Alpha Lipoic Acid and Polycystic Ovary Syndrome

NCT ID: NCT00505427

Last Updated: 2013-07-01

Basic Information

• Recruitment Status: COMPLETED
• Clinical Phase: PHASE1
• Total Enrollment: 22 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2006-03-31
• Study Completion Date: 2010-07-31

Brief Summary

The study will recruit 40 subjects with Polycystic Ovary Syndrome (PCOS) as defined by the NIH criteria. The subjects will be pre-screened for insulin sensitivity using fasting insulin and glucose levels and oral glucose tolerance test. The 20 most insulin resistant subjects will undergo measurements of in vivo insulin action by hyperinsulinemic, euglycemic clamp. Body composition will be measured by dual-energy X-ray absorptiometry (DEXA). Plasma lipids and markers of oxidative stress will be measured. They will then receive open label controlled release alpha lipoic acid (CRLA) at 800 mg twice daily for 16 weeks. After treatment hyperinsulinemic euglycemic clamps, DEXA, plasma lipids and markers of oxidative stress will be repeated.

Hypotheses: LA will improve insulin sensitivity in PCOS subjects; LA will reduce oxidative stress, testosterone levels and improve cardiovascular risk factors.

Detailed Description

Insulin resistance commonly occurs in patients with Polycystic Ovary Syndrome (PCOS) and may be responsible for many of the long term complications of PCOS. Patients with PCOS are at increased risk for developing type 2 diabetes and the metabolic syndrome (hypertension, dyslipidemia and cardiovascular disease). Data suggest that oxidative stress contributes to insulin resistance and thus inhibitors of oxidative stress improve insulin action. Alpha Lipoic Acid (LA) is synthesized in the liver and other tissues and is a key component of several mitochondrial enzyme complexes responsible for oxidative glucose metabolism and cellular energy production. When used pharmacologically, LA functions as a safe and effective antioxidant, recycling vitamins C and E,elevating glutathione levels,and lowering reactive oxygen species. Cell culture studies reveal that LA reverses the effects of oxidative stress and improving insulin action. Preliminary clinical data indicate that antioxidants may improve insulin resistance in PCOS patients. We propose, therefore, to study LA's effects on insulin-stimulated glucose uptake (insulin clamp) in a well characterized population of insulin resistant PCOS patients. Because these patients usually present in the adolescent and teenage years, the development of safe, long-term, treatment strategies are needed.

Conditions

Insulin Resistance; Oxidative Stress

Study Design

• Allocation Method: NON_RANDOMIZED
• Intervention Model: SINGLE_GROUP
• Primary Study Purpose: TREATMENT
• Blinding Strategy: NONE

Interventions

Alpha Lipoic Acid

Intervention Type: DIETARY_SUPPLEMENT

Eligibility Criteria

Inclusion Criteria

• PCOS diagnosis
• 18 years of age or older
• Body Mass Index below 35
• Willing to use any form of contraception for the duration of the study

Exclusion Criteria

• Diabetes
• Pregnancy
• Liver or heart disease or other health problems
• Taking medications that affect insulin resistance

• Minimum Eligible Age: 18 Years
• Maximum Eligible Age: 50 Years
• Eligible Sex: FEMALE
• Accepts Healthy Volunteers: No

Sponsors

National Institutes of Health (NIH)

NIH

Sponsor Role: collaborator

University of California, San Francisco

OTHER

Sponsor Role: lead

Responsible Party

Responsibility Role: SPONSOR

Principal Investigators

Umesh Masharani, MD

Role: PRINCIPAL_INVESTIGATOR

University of California, San Francisco

Ira Goldfine, MD

Role: PRINCIPAL_INVESTIGATOR

University of California, San Francisco

Locations

University of California at San Francisco

San Francisco, California, United States

Countries

United States

References

Masharani U, Gjerde C, Evans JL, Youngren JF, Goldfine ID. Effects of controlled-release alpha lipoic acid in lean, nondiabetic patients with polycystic ovary syndrome. J Diabetes Sci Technol. 2010 Mar 1;4(2):359-64. doi: 10.1177/193229681000400218.

Reference Type: DERIVED

PMID: 20307398 (View on PubMed)

Other Identifiers

8476-27691-01

Identifier Type: -

Identifier Source: org_study_id