Ghrelin, Non-esterified fatty acids, Growth hormone, Insulin, Cycloergometer exercise
- Medical subject headings
- Obesity, Insulin Resistance
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Jun 2007 (estimated)
- Study startMar 2004
- Study completionDec 2006
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (15)Papers the sponsor has linked to this study.
- Other trials for ObesityStudies of the same condition, open and under way.
- More trials run by Istituto Auxologico ItalianoThe 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
- Observational
- Observational model
- Case-control
- Time perspective
- Other
- Enrolment
- 16 participants (actual)
Sponsor and investigators
- Lead sponsor
- Istituto Auxologico Italiano
- Sponsor type
- University, hospital or other
- Investigators
- Paolo Marzullo, MD, PhD, Principal investigator, Division of General Medicine
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00486161
- Sponsor's protocol ID
- 18C403
- Acronym
- aeroghre
- Status last verified
- Jun 2007
- First submitted
- 11 Jun 2007
- Last updated
- 13 Jun 2007
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999 Dec 9;402(6762):656-60. doi: 10.1038/45230.
PubMed 10604470Shintani M, Ogawa Y, Ebihara K, Aizawa-Abe M, Miyanaga F, Takaya K, Hayashi T, Inoue G, Hosoda K, Kojima M, Kangawa K, Nakao K. Ghrelin, an endogenous growth hormone secretagogue, is a novel orexigenic peptide that antagonizes leptin action through the activation of hypothalamic neuropeptide Y/Y1 receptor pathway. Diabetes. 2001 Feb;50(2):227-32. doi: 10.2337/diabetes.50.2.227.
PubMed 11272130van der Lely AJ, Tschop M, Heiman ML, Ghigo E. Biological, physiological, pathophysiological, and pharmacological aspects of ghrelin. Endocr Rev. 2004 Jun;25(3):426-57. doi: 10.1210/er.2002-0029.
PubMed 15180951Ariyasu H, Takaya K, Hosoda H, Iwakura H, Ebihara K, Mori K, Ogawa Y, Hosoda K, Akamizu T, Kojima M, Kangawa K, Nakao K. Delayed short-term secretory regulation of ghrelin in obese animals: evidenced by a specific RIA for the active form of ghrelin. Endocrinology. 2002 Sep;143(9):3341-50. doi: 10.1210/en.2002-220225.
PubMed 12193546Baldanzi G, Filigheddu N, Cutrupi S, Catapano F, Bonissoni S, Fubini A, Malan D, Baj G, Granata R, Broglio F, Papotti M, Surico N, Bussolino F, Isgaard J, Deghenghi R, Sinigaglia F, Prat M, Muccioli G, Ghigo E, Graziani A. Ghrelin and des-acyl ghrelin inhibit cell death in cardiomyocytes and endothelial cells through ERK1/2 and PI 3-kinase/AKT. J Cell Biol. 2002 Dec 23;159(6):1029-37. doi: 10.1083/jcb.200207165. Epub 2002 Dec 16.
PubMed 12486113Ghigo E, Broglio F, Arvat E, Maccario M, Papotti M, Muccioli G. Ghrelin: more than a natural GH secretagogue and/or an orexigenic factor. Clin Endocrinol (Oxf). 2005 Jan;62(1):1-17. doi: 10.1111/j.1365-2265.2004.02160.x.
PubMed 15638864St-Pierre DH, Karelis AD, Coderre L, Malita F, Fontaine J, Mignault D, Brochu M, Bastard JP, Cianflone K, Doucet E, Imbeault P, Rabasa-Lhoret R. Association of acylated and nonacylated ghrelin with insulin sensitivity in overweight and obese postmenopausal women. J Clin Endocrinol Metab. 2007 Jan;92(1):264-9. doi: 10.1210/jc.2006-1603. Epub 2006 Oct 24.
PubMed 17062757Korner J, Bessler M, Cirilo LJ, Conwell IM, Daud A, Restuccia NL, Wardlaw SL. Effects of Roux-en-Y gastric bypass surgery on fasting and postprandial concentrations of plasma ghrelin, peptide YY, and insulin. J Clin Endocrinol Metab. 2005 Jan;90(1):359-65. doi: 10.1210/jc.2004-1076. Epub 2004 Oct 13.
PubMed 15483088Marzullo P, Verti B, Savia G, Walker GE, Guzzaloni G, Tagliaferri M, Di Blasio A, Liuzzi A. The relationship between active ghrelin levels and human obesity involves alterations in resting energy expenditure. J Clin Endocrinol Metab. 2004 Feb;89(2):936-9. doi: 10.1210/jc.2003-031328.
PubMed 14764817Dall R, Kanaley J, Hansen TK, Moller N, Christiansen JS, Hosoda H, Kangawa K, Jorgensen JO. Plasma ghrelin levels during exercise in healthy subjects and in growth hormone-deficient patients. Eur J Endocrinol. 2002 Jul;147(1):65-70. doi: 10.1530/eje.0.1470065.
PubMed 12088921Schmidt A, Maier C, Schaller G, Nowotny P, Bayerle-Eder M, Buranyi B, Luger A, Wolzt M. Acute exercise has no effect on ghrelin plasma concentrations. Horm Metab Res. 2004 Mar;36(3):174-7. doi: 10.1055/s-2004-814342.
PubMed 15057671Kraemer RR, Durand RJ, Acevedo EO, Johnson LG, Kraemer GR, Hebert EP, Castracane VD. Rigorous running increases growth hormone and insulin-like growth factor-I without altering ghrelin. Exp Biol Med (Maywood). 2004 Mar;229(3):240-6. doi: 10.1177/153537020422900304.
PubMed 14988516Vestergaard ET, Dall R, Lange KH, Kjaer M, Christiansen JS, Jorgensen JO. The ghrelin response to exercise before and after growth hormone administration. J Clin Endocrinol Metab. 2007 Jan;92(1):297-303. doi: 10.1210/jc.2006-1435. Epub 2006 Oct 10.
PubMed 17032714Broom DR, Stensel DJ, Bishop NC, Burns SF, Miyashita M. Exercise-induced suppression of acylated ghrelin in humans. J Appl Physiol (1985). 2007 Jun;102(6):2165-71. doi: 10.1152/japplphysiol.00759.2006. Epub 2007 Mar 8.
PubMed 17347386Marzullo P, Salvadori A, Brunani A, Verti B, Walker GE, Fanari P, Tovaglieri I, De Medici C, Savia G, Liuzzi A. Acylated ghrelin decreases during acute exercise in the lean and obese state. Clin Endocrinol (Oxf). 2008 Dec;69(6):970-1. doi: 10.1111/j.1365-2265.2008.03275.x. Epub 2008 Apr 14. No abstract available.
PubMed 18419786
Study at a glance
From the registry record, last updated by the sponsor on 13 Jun 2007. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Evaluation of Acylated Ghrelin Response Following Acute Exercise in Relation to Adiposity, Metabolic Homeostasis and Growth Hormone Secretion
- ClinicalTrials.gov ID
- NCT00486161
- Acronym / sponsor ID
- aeroghre / 18C403
- Conditions
- Obesity
- Keywords
- Obesity, Ghrelin, Non-esterified fatty acids, Growth hormone, Insulin, Cycloergometer exercise
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 16 participants (actual)
- Lead sponsor
- Istituto Auxologico ItalianoUniversity, hospital or other
- Study start
- Mar 2004
- Study completion
- Dec 2006 (actual)
- First posted
- 13 Jun 2007 (estimated)
- 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.
Ghrelin is a GH-secretagogue gastrointestinal hormone that regulates feeding behavior by interacting directly with hypothalamic centers in concert with other negative and permissive neuromodulators. Ghrelin is involved in controlling energy balance in the short-term and long-term, and its levels are inversely related to the degree of obesity, insulin-resistance and energy accumulation. Consequently, obesity bears decreased ghrelin levels which increase upon weight loss, energy depletion and long-term exercise programs. Nevertheless, the role of acute exercise on the secretion of the bioactive component of ghrelin is yet unknown in conditions of normal and excessive body weight.
Our study examines acylated and total ghrelin secretion following a cycloergometric exercise test in obese and age- and sex-matched lean subjects to document if ghrelin components change as a function of fat accumulation, insulin homeostasis, growth hormone secretion, non-esterified fatty acid availability and exercise performance. Our study aims at testing the hypothesis that ghrelin components may be regulated by acute exercise, with concentrations at the exercise peak being related to acute metabolic homeostasis. Targetting this purpose may help to clarify ghrelin involvement in acute conditions unrelated to gastrointestinal activities.
Detailed description
- Ghrelin is the natural ligand of the hypothalamic GH-secretagogue receptor (GHS-R)-1a (1). Over the time, it has been documented that ghrelin predominantly functions as a central modulator of energy homeostasis via NP-Y and AgRP-containing neurons located in the arcuate nucleus of the hypothalamus (2). It thus promotes the drive to eat and governs long-term energy accumulation; clearly, circulating ghrelin concentrations are related to energy balance based on the following evidences (3):
- ghrelin levels are acutely modulated by food intake and glucose administration
- long-term ghrelin homeostasis reflects adiposity, insulin resistance and chronic exercise
- in fasting and postabsorptive conditions, a negative correlation exists between ghrelin and resting energy expenditure independent of variations in insulin levels, energy intake, body composition or body weight. In summary, circulating ghrelin levels are approximately 30% lower than normal; are inversely related to increasing body fat, leptin and insulin levels; and are far less responsive to post-meal inhibition than in controls (3).
- In the circulation, ghrelin is found as acylated and desacylated peptide. Ser(3)-octanoylation is a prerequisite for ghrelin biological activity (3). Des-octanoyl ghrelin variants have been additionally identified (4,5) and found to exert novel antiapoptotic effects in primary adult and cultured rat cardiomyocytes (6). Using specific immunoassays recognizing active (N-terminus) and total (N- plus C-terminus) ghrelin levels, assessment of circulating ghrelin concentrations helped to further discriminate specific functions of each at the hypothalamic level (7), on insulin sensitivity (8) or after bariatric surgery (9). Also, an association has been documented between obesity and total and acylated ghrelin concentrations, being respectively 30% and 56% lower than normal (10). Our laboratory showed previously that stratification of obese patients by the ratio of measured/predicted resting energy expenditure, allowed to detect a positive relationship between acylated ghrelin levels and the efficiency of energy expenditure (10). Speculatively, this could be interpreted as an obesity-related compensatory mechanism acting to contain the orexigenic signals afferent to the brain.
- Studies on ghrelin responsiveness to cycloergometer exercise, treadmill exercise or long-distance marathons, originally showed no variation of ghrelin secretion (11-13). More recently, significant decrements of ghrelin levels following acute exercise bouts has been observed in elite athletes and their healthy controls, as well as in lean individuals (14, 15). While these findings suggested a link of ghrelin suppression with GH rise on one side and appetite regulation upon exercise on the other, little is known on the metabolic mechanisms regulating ghrelin response to acute exercise in the lean and obese state.
Based on these observations, our comparative study aims at exploring the response of ghrelin components to a standardized maximal exercise test in the lean and obese state, to identify the neuroendocrine and metabolic predictors of ghrelin response in these groups and document if ghrelin components change as a function of fat accumulation, insulin homeostasis, growth hormone secretion, non-esterified fatty acid availability and exercise performance.
Study design
- Observational model
- Case-control
- Time perspective
- Other
Who may qualify
- Ages
- 20 to 45 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (2 listed)
- healthy status
- lean (BMI < 25 kg/m2) and obese subjects (BMI>30 kg/m2)
Key exclusion criteria (5 listed)
- cardiovascular disease
- gastrointestinal disease
- diabetes mellitus
- alcohol consumption (wine or equivalents) > 125 ml Day
- physical inability
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 13 Jun 2007.
- Background: PubMed 10604470Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999 Dec 9;402(6762):656-60. doi: 10.1038/45230.
- Background: PubMed 11272130Shintani M, Ogawa Y, Ebihara K, Aizawa-Abe M, Miyanaga F, Takaya K, Hayashi T, Inoue G, Hosoda K, Kojima M, Kangawa K, Nakao K. Ghrelin, an endogenous growth hormone secretagogue, is a novel orexigenic peptide that antagonizes leptin action through the activation of hypothalamic neuropeptide Y/Y1 receptor pathway. Diabetes. 2001 Feb;50(2):227-32. doi: 10.2337/diabetes.50.2.227.
- Background: PubMed 15180951van der Lely AJ, Tschop M, Heiman ML, Ghigo E. Biological, physiological, pathophysiological, and pharmacological aspects of ghrelin. Endocr Rev. 2004 Jun;25(3):426-57. doi: 10.1210/er.2002-0029.
- Background: PubMed 12193546Ariyasu H, Takaya K, Hosoda H, Iwakura H, Ebihara K, Mori K, Ogawa Y, Hosoda K, Akamizu T, Kojima M, Kangawa K, Nakao K. Delayed short-term secretory regulation of ghrelin in obese animals: evidenced by a specific RIA for the active form of ghrelin. Endocrinology. 2002 Sep;143(9):3341-50. doi: 10.1210/en.2002-220225.
- Background: PubMed 12486113Baldanzi G, Filigheddu N, Cutrupi S, Catapano F, Bonissoni S, Fubini A, Malan D, Baj G, Granata R, Broglio F, Papotti M, Surico N, Bussolino F, Isgaard J, Deghenghi R, Sinigaglia F, Prat M, Muccioli G, Ghigo E, Graziani A. Ghrelin and des-acyl ghrelin inhibit cell death in cardiomyocytes and endothelial cells through ERK1/2 and PI 3-kinase/AKT. J Cell Biol. 2002 Dec 23;159(6):1029-37. doi: 10.1083/jcb.200207165. Epub 2002 Dec 16.
- Background: PubMed 15638864Ghigo E, Broglio F, Arvat E, Maccario M, Papotti M, Muccioli G. Ghrelin: more than a natural GH secretagogue and/or an orexigenic factor. Clin Endocrinol (Oxf). 2005 Jan;62(1):1-17. doi: 10.1111/j.1365-2265.2004.02160.x.
- Background: PubMed 17062757St-Pierre DH, Karelis AD, Coderre L, Malita F, Fontaine J, Mignault D, Brochu M, Bastard JP, Cianflone K, Doucet E, Imbeault P, Rabasa-Lhoret R. Association of acylated and nonacylated ghrelin with insulin sensitivity in overweight and obese postmenopausal women. J Clin Endocrinol Metab. 2007 Jan;92(1):264-9. doi: 10.1210/jc.2006-1603. Epub 2006 Oct 24.
- Background: PubMed 15483088Korner J, Bessler M, Cirilo LJ, Conwell IM, Daud A, Restuccia NL, Wardlaw SL. Effects of Roux-en-Y gastric bypass surgery on fasting and postprandial concentrations of plasma ghrelin, peptide YY, and insulin. J Clin Endocrinol Metab. 2005 Jan;90(1):359-65. doi: 10.1210/jc.2004-1076. Epub 2004 Oct 13.
- Background: PubMed 14764817Marzullo P, Verti B, Savia G, Walker GE, Guzzaloni G, Tagliaferri M, Di Blasio A, Liuzzi A. The relationship between active ghrelin levels and human obesity involves alterations in resting energy expenditure. J Clin Endocrinol Metab. 2004 Feb;89(2):936-9. doi: 10.1210/jc.2003-031328.
- Background: PubMed 12088921Dall R, Kanaley J, Hansen TK, Moller N, Christiansen JS, Hosoda H, Kangawa K, Jorgensen JO. Plasma ghrelin levels during exercise in healthy subjects and in growth hormone-deficient patients. Eur J Endocrinol. 2002 Jul;147(1):65-70. doi: 10.1530/eje.0.1470065.
- Background: PubMed 15057671Schmidt A, Maier C, Schaller G, Nowotny P, Bayerle-Eder M, Buranyi B, Luger A, Wolzt M. Acute exercise has no effect on ghrelin plasma concentrations. Horm Metab Res. 2004 Mar;36(3):174-7. doi: 10.1055/s-2004-814342.
- Background: PubMed 14988516Kraemer RR, Durand RJ, Acevedo EO, Johnson LG, Kraemer GR, Hebert EP, Castracane VD. Rigorous running increases growth hormone and insulin-like growth factor-I without altering ghrelin. Exp Biol Med (Maywood). 2004 Mar;229(3):240-6. doi: 10.1177/153537020422900304.
- Institution's description of scientific activitiesLink provided by the sponsor.
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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.
Paolo Marzullo, MD, PhD principal investigator
Division of General Medicine
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Obesity, run by Istituto Auxologico Italiano at 1 site in Italy.
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 2 inclusion and 5 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: finished, as of the sponsor's last update on 13 Jun 2007. 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 Italy. 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?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00486161, which also lists 15 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 13 Jun 2007.