NCT01846533

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.

Trial Health

43
At Risk

Trial Health Score

Automated assessment based on enrollment pace, timeline, and geographic reach

Trial has exceeded expected completion date
Enrollment
1,200

participants targeted

Target at P75+ for all trials

Timeline
Completed

Started May 2013

Typical duration for all trials

Geographic Reach
1 country

1 active site

Status
unknown

Health score is calculated from publicly available data and should be used for screening purposes only.

Trial Relationships

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Study Timeline

Key milestones and dates

First Submitted

Initial submission to the registry

May 1, 2013

Completed
Same day until next milestone

Study Start

First participant enrolled

May 1, 2013

Completed
2 days until next milestone

First Posted

Study publicly available on registry

May 3, 2013

Completed
2.6 years until next milestone

Primary Completion

Last participant's last visit for primary outcome

December 1, 2015

Completed
Same day until next milestone

Study Completion

Last participant's last visit for all outcomes

December 1, 2015

Completed
Last Updated

July 30, 2015

Status Verified

July 1, 2015

Enrollment Period

2.6 years

First QC Date

May 1, 2013

Last Update Submit

July 28, 2015

Conditions

Outcome Measures

Primary Outcomes (1)

  • Osteoprosis in type 2 diabetic patients- a cohort study

    three years

Eligibility Criteria

Age40 Years+
Sexall
Healthy VolunteersYes
Age GroupsAdult (18-64), Older Adult (65+)
Sampling MethodProbability Sample
Study Population

type 2 diabetic patients

Contact the study team to confirm eligibility.

Sponsors & Collaborators

Study Sites (1)

National Taiwan University Hospital

Taipei, 100, Taiwan

RECRUITING

Biospecimen

Retention: SAMPLES WITHOUT DNA

CBC/DC \& BCS

MeSH Terms

Conditions

Diabetes Mellitus, Type 2Osteoporosis

Condition Hierarchy (Ancestors)

Diabetes MellitusGlucose Metabolism DisordersMetabolic DiseasesNutritional and Metabolic DiseasesEndocrine System DiseasesBone Diseases, MetabolicBone DiseasesMusculoskeletal Diseases

Study Officials

  • Kuo Chin Huang, PhD

    Department of Family Medicine, National Taiwan University Hospital

    PRINCIPAL INVESTIGATOR

Study Design

Study Type
observational
Observational Model
COHORT
Time Perspective
CROSS SECTIONAL
Sponsor Type
OTHER
Responsible Party
SPONSOR

Study Record Dates

First Submitted

May 1, 2013

First Posted

May 3, 2013

Study Start

May 1, 2013

Primary Completion

December 1, 2015

Study Completion

December 1, 2015

Last Updated

July 30, 2015

Record last verified: 2015-07

Locations