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Osteoprosis in Type 2 Diabetic Patients- a Cohort Study

The recruitment status of this study is unknown. The completion date has passed and the status has not been verified in more than two years.
Verified July 2015 by National Taiwan University Hospital.
Recruitment status was:  Recruiting
Sponsor:
ClinicalTrials.gov Identifier:
NCT01846533
First Posted: May 3, 2013
Last Update Posted: July 30, 2015
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Information provided by (Responsible Party):
National Taiwan University Hospital
May 1, 2013
May 3, 2013
July 30, 2015
May 2013
December 2015   (Final data collection date for primary outcome measure)
Osteoprosis in type 2 diabetic patients- a cohort study [ Time Frame: three years ]
Same as current
Complete list of historical versions of study NCT01846533 on ClinicalTrials.gov Archive Site
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Osteoprosis in Type 2 Diabetic Patients- a Cohort Study
Osteoprosis in Type 2 Diabetic Patients- a Cohort 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.
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.
Observational
Observational Model: Cohort
Time Perspective: Cross-Sectional
Not Provided
Retention:   Samples Without DNA
Description:
CBC/DC & BCS
Probability Sample
type 2 diabetic patients
  • Type 2 Diabetes Mellitus
  • Osteoporosis
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Unknown status
1200
December 2015
December 2015   (Final data collection date for primary outcome measure)
  1. inclusion:40-99 years old with type 2 DM patient
  2. exclusion:organization people
Sexes Eligible for Study: All
40 Years and older   (Adult, Senior)
Yes
Contact information is only displayed when the study is recruiting subjects
Taiwan
 
 
NCT01846533
201212080RINC
No
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National Taiwan University Hospital
National Taiwan University Hospital
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Principal Investigator: Kuo Chin Huang, PhD Department of Family Medicine, National Taiwan University Hospital
National Taiwan University Hospital
July 2015