Osteoprosis in Type 2 Diabetic Patients- a Cohort Study

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. Identifier: NCT01846533
Recruitment Status : Unknown
Verified July 2015 by National Taiwan University Hospital.
Recruitment status was:  Recruiting
First Posted : May 3, 2013
Last Update Posted : July 30, 2015
Information provided by (Responsible Party):
National Taiwan University Hospital

Brief 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. (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.

Condition or disease
Type 2 Diabetes Mellitus Osteoporosis

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 Type : Observational
Estimated Enrollment : 1200 participants
Observational Model: Cohort
Time Perspective: Cross-Sectional
Official Title: Osteoprosis in Type 2 Diabetic Patients- a Cohort Study
Study Start Date : May 2013
Estimated Primary Completion Date : December 2015
Estimated Study Completion Date : December 2015

Resource links provided by the National Library of Medicine

MedlinePlus related topics: Osteoporosis

Primary Outcome Measures :
  1. Osteoprosis in type 2 diabetic patients- a cohort study [ Time Frame: three years ]

Biospecimen Retention:   Samples Without DNA

Information from the National Library of Medicine

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Ages Eligible for Study:   40 Years and older   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes
Sampling Method:   Probability Sample
Study Population
type 2 diabetic patients
  1. inclusion:40-99 years old with type 2 DM patient
  2. exclusion:organization people

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT01846533

National Taiwan University Hospital Recruiting
Taipei, Taiwan, 100
Contact: Kuo Chin Huang, PhD    886-23123456 ext 66081   
Sponsors and Collaborators
National Taiwan University Hospital
Principal Investigator: Kuo Chin Huang, PhD Department of Family Medicine, National Taiwan University Hospital

Responsible Party: National Taiwan University Hospital Identifier: NCT01846533     History of Changes
Other Study ID Numbers: 201212080RINC
First Posted: May 3, 2013    Key Record Dates
Last Update Posted: July 30, 2015
Last Verified: July 2015

Additional relevant MeSH terms:
Diabetes Mellitus
Diabetes Mellitus, Type 2
Glucose Metabolism Disorders
Metabolic Diseases
Endocrine System Diseases
Bone Diseases, Metabolic
Bone Diseases
Musculoskeletal Diseases