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CompletedNCT00805207SCORUpdated Aug 1, 2018Results posted

Sex Steroids, Sleep, and Metabolic Dysfunction in Women

An interventional study of Progesterone and testosterone in Polycystic Ovary Syndrome (PCOS), Obstructive Sleep Apnea and Obesity, sponsored by Washington University School of Medicine. Completed at 1 site in United States. Open to participants aged 18 Years to 75 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2018-08-01.

Sponsored by Washington University School of Medicine · Not applicable, Interventional, and Other

Phase
Not applicable
Study type
Interventional
Enrollment
61
Allocation
Non-randomized
Ages
18 Years to 75 Years
Sex
All
01

Study summary

Increased plasma triglyceride concentration is a common feature of the metabolic abnormalities associated with obesity and a major risk factor for cardiovascular disease. Obesity is a major risk factor for two conditions that appear to be increasing in prevalence in women: the polycystic ovary syndrome (PCOS) and sleep disordered breathing. PCOS affects 5-8% of women. Sleep disordered breathing affects up to 10% of women. Obstructive sleep apnea (OSA) is the most common cause for sleep disordered breathing and particularly prevalent in obese women with PCOS (\~50%). Both PCOS and OSA augment the increase in plasma triglyceride (TG) concentration associated with obesity, and the effects of PCOS and OSA on plasma TG concentration appear to be additive. The mechanisms responsible for the adverse effects on plasma TG metabolism are not known. The primary goal of this project, therefore, is to determine the mechanisms responsible for the increase in plasma TG concentration in obese women with PCOS and OSA. It is our general hypothesis that alterations in the hormonal milieu that are characteristic of these two conditions are, at least in part, responsible for the increase in plasma TG concentration in obese women with the conditions. Furthermore, we hypothesize that the hormonal aberrations characteristic of the two conditions are particularly harmful to obese, compared with lean, women.

The effects of PCOS on skeletal muscle protein metabolism are also not known. However, sex hormones are thought to be important regulators of muscle protein turnover suggesting that muscle protein metabolism is likely to be affected by PCOS. We will examine this by determining the effect of individual sex hormones on muscle protein metabolism and hypothesize that testosterone administration will stimulate muscle protein metabolism while estrogen and progesterone administration will inhibit muscle protein metabolism.

02

Conditions studied

  • Polycystic Ovary Syndrome (PCOS)
  • Obstructive Sleep Apnea
  • Obesity

Keywords

  • sleep apnea
  • obese
  • Very-low density lipoprotein (VLDL) metabolism
  • isotope tracer
  • women
03

In context

Polycystic Ovary Syndrome

944 studies on the registry are indexed under Polycystic Ovary Syndrome; 174 are open to participants now.

This study's enrollment of 61 is below the median of 70 across 685 interventional studies indexed under Polycystic Ovary Syndrome.

Browse Polycystic Ovary Syndrome studies →

Lead sponsor

Washington University School of Medicine is the lead sponsor of 1,765 studies on the registry; 271 are open to participants now.

Of its 324 completed or terminated interventional studies of FDA-regulated products, 212 (65%) have results posted.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
18 Years to 75 Years
Sexes eligible
All
Accepts healthy volunteers
Yes

Inclusion criteria

  • Women aged 18-75 years and men 45-75 years
  • Healthy lean, overweight and obese women (BMI 18-40 kg/m2) and obese men (BMI 30-40 kg/m2)
  • Obese women (BMI 30-40 kg/m2) with OSA or PCOS

Exclusion criteria

Exclusion Criteria:

  • Pregnant, lactating, peri- or postmenopausal women will be excluded from the study because of potential confounding influences of these factors and potential ethical concerns (pregnant women)
  • Women taking medications known to affect substrate metabolism and those with evidence of significant organ dysfunction (e.g. impaired glucose tolerance, diabetes mellitus, liver disease, hypo- or hyper-thyroidism) other than PCOS and OSA
  • Severe hypertriglyceridemia (fasting plasma TG concentration >400 mg/dl)
  • Subjects with OSA who have an apnea-hypopnea index (AHI) score >30 (the total number of obstructive events divided by the total hours of sleep) will be excluded and instructed to seek medical care
05

Study design

Phase
Not applicable
Primary purpose
Other
Allocation
Non-randomized
Intervention model
Parallel assignment
Masking
None (open label)
Enrollment
61 participants (actual)

Study arms

  • Experimental
    Progesterone - PCOS

    Women with obesity and polycystic ovary syndrome

    Drug: Progesterone

  • Experimental
    Testosterone - premenopausal women

    Healthy premenopausal women.

    Drug: testosterone

  • Experimental
    Continuous positive airway pressure

    Women and men with obesity and obstructive sleep apnea

    Device: continuous positive airway pressure

  • Experimental
    Glucocorticoid

    Lean and obese healthy women, and obese men

    Drug: glucocorticoid

  • Experimental
    Estrogen

    Postmenopausal women

    Drug: Estrogen

  • Other
    control

    Postmenopausal women - tested before and after no treatment. Duration between before and after testing ranged from 31 to 78 days with an average of 46 days between visits

    Other: Control

  • No intervention
    control - baseline testing only

    Healthy men and women

  • Experimental
    Progesterone - Postmenopausal women

    Postmenopausal women

    Drug: Progesterone

  • Experimental
    Testosterone - Postmenopausal women

    Postmenopausal women

    Drug: testosterone

Interventions

  • DrugProgesterone

    Micronized progesterone, 100 mg/d vaginally. The intervention lasts 70 days in total and consisted of 14 days on treatment, 14 days off treatment, 14 days on treatment, 14 days off treatment and a final 14 days on treatment. Testing is performed before and at the end of the 70 day intervention.

    Also known as: Endometrin

  • Drugtestosterone

    Testosterone gel 1250 ug/d applied transdermally for a total of 21 days. Testing is performed before and at the end of the 21 day intervention.

    Also known as: 1% AndroGel

  • Drugglucocorticoid

    Dexamethasone 0.013 mg/kg fat-free mass daily taken orally for a total of 21 days. Testing is performed before and at the end of the 21 day intervention.

  • Devicecontinuous positive airway pressure

    Breathe through the mask of a continuous positive airway pressure device every night when sleep, for 6 weeks. Testing is performed before and at the end of the 6 week intervention.

  • DrugEstrogen

    Estrogen treatment (100 ug Estradiol daily) administered transdermally by using continuous delivery patches. The intervention lasted 70 days in total and consisted of 14 days on treatment, 14 days off treatment, 14 days on treatment, 14 days off treatment and a final 14 days on treatment.

    Also known as: Estradiol Patch, Mylan Pharmaceuticals Inc.

  • OtherControl

    No treatment with studies performed 31 to 72 days apart

06

What researchers measure

Primary outcomes

  1. Very-Low Density Lipoprotein-Triglyceride (VLDL-TG) Secretion Rate

    VLDL was isolated from plasma by ultracentrifugation with the tracer-to-tracee (TTR) of free glycerol in plasma and glycerol in VLDL-TG determined by gas chromatography-mass spectrometry. The fractional turnover rates of VLDL-TG was determined by fitting the glycerol TTR time courses in plasma and in VLDL-TG to a multicompartmental model. The hepatic (liver) secretion rates of VLDL-TG was calculated by multiplying the fractional turnover rates of VLDL-TG by the of VLDL-TG concentration.

    Time frame: Before and at the end of interventions

Secondary outcomes

  1. Very-Low Density Lipoprotein-Triglyceride (VLDL-TG) Concentration

    VLDL was isolated from plasma by ultracentrifugation with VLDL-TG concentration measured by using a colorimetric enzymatic kit (Sigma-Aldrich, St. Louis, MO).

    Time frame: Before and at the end of the interventions

  2. VLDL-TG Plasma Clearance Rate (Means)

    VLDL was isolated from plasma by ultracentrifugation with the tracer-to-tracee (TTR) of free glycerol in plasma and glycerol in VLDL-TG determined by gas chromatography-mass spectrometry. The fractional turnover rates of VLDL-TG was determined by fitting the glycerol TTR time courses in plasma and in VLDL-TG to a multicompartmental model. The plasma clearance rate of VLDL-TG was calculated by dividing the VLDL-TG secretion rate by the VLDL-TG concentration.

    Time frame: Before and at the end of the interventions

  3. VLDL-TG Plasma Clearance Rate (Medians)

    VLDL was isolated from plasma by ultracentrifugation with the tracer-to-tracee (TTR) of free glycerol in plasma and glycerol in VLDL-TG determined by gas chromatography-mass spectrometry. The fractional turnover rates of VLDL-TG was determined by fitting the glycerol TTR time courses in plasma and in VLDL-TG to a multicompartmental model. The plasma clearance rate of VLDL-TG was calculated by dividing the VLDL-TG secretion rate by the VLDL-TG concentration.

    Time frame: Before and at the end of the interventions

  4. Basal, Postabsorptive Fractional Synthesis Rates of Muscle Protein Synthesis

    The fractional synthesis rate (FSR) of muscle protein synthesis was determined by assessing the incorporation of \[5,5,5-2H3\]leucine into muscle proteins. \[5,5,5-2H3\]leucine was infused for 5 hours with muscle biopsies obtained from the vastus lateralis muscle in the thigh 2 and 5 hours. The leucine tracer-to-tracee ratio (TTR) in muscle protein and the muscle free leucine pool was determined by gas chromatography-mass spectrometry (GCMS) and the FSR of muscle proteins calculated using a standard precursor-product model. The FSR was calculated as %/h, which reflects the percent of all proteins in the muscle that were synthesized (made) per hour.

    Time frame: Before and at the end of the intervention

07

Results

Posted Aug 1, 2018

Participant flow

Participant flow — Overall Study
MilestoneProgesterone - PCOSProgesterone - Postmenopausal WomenTestosterone - Premenopausal WomenTestosterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing Only
Started19126312666
Completed1711629666
Not completed021013000
Withdrew: Protocol violation001000000
Withdrew: Physician decision010001000
Withdrew: Withdrawal by subject010012000

Outcome measures

PrimaryVery-Low Density Lipoprotein-Triglyceride (VLDL-TG) Secretion Rate

VLDL was isolated from plasma by ultracentrifugation with the tracer-to-tracee (TTR) of free glycerol in plasma and glycerol in VLDL-TG determined by gas chromatography-mass spectrometry. The fractional turnover rates of VLDL-TG was determined by fitting the glycerol TTR time courses in plasma and in VLDL-TG to a multicompartmental model. The hepatic (liver) secretion rates of VLDL-TG was calculated by multiplying the fractional turnover rates of VLDL-TG by the of VLDL-TG concentration.

Time frame:
Before and at the end of interventions
Reported as:
Mean · umol/min/L plasma
Very-Low Density Lipoprotein-Triglyceride (VLDL-TG) Secretion Rate
umol/min/L plasmaTestosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing Only
Before3.13 ± 2.112.03 ± 0.354.663.36 ± 1.652.87 ± 0.033.80 ± 1.522.87 ± 0.862.47 ± 0.853.53 ± 2.88
After3.00 ± 1.582.11 ± 0.807.773.24 ± 1.553.94 ± 0.423.42 ± 2.012.94 ± 1.402.57 ± 1.26—
Statistical analysis
  • Testosterone - Premenopausal Women · t-test, 2 sided · p = 0.85
  • Glucocorticoid · t-test, 2 sided · p = 0.70
  • Testosterone - Postmenopausal Women vs Progesterone - Postmenopausal Women vs Estrogen vs Control · ANOVA · p = 0.88 (P-value is the main effect of treatment (i.e., Before vs. After) from ANOVA)VLDL-TG secretion rates were skewed and log transformed prior to performing ANOVA
  • Testosterone - Postmenopausal Women vs Progesterone - Postmenopausal Women vs Estrogen vs Control · ANOVA · p = 0.26 (P-value is the main effect of group (i.e., Testosterone, Progesterone, Estrogen and Control) from ANOVA)VLDL-TG secretion rates were skewed and log transformed prior to performing ANOVA
  • Testosterone - Postmenopausal Women vs Progesterone - Postmenopausal Women vs Estrogen vs Control · ANOVA · p = 0.98 (P value is the group by treatment interaction from the ANOVA)VLDL-TG secretion rates were skewed and log transformed prior to performing ANOVA
SecondaryVery-Low Density Lipoprotein-Triglyceride (VLDL-TG) Concentration

VLDL was isolated from plasma by ultracentrifugation with VLDL-TG concentration measured by using a colorimetric enzymatic kit (Sigma-Aldrich, St. Louis, MO).

Time frame:
Before and at the end of the interventions
Reported as:
Mean · mmol/L
Very-Low Density Lipoprotein-Triglyceride (VLDL-TG) Concentration
mmol/LTestosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing Only
Before0.31 ± 0.290.18 ± 0.090.750.42 ± 0.180.50 ± 0.060.35 ± 0.160.50 ± 0.280.30 ± 0.150.32 ± 0.17
After0.40 ± 0.500.18 ± 0.101.030.44 ± 0.360.64 ± 0.180.33 ± 0.220.35 ± 0.220.28 ± 0.16—
Statistical analysis
  • Testosterone - Premenopausal Women · t-test, 2 sided · p = 0.31
  • Glucocorticoid · t-test, 2 sided · p = 0.82
  • Estrogen vs Control · ANCOVA · p = <0.05
  • Progesterone - Postmenopausal Women vs Control · ANCOVA · p = 0.87
  • Testosterone - Postmenopausal Women vs Control · ANCOVA · p = 0.57
SecondaryVLDL-TG Plasma Clearance Rate (Means)

VLDL was isolated from plasma by ultracentrifugation with the tracer-to-tracee (TTR) of free glycerol in plasma and glycerol in VLDL-TG determined by gas chromatography-mass spectrometry. The fractional turnover rates of VLDL-TG was determined by fitting the glycerol TTR time courses in plasma and in VLDL-TG to a multicompartmental model. The plasma clearance rate of VLDL-TG was calculated by dividing the VLDL-TG secretion rate by the VLDL-TG concentration.

Time frame:
Before and at the end of the interventions
Reported as:
Mean · mL/min
VLDL-TG Plasma Clearance Rate (Means)
mL/minTestosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing Only
Before42.2 ± 16.335.1 ± 16.520.321.2 ± 7.519.1 ± 2.733.8 ± 11.317.4 ± 6.722.6 ± 9.033.1 ± 13.1
After58.1 ± 51.634.5 ± 15.824.624.9 ± 15.320.8 ± 2.834.3 ± 21.925.1 ± 6.123.3 ± 5.0—
Statistical analysis
  • Glucocorticoid · t-test, 2 sided · p = 0.94
  • Estrogen vs Control · ANCOVA · p = <0.05
  • Progesterone - Postmenopausal Women vs Control · ANCOVA · p = 0.53
  • Testosterone - Postmenopausal Women vs Control · ANCOVA · p = 0.23
SecondaryVLDL-TG Plasma Clearance Rate (Medians)

VLDL was isolated from plasma by ultracentrifugation with the tracer-to-tracee (TTR) of free glycerol in plasma and glycerol in VLDL-TG determined by gas chromatography-mass spectrometry. The fractional turnover rates of VLDL-TG was determined by fitting the glycerol TTR time courses in plasma and in VLDL-TG to a multicompartmental model. The plasma clearance rate of VLDL-TG was calculated by dividing the VLDL-TG secretion rate by the VLDL-TG concentration.

Time frame:
Before and at the end of the interventions
Reported as:
Median · mL/min
VLDL-TG Plasma Clearance Rate (Medians)
mL/minTestosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing Only
Before40.6 (33.8 to 52.9)32.1 (23.1 to 47.8)20.320.8 (15.4 to 25.4)19.1 (18.1 to 20.1)35.8 (29.6 to 40.5)14.4 (12.7 to 20.5)19.6 (16.6 to 26.8)33.4 (22.8 to 43.7)
After43.6 (19.4 to 63.5)32.7 (24.4 to 48.1)20.322.8 (15.7 to 34.3)20.8 (19.9 to 21.8)27.4 (21.5 to 38.7)24.2 (22.0 to 29.1)22.3 (19.0 to 26.9)—
Statistical analysis
  • Testosterone - Premenopausal Women · Wilcoxon (Mann-Whitney) · p = 0.80
SecondaryBasal, Postabsorptive Fractional Synthesis Rates of Muscle Protein Synthesis

The fractional synthesis rate (FSR) of muscle protein synthesis was determined by assessing the incorporation of \[5,5,5-2H3\]leucine into muscle proteins. \[5,5,5-2H3\]leucine was infused for 5 hours with muscle biopsies obtained from the vastus lateralis muscle in the thigh 2 and 5 hours. The leucine tracer-to-tracee ratio (TTR) in muscle protein and the muscle free leucine pool was determined by gas chromatography-mass spectrometry (GCMS) and the FSR of muscle proteins calculated using a standard precursor-product model. The FSR was calculated as %/h, which reflects the percent of all proteins in the muscle that were synthesized (made) per hour.

Time frame:
Before and at the end of the intervention
Reported as:
Mean · %/h
Basal, Postabsorptive Fractional Synthesis Rates of Muscle Protein Synthesis
%/hTestosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing Only
Before0.064 ± 0.0230.056 ± 0.0070.0490.054 ± 0.12—0.059 ± 0.0070.063 ± 0.0160.064 ± 0.012—
After0.092 ± 0.0240.079 ± 0.0300.0830.085 ± 0.018—0.061 ± 0.0370.063 ± 0.0260.067 ± 0.011—
Statistical analysis
  • Testosterone - Premenopausal Women · t-test, 2 sided · p = <0.001
  • Testosterone - Postmenopausal Women vs Progesterone - Postmenopausal Women vs Estrogen vs Control · ANOVA · p = <0.01 (P-value is the main effect of treatment (i.e., Before vs. After) from ANOVA)
  • Testosterone - Postmenopausal Women vs Progesterone - Postmenopausal Women vs Estrogen vs Control · ANOVA · p = 0.96 (P-value is the main effect of group (i.e., Testosterone, Progesterone, Estrogen and Control) from ANOVA)
  • Testosterone - Postmenopausal Women vs Progesterone - Postmenopausal Women vs Estrogen vs Control · ANOVA · p = <0.05 (P value is the group by treatment interaction from the ANOVA)
  • Testosterone - Postmenopausal Women · Tukey test · p = <0.01
  • Progesterone - Postmenopausal Women · Tukey test · p = <0.01
  • Estrogen · Tukey test · p = >0.10
  • Control · Tukey test · p = >0.10

Adverse events

Collected over Adverse events were monitored over the following periods; Estrogen = 70 days (consisted of 14 days on treatment, 14 days off treatment, 14 days on treatment, 14 days off treatment and a final 14 days on treatment.); Testosterone = 21 days; continuous positive airway pressure = 6 weeks; Dexamethasone = 21 days; Progesterone = 70 days (consisted of 14 days on, 14 days off, 14 days on, 14 days off and a final 14 days on treatment); Control (no treatment) = 31 to 72 days between testing visits.. Non-serious events are listed at a 0% frequency threshold.

Adverse event summary by group
GroupDeathsSeriousOther
Testosterone - Premenopausal Women0/12 (0%)0/12 (0%)0/12 (0%)
Testosterone - Postmenopausal Women0/6 (0%)0/6 (0%)0/6 (0%)
Progesterone - PCOS0/1 (0%)0/1 (0%)0/3 (0%)
Progesterone - Postmenopausal Women0/9 (0%)0/9 (0%)3/9 (33.3%)
Continuous Positive Airway Pressure0/3 (0%)0/3 (0%)0/3 (0%)
Glucocorticoid0/12 (0%)0/12 (0%)0/12 (0%)
Estrogen0/6 (0%)0/6 (0%)1/6 (16.7%)
Control0/6 (0%)0/6 (0%)0/6 (0%)
Control - Baseline Testing Only0/6 (0%)0/6 (0%)0/6 (0%)
Most frequent other events
Most frequent other events
EventTestosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing Only
AcneSkin and subcutaneous tissue disorders0/120/60/30/90/30/121/60/60/6
Vaginal dischargeReproductive system and breast disorders0/120/60/30/90/30/121/60/60/6
ItchinessSkin and subcutaneous tissue disorders0/120/60/31/90/30/120/60/60/6
ShakingMusculoskeletal and connective tissue disorders0/120/60/31/90/30/120/60/60/6
VomitingGastrointestinal disorders0/120/60/31/90/30/120/60/60/6
DiarrheaGastrointestinal disorders0/120/60/31/90/30/120/60/60/6
Broken ankleMusculoskeletal and connective tissue disorders0/120/60/31/90/30/120/60/60/6

Baseline characteristics

Age, Continuous
Age, Continuous(years)Testosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing OnlyTotal
Mean35 ± 857 ± 622 ± 063 ± 762 ± 1238 ± 1359 ± 1064 ± 641 ± 1549 ± 16
Sex: Female, Male
Sex: Female, Male(Participants)Testosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing OnlyTotal
Female126192966556
Male0000130015
Race (NIH/OMB)
Race (NIH/OMB)(Participants)Testosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing OnlyTotal
American Indian or Alaska Native0000000000
Asian0000010001
Native Hawaiian or Other Pacific Islander0000000000
Black or African American72022300319
White54171866341
More than one race0000000000
Unknown or Not Reported0000000000
Region of Enrollment
Region of Enrollment(participants)Testosterone - Premenopausal WomenTestosterone - Postmenopausal WomenProgesterone - PCOSProgesterone - Postmenopausal WomenContinuous Positive Airway PressureGlucocorticoidEstrogenControlControl - Baseline Testing OnlyTotal
United States1261931266661
08

Study locations

1 site
  • Washington University School of Medicine
    Saint Louis, Missouri 63110, United States
09

References and documents

Publications

  • Wang X, Magkos F, Patterson BW, Reeds DN, Kampelman J, Mittendorfer B. Low-dose dexamethasone administration for 3 weeks favorably affects plasma HDL concentration and composition but does not affect very low-density lipoprotein kinetics. Eur J Endocrinol. 2012 Aug;167(2):217-23. doi: 10.1530/EJE-12-0180. Epub 2012 May 22. PubMed 22619349 ↗
  • Wang X, Smith GI, Patterson BW, Reeds DN, Kampelman J, Magkos F, Mittendorfer B. Testosterone increases the muscle protein synthesis rate but does not affect very-low-density lipoprotein metabolism in obese premenopausal women. Am J Physiol Endocrinol Metab. 2012 Mar 15;302(6):E740-6. doi: 10.1152/ajpendo.00533.2011. Epub 2012 Jan 17. PubMed 22252942 ↗
  • Smith GI, Reeds DN, Okunade AL, Patterson BW, Mittendorfer B. Systemic delivery of estradiol, but not testosterone or progesterone, alters very low density lipoprotein-triglyceride kinetics in postmenopausal women. J Clin Endocrinol Metab. 2014 Jul;99(7):E1306-10. doi: 10.1210/jc.2013-4470. Epub 2014 Apr 2. PubMed 24694337 ↗
  • Smith GI, Yoshino J, Reeds DN, Bradley D, Burrows RE, Heisey HD, Moseley AC, Mittendorfer B. Testosterone and progesterone, but not estradiol, stimulate muscle protein synthesis in postmenopausal women. J Clin Endocrinol Metab. 2014 Jan;99(1):256-65. doi: 10.1210/jc.2013-2835. Epub 2013 Dec 20. PubMed 24203065 ↗
10

Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Aug 1, 2018, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
11

Registry details

Key details

Study ID
NCT00805207
Lead sponsor
Washington University School of Medicine
Responsible party
Sponsor
First posted
Dec 9, 2008
Start date
Sep 2007
Primary completion
Mar 2013
Completion
Mar 2013
Results posted
Aug 1, 2018
Last update
Aug 1, 2018

Study contacts

Bettina Mittendorfer, PhD
principal investigator · Washington University School of Medicine

Oversight

Data monitoring committee
No
View the source record on ClinicalTrials.gov ↗

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