Type 2 Diabetes MellitusNCT01846533
Osteoprosis in Type 2 Diabetic Patients- a Cohort Study
An observational study of Type 2 Diabetes Mellitus and Osteoporosis, run by National Taiwan University Hospital at 1 site in Taiwan.
Trial summary
Some possible humoural and cellular mechanism for diabetes related osteoporosis/fractures were proposed and summarzied as the following, (1)Diabetes mellitus increases osteoclast function but decreases osteoblast function, thereby leading to accelerated bone loss, osteopenia and osteoporosis. Read more about this study
- Who is it for?
- Ages 40 years and olderHealthy volunteers can take part
- Conditions the study is for
- Type 2 Diabetes Mellitus, Osteoporosis
- How many people
- 1,200 participants
- Where
- 1 siteTaiwan
- Study dates
- May 2013to Dec 2015
- 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 40 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: type 2 diabetic patients
- inclusion:40-99 years old with type 2 DM patient
- exclusion:organization people
Trial locations and contacts
1 site in 1 country.
Taiwan1 site, 1 recruiting
- Recruiting
National Taiwan University Hospital
Taipei, 100
Kuo Chin Huang, PhD, 886-23123456 ext. 66081, bretthuang@ntu.edu.tw
About this study
Some possible humoural and cellular mechanism for diabetes related osteoporosis/fractures were proposed and summarzied as the following, (1)Diabetes mellitus increases osteoclast function but decreases osteoblast function, thereby leading to accelerated bone loss, osteopenia and osteoporosis. (2)DM/hyperglycemia induces production of macrophage colony stimulating factor (MCSF), tumor necrosis factor (TNF)-α and receptor activator of nuclear factor-κB ligand (RANKL), all of which are osteoblast-derived activators of osteoclast proliferation and differentiation. (3) DM/hyperglycemia suppresses osteoblast proliferation and function, in part, by decreasing runtrelated transcription factor (Runx)-2, osteocalcin and osteopontin expressions. (4)Adipogenic differentiation of mesenchymal stem cells is increased as indicated by the overexpression of adipocyte differentiation markers, including peroxisome proliferator-activated receptor (PPAR)-g, adipocyte fatty acid binding protein (aP2), adipsin and resistin. A decrease in neovascularization may further aggravate bone loss. (5)Bone quality is also reduced as a result of advanced glycation end products (AGE) production, which may eventually result in low impact or fragility fractures. DM are associated osteoporosis/fracture. The underlying mechanism, especially of type 2 DM, mandates a DM-osteoporosis cohort to elucidate. In clinical practice, to developed preventive strategies from osteoporotic-fracture is also necessary.
Read the detailed description
It is becoming apparent that both type 1 and type 2 diabetes mellitus are associated with an increased risk for osteoporosis-associated fractures. A meta-analysis by Vestergaard showed that patients with type 1 DM have decreased bone mineral density and increased fracture risk. This study noted a 6.9 relative risk of hip fracture, when the expected relative risk of fracture was only 1.4 based on the BMD. This finding suggests that the increased fracture risk is not entirely accounted for by the lower BMD. It has been demonstrated that the presence of diabetic microvascular complications, including ophthalmic, nephropathic, and neurological, lead to a higher risk of hip fracture in patients with type 1 DM. Unlike patients with type 1 DM, patients with type 2 DM have an average or higher BMD than age-matched controls. However, several studies have demonstrated that patients with type 2 DM have a higher risk of hip, proximal humerus, and foot fractures. Data from the Women's Health Initiative Observational Study indicate that post-menopausal women with diabetes are at an increased risk of hip, foot, and spine fractures, and fractures overall. For a given BMD, diabetic bone appears to be less strong and therefore more likely to fracture. Insulin-like growth factor (IGF)-1, insulin, bone morphogenetic proteins and osteoprotegerin (OPG), serve as anabolic signals to promote bone formation. Among these anabolic mediators, liver-derived IGF-1 is of particular interest since profound growth retardation, small bone size, low BMD and osteoporosis were reported in IGF-1 and IGF-1 receptor deficiencies. Furthermore, insulin was found to directly induce osteogenic action by increasing cell proliferation, differentiation, alkaline phosphatase activity and expression of type Ⅰcollagen and osteocalcin in human osteoblast-like MG-63 cells. Type 1 DM featuring low circulating insulin and IGF-1 levels usually occurs in young children prior to peak bone mass attainment, whereas type 2 DM is common in adults who have already attained peak bone mass.
- Conditions
- Type 2 Diabetes Mellitus, Osteoporosis
- Medical subject headings
- Diabetes Mellitus, Type 2, Osteoporosis
What is being measured
The primary outcome is the main question the study is designed to answer.
Osteoprosis in type 2 diabetic patients- a cohort study
Measured: three years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 May 2013 (estimated)
- Study startMay 2013
- Primary completionDec 2015 (estimated)
- Study completionDec 2015 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Type 2 Diabetes MellitusStudies of the same condition, open and under way.
- More trials run by National Taiwan University HospitalThe 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
- Cohort
- Time perspective
- Cross-sectional
- Enrolment
- 1,200 participants (estimated)
Sponsor and investigators
- Lead sponsor
- National Taiwan University Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Kuo Chin Huang, PhD, Principal investigator, Department of Family Medicine, National Taiwan University Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01846533
- Sponsor's protocol ID
- 201212080RINC
- Status last verified
- Jul 2015
- First submitted
- 1 May 2013
- Last updated
- 30 Jul 2015
- Results posted
- No
- Data monitoring committee
- No
Study at a glance
From the registry record, last updated by the sponsor on 30 Jul 2015. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Osteoprosis in Type 2 Diabetic Patients- a Cohort Study
- ClinicalTrials.gov ID
- NCT01846533
- Acronym / sponsor ID
- 201212080RINC
- Conditions
- Type 2 Diabetes Mellitus, Osteoporosis
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 1,200 participants (estimated)
- Lead sponsor
- National Taiwan University HospitalUniversity, hospital or other
- Study start
- May 2013
- Primary completion
- Dec 2015 (estimated)
- Study completion
- Dec 2015 (estimated)
- First posted
- 3 May 2013 (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.
Some possible humoural and cellular mechanism for diabetes related osteoporosis/fractures were proposed and summarzied as the following, (1)Diabetes mellitus increases osteoclast function but decreases osteoblast function, thereby leading to accelerated bone loss, osteopenia and osteoporosis. (2)DM/hyperglycemia induces production of macrophage colony stimulating factor (MCSF), tumor necrosis factor (TNF)-α and receptor activator of nuclear factor-κB ligand (RANKL), all of which are osteoblast-derived activators of osteoclast proliferation and differentiation. (3) DM/hyperglycemia suppresses osteoblast proliferation and function, in part, by decreasing runtrelated transcription factor (Runx)-2, osteocalcin and osteopontin expressions. (4)Adipogenic differentiation of mesenchymal stem cells is increased as indicated by the overexpression of adipocyte differentiation markers, including peroxisome proliferator-activated receptor (PPAR)-g, adipocyte fatty acid binding protein (aP2), adipsin and resistin. A decrease in neovascularization may further aggravate bone loss. (5)Bone quality is also reduced as a result of advanced glycation end products (AGE) production, which may eventually result in low impact or fragility fractures. DM are associated osteoporosis/fracture. The underlying mechanism, especially of type 2 DM, mandates a DM-osteoporosis cohort to elucidate. In clinical practice, to developed preventive strategies from osteoporotic-fracture is also necessary.
Detailed description
It is becoming apparent that both type 1 and type 2 diabetes mellitus are associated with an increased risk for osteoporosis-associated fractures. A meta-analysis by Vestergaard showed that patients with type 1 DM have decreased bone mineral density and increased fracture risk. This study noted a 6.9 relative risk of hip fracture, when the expected relative risk of fracture was only 1.4 based on the BMD. This finding suggests that the increased fracture risk is not entirely accounted for by the lower BMD. It has been demonstrated that the presence of diabetic microvascular complications, including ophthalmic, nephropathic, and neurological, lead to a higher risk of hip fracture in patients with type 1 DM. Unlike patients with type 1 DM, patients with type 2 DM have an average or higher BMD than age-matched controls. However, several studies have demonstrated that patients with type 2 DM have a higher risk of hip, proximal humerus, and foot fractures. Data from the Women's Health Initiative Observational Study indicate that post-menopausal women with diabetes are at an increased risk of hip, foot, and spine fractures, and fractures overall. For a given BMD, diabetic bone appears to be less strong and therefore more likely to fracture. Insulin-like growth factor (IGF)-1, insulin, bone morphogenetic proteins and osteoprotegerin (OPG), serve as anabolic signals to promote bone formation. Among these anabolic mediators, liver-derived IGF-1 is of particular interest since profound growth retardation, small bone size, low BMD and osteoporosis were reported in IGF-1 and IGF-1 receptor deficiencies. Furthermore, insulin was found to directly induce osteogenic action by increasing cell proliferation, differentiation, alkaline phosphatase activity and expression of type Ⅰcollagen and osteocalcin in human osteoblast-like MG-63 cells. Type 1 DM featuring low circulating insulin and IGF-1 levels usually occurs in young children prior to peak bone mass attainment, whereas type 2 DM is common in adults who have already attained peak bone mass.
Study design
- Observational model
- Cohort
- Time perspective
- Cross-sectional
Who may qualify
- Ages
- 40 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- type 2 diabetic patients
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
Osteoprosis in type 2 diabetic patients- a cohort study
Time frame: three years
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 30 Jul 2015.
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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.
Kuo Chin Huang, PhD principal investigator
Department of Family Medicine, National Taiwan University Hospital
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 Type 2 Diabetes Mellitus and Osteoporosis, run by National Taiwan University Hospital at 1 site in Taiwan.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
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 30 Jul 2015. 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 Taiwan. 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?
Each site lists its own contact: choose the nearest one under Trial locations. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Osteoprosis in type 2 diabetic patients- a cohort study (time frame: three years). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
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 30 Jul 2015.