Biologic Effects of Dehydroepiandrosterone (DHEA) in Humans

NCT ID: NCT00099697

Last Updated: 2009-12-11

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

NA

Total Enrollment

56 participants

Study Classification

INTERVENTIONAL

Study Start Date

2001-06-30

Study Completion Date

2004-02-29

Brief Summary

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The purpose of this study is to determine whether DHEA replacement therapy decreases abdominal fat and improves insulin sensitivity.

Detailed Description

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Studies on rats and mice have shown that the adrenal hormone dehydroepiandrosterone (DHEA) reduces abdominal visceral fat and protects against insulin resistance. This study was done to learn if DHEA replacement therapy decreases abdominal obesity and improves insulin action in humans.

Participants were randomly assigned to receive 50 mg per day of DHEA or a placebo at bedtime for 6 months. Participants underwent magnetic resonance imaging (MRI) and oral glucose tolerance tests at the beginning and conclusion of the study. Other tests included measurements of hormones and lipids.

Conditions

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Aging Obesity Insulin Resistance

Keywords

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abdominal fat dehydroepiandrosterone Insulin sensitivity

Study Design

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Allocation Method

RANDOMIZED

Primary Study Purpose

PREVENTION

Blinding Strategy

DOUBLE

Interventions

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DHEA

Intervention Type DRUG

Eligibility Criteria

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Inclusion Criteria

* 65 to 78 years old
* Physically healthy
* Non-smoker
* On stable medications for at least 6 months
* Stable body weight for the past year

Exclusion Criteria

* Serious active medical problems
* Hormone therapy
* Abnormal PSA (prostate specific antigen) in men
Minimum Eligible Age

65 Years

Maximum Eligible Age

78 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

NIH

Sponsor Role collaborator

National Center for Research Resources (NCRR)

NIH

Sponsor Role collaborator

National Institute on Aging (NIA)

NIH

Sponsor Role lead

Principal Investigators

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John O. Holloszy, MD

Role: PRINCIPAL_INVESTIGATOR

Washington University School of Medicine

Dennis T. Villareal, MD

Role: PRINCIPAL_INVESTIGATOR

Washington University School of Medicine

Locations

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Washington University School of Medicine

St Louis, Missouri, United States

Site Status

Countries

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United States

References

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Hansen PA, Han DH, Nolte LA, Chen M, Holloszy JO. DHEA protects against visceral obesity and muscle insulin resistance in rats fed a high-fat diet. Am J Physiol. 1997 Nov;273(5):R1704-8. doi: 10.1152/ajpregu.1997.273.5.R1704.

Reference Type BACKGROUND
PMID: 9374813 (View on PubMed)

Han DH, Hansen PA, Chen MM, Holloszy JO. DHEA treatment reduces fat accumulation and protects against insulin resistance in male rats. J Gerontol A Biol Sci Med Sci. 1998 Jan;53(1):B19-24. doi: 10.1093/gerona/53a.1.b19.

Reference Type BACKGROUND
PMID: 9467418 (View on PubMed)

Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone mineral density and body composition in elderly women and men. Clin Endocrinol (Oxf). 2000 Nov;53(5):561-8. doi: 10.1046/j.1365-2265.2000.01131.x.

Reference Type BACKGROUND
PMID: 11106916 (View on PubMed)

Villareal DT, Holloszy JO. Effect of DHEA on abdominal fat and insulin action in elderly women and men: a randomized controlled trial. JAMA. 2004 Nov 10;292(18):2243-8. doi: 10.1001/jama.292.18.2243.

Reference Type RESULT
PMID: 15536111 (View on PubMed)

Other Identifiers

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5P60AG013629

Identifier Type: NIH

Identifier Source: secondary_id

View Link

5R01AG020076

Identifier Type: NIH

Identifier Source: secondary_id

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5K23RR016191

Identifier Type: NIH

Identifier Source: secondary_id

View Link

3P30DK056341

Identifier Type: NIH

Identifier Source: secondary_id

View Link

5P60DK020579

Identifier Type: NIH

Identifier Source: secondary_id

View Link

2M01RR000036

Identifier Type: NIH

Identifier Source: secondary_id

View Link

AG0013

Identifier Type: -

Identifier Source: org_study_id