Effect of NF-кB Dependent Proinflammation on Osteogenic D... | NCT02286128

Studies
Effect of NF-кB Dependent Proinflammation on Osteogenic Differentiation of the Mesenchymal Stem Cells in Type 2 Diabetes

NCT02286128

Sponsor

Chiang Mai University

Status

Completed

Last Update Posted

Jul 12, 2018Actual

Enrollment

75Actual

Phase

Not provided

Conditions

Type 2 Diabetes

Interventions

Not provided

Countries

Thailand

Protocol Section

Identification Module Status Module Sponsor/Collaborators Module Oversight Module Description Module Conditions Module Design Module Arms/Interventions Module Outcomes Module Eligibility Module Contacts/Locations Module References Module IPD Sharing Statement Module

Results Section

Participant Flow Module Baseline Characteristics Module Outcome Measures Module Adverse Events Module More Info Module

Annotation Section

Annotation Module

Document Section

Large Document Module

Derived Section

Miscellaneous Info Module Condition Browse Module Intervention Browse Module

Protocol Section

Identification Module

NCT ID

Results Section

No data available

No data is available for this block.

Annotation Section

Annotation Module

Unposted Annotation

Unposted Responsible Party

Document Section

No data available

No data is available for this block.

Derived Section

Miscellaneous Info Module

Version Holder

Status Module

Record Verification Date

Jul 2018

Overall Recruitment Status or Expanded Access Status

Completed

Last Known Status

Not provided

Delayed Posting

Not provided

Why Stopped

Not provided

Expanded Access Info

Start Date

Nov 2014Actual

Primary Completion Date

May 3, 2018Actual

Completion Date

May 3, 2018Actual

First Submitted Date

Oct 28, 2014

First Submission Date that Met QC Criteria

Nov 5, 2014

First Posted Date

Nov 7, 2014Estimated

Results Waived

Not provided

Results First Submitted Date

Not provided

Results First Submitted that Met QC Criteria

Not provided

Results First Posted Date

Not provided

Certification/Extension (aka Delayed Results) First Submitted Date

Not provided

Certification/Extension First Submitted that Passed QC Review

Not provided

Certification/Extension First Posted Date

Not provided

Last Update Submitted Date

Jul 11, 2018

Last Update Posted Date

Jul 12, 2018Actual

Sponsor/Collaborators Module

Responsible Party, by Official Title

Mattabhorn Phornphutkul, Assistant Professor, Chiang Mai UniversityPrincipal Investigator

Lead Sponsor

Chiang Mai UniversityOTHER

Collaborators

Not provided

Oversight Module

Has Data Monitoring Committee (DMC)

Is FDA Regulated Drug

Not provided

Is FDA Regulated Device

Not provided

Is Unapproved Device

Not provided

Pediatric Postmarket Surveillance of a Device Product

Not provided

Product Exported from US

Not provided

FDAAA801 Violation

Not provided

Description Module

Brief Summary

This study determines whether NF-кB dependent proinflammatory state found in type 2 diabetes yield to a higher RAGE activation in the mesenchymal stem cell, as well as the effects of the proinflammation on osteoblast differentiation impairment and cellular apoptosis in type 2 diabetic patients. This study will compare non-diabetic control subjects and type 2 diabetic patients with metformin monotherapy failure in the aspect of 1) serum markers for NF-кB dependent proinflammatory state and its intracellular signals, 2) osteogenic differentiation and apoptosis of the mesenchymal stem cells, and 3) serum AGE, RAGE and cellular RAGE activation.

Detailed Description

This study aims to explore whether proinflammation in type 2 diabetes is an mechanism underlined higher RAGE activation and osteoblast differentiation defect demonstrated in the MSC of type 2 diabetes, as well as the effects of the proinflammation on cellular differentiation and apoptosis of the MSC. Type 2 diabetes was known to be in proinflammatory state due to NF-кB-dependent cytokine secretion (for example, TNF-α, IL1 and IL6), which in turn contribute to NF-кB upregulation. Because RAGE expression is partly regulated by NF-кB signal, the NF-кB upregulation in proinflammatory state observed in type 2 diabetes may entail RAGE overactivation in this population. Therefore, the proinflammatory state and its correlation to cellular NF-кB-dependent RAGE activation is noteworthy to be determined in the MSC of type 2 diabetes. Furthermore, the effect of proinflammation on differentiation potential and apoptosis of the MSC in type 2 diabetes remains to be elucidated.

Design Module

Study Type

Observational

Number of References to an Expanded Access Study

Not provided

Expanded Access Types

Not provided

Patient Registry

Target Follow-Up Duration

Not provided

Phases

Not provided

Interventional Study Design

Allocation

Not provided

Intervention Model

Biospecimen

Retention

Enrollment

75Actual

Arms/Interventions Module

Arm Groups

Label	Type	Description	Intervention Names
Non-diabetic controls		Age-matched non-diabetic subjects
Type 2 diabetes		Type 2 diabetes with metformin monotherapy failure

Interventions

Not provided

Outcomes Module

Primary Outcomes

Measure	Description	Time Frame
Correlation between NF-кB dependent-proinflammation markers and osteoblast-specific gene expression in the MSC to measure the effects of NF-кB dependent-proinflammation on differentiation potential toward osteoblast in type 2 diabetes.		2-4 weeks

Secondary Outcomes

Measure	Description	Time Frame
Correlation between NF-кB dependent-proinflammation markers and apoptotic marker expression in the MSC to measure effects of NF-кB dependent-proinflammation on cellular apoptosis in type 2 diabetes.		2-4 weeks
Correlation between NF-кB dependent-proinflammation markers and the expression of RAGE and its downstream signals in the MSC to measure effects of NF-кB dependent-proinflammation on cellular RAGE activation in type 2 diabetes.

Other Outcomes

Not provided

Eligibility Module

Eligibility Criteria

Inclusion Criteria:

Patients with type 2 diabetes who has HbA1c higher than 6.5% with metformin monotherapy and age-matched non-diabetes control subjects who signed consent form to be in the study.

Exclusion Criteria:

Patients who use thiazolidinedione, steroid, immunosuppressive medications, antiresorptive agents or anabolic therapy for osteoporosis.
Patients with elevated serum creatinine higher than 1.4 in female and 1.5 in male.
Patients with metastases cancer or hematologic malignancy.

Accepts Healthy Volunteers

Yes

Sex

All

Sex/Gender Based

Not provided

Sex/Gender Description

Not provided

Minimum Age

18 Years

Maximum Age

Not provided

Standard Ages

AdultOlder Adult

Study Population

This study will include 30 non-diabetic control subjects, and 45 type 2 diabetic patients who has HbA1c higher than 6.5% with metformin monotherapy.

Sampling Method

Non-Probability Sample

Contacts/Locations Module

Central Contacts

Not provided

Overall Officials

Name	Affiliation	Role
Mattabhorn Phornphutkul, M.D, Ph.D	Chiang Mai University	Principal Investigator

Locations

Facility	Status	City	State	ZIP	Country	Contacts
Mattabhorn Phornputkul		Chiang Mai		50200	Thailand

IPD Sharing Statement Module

Plan to Share IPD

Description

Not provided

Types

Not provided

Time Frame

Not provided

Access Criteria

Not provided

URL

Not provided

Type	Date	Date Unknown
Release	Nov 23, 2018
Reset	Mar 15, 2019
Release	Jul 25, 2019
Reset	Aug 28, 2019

Submission Tracking

Estimated Results First Submitted Date

Nov 23, 2018

First MCP Posted Date

Not provided

Submission Infos

Release Date	Unrelease Date	Unrelease Date Unknown	Reset Date	MCP Release Number
Nov 23, 2018			Mar 15, 2019
Jul 25, 2019

Condition Browse Module

MeSH Terms

ID	Term
D003924	Diabetes Mellitus, Type 2

Ancestor Terms

ID	Term
D003920	Diabetes Mellitus
D044882	Glucose Metabolism Disorders
D008659	Metabolic Diseases
D009750	Nutritional and Metabolic Diseases

Browse Leaves

Not provided

Browse Branches

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