TerminatedNCT01472445Updated Apr 23, 2026Results posted

Vitamin D and Breast Cancer: Does Weight Make a Difference?

A Phase 2 interventional study of Vitamin D in Breast Cancer, sponsored by Melinda Telli. Terminated at 1 site in United States. Open to female participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2026-04-23.

Sponsored by Melinda Telli · Phase 2, Interventional, and Basic science

Why this study was terminated

Slow accrual

Phase: Phase 2
Study type: Interventional
Enrollment: 41
Allocation: Randomized
Ages: 18 Years and older
Sex: Female

Study summary

This is a research study of the effect of Vitamin D on breast cancer. We hope to learn whether Vitamin D can change characteristics of certain genes in a breast cancer tumor that affect its growth. We believe some of these characteristics may be influenced by body weight.

Read the detailed description

Vitamin D3 (cholecalciferol, colecalciferol) is one of type of vitamin D which is made by the skin when exposed to sunlight; it is also found in some foods and can be taken as a dietary supplement. It is used to treat and prevent vitamin D deficiency and associated diseases, including rickets. Vitamin D3 may have a role obesity and cancer biology. In the body, Vitamin D3 is metabolized to the active form 1,25-dihydroxycholecalciferol (calcitriol, 1,25-(OH)2vitamin D3).

This protocol is a randomized, controlled, and blinded clinical trial in obese and non-obese breast cancer patients in whom the effects of vitamin D supplementation will be evaluated in the neoadjuvant setting. Changes in biomarker expression levels in blood will be assessed from baseline to post-treatment (post-surgery).

Per protocol (see title), the treatment groups are defined as those participants with body mass index (BMI) ≤ 25 ("non-obese") and > 25 ("obese"). Within each treatment group, dose of Vitamin D3 was stratified between 400 IU/day (control) and 10,000 IU/day (experimental). All analyses were typically conducted between BMI cohorts stratified by Vitamin D3 dose.

Protocol Primary Objective: "To determine whether dietary vitamin D can reverse the negative effects of obesity and insulin resistance as reflected by changes in breast cancer gene expression patterns in obese and non obese subjects diagnosed with breast cancer."

Protocol Secondary Objectives: "To determine whether dietary vitamin D can reverse the negative effects of obesity and insulin resistance as reflected by serum biomarkers of insulin resistance and adipokine secretion in obese and non obese subjects diagnosed with breast cancer."

The following markers will be part of this study.

Insulin-like growth factor-binding protein 3 (IGFBP-3) is a Vitamin D target, and the most abundant of 6 different IGFBPs. The insulin-like growth factors 1 and 2 (IGF-1 and IGF-2) binds to IGFBP-3 with high affinity, which helps lengthen the half-life of circulating IGFs in all tissues. Through this binding action, IGFBP-3 exerts anti-proliferative effects by blocking the ability of IGFs to activate the IGF-1 receptor (IGF1R, which stimulates cell proliferation). IGFBP-3 levels were assessed on the basis of mRNA levels.
p21 [also known as p21Cip1; p21Waf1, cyclin-dependent kinase inhibitor 1 (CDKI1) or cyclin-dependent kinase (CDK)-interacting protein 1 (CDKIP1)] is the primary mediator of p53-dependent cell cycle arrest in response to DNA damage, and is a proliferation; apoptosis; and invasion biomarker. p21 is primarily associated with inhibition of CDK2, but is capable of inhibiting all cyclin/CDK complexes. p21 3 levels were assessed on the basis of mRNA levels.
Matrix metalloproteinase-11 (MMP-11), aka Stromelysin-3 (SL-3), is involved in the breakdown of extracellular matrix in the disease processes of metastasis and arthritis, as well as various normal physiological processes, such as embryonic development, reproduction, and tissue remodeling. MMP-11 levels were assessed on the basis of mRNA levels.
Ki-67 ("Antigen Identified By Monoclonal Antibody Ki-67", Antigen Ki67) is the protein produced by the gene MKI67, and is a nuclear protein that is associated with cellular proliferation and ribosomal RNA transcription. Ki-67 is a recognized biomarker for mitotic rate and cellular, but is absent in resting (quiescent) cells (Stage G0). In breast cancer, Ki67 identifies a subset of patients with ER-positive breast cancer that is highly proliferative, and who derive greater benefit from adjuvant chemotherapy. MKI67 levels were assessed on the basis of mRNA levels.
ESR1 is the gene encoding estrogen receptor alpha (ERα), also known as NR3A1 (nuclear receptor subfamily 3, group A, member 1), and is a nuclear receptor that is activated by the sex hormone estrogen. ERα plays a role in the physiological development and function of a variety of organ systems to varying degrees, including the reproductive, central nervous, skeletal, and cardiovascular systems. Genetic polymorphisms in ESR1 have been associated with breast cancer. ESR1 levels were assessed on the basis of mRNA levels.
Leptin is a stimulator of adipose stromal cell estrogen synthesis and a breast cancer growth promoter. Serum levels of leptin correlate with body mass index (BMI, a measure of obesity) and breast cancer risk. Leptin receptors are expressed by breast cancer cells and leptin can promote (regulate) breast cancer cell proliferation. Leptin levels were measured by Western blot or immunohistochemical (IHC) methodology.
Adiponectin inhibits breast cancer growth. Adiponectin receptors are expressed by breast cancer cells and adiponectin can inhibit (regulate) breast cancer cell proliferation by stimulating apoptosis in estrogen receptor (ER)+ Breast cancer cells and suppressing estrogen-stimulated cell growth. Adiponectin levels were measured by Western blot or immunohistochemical (IHC) methodology.
Homeostasis Model of Assessment - Insulin Resistance (HOMA-IR) is a standard determination of insulin resistance based on fasting insulin and glucose levels.
cRP (C-reactive protein) is an inflammation marker produced by the liver. High levels of CRP in the blood are indicative of a wide variety of conditions, including cancer. cRP levels were measured by Western blot or immunohistochemical (IHC) methodology.

Conditions studied

Breast Cancer

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Keywords

Vitamin D
Obesity

In context

Breast Neoplasms

12,544 studies on the registry are indexed under Breast Neoplasms; 2,892 are open to participants now.

This study's enrollment of 41 is below the median of 72 across 9,303 interventional studies indexed under Breast Neoplasms.

Browse Breast Neoplasms studies →

Lead sponsor

Melinda Telli is the lead sponsor of 2 studies on the registry; none are open to participants now.

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

Who can participate

Ages eligible: 18 Years and older
Sexes eligible: Female
Accepts healthy volunteers: No

Inclusion criteria

Women who have undergone a core needle biopsy demonstrating an operable breast cancer whom have not yet had any further therapy.
No prior therapy for breast cancer.
Age 18 years or older.
Any menopausal status
Planned surgical resection of breast cancer or repeat core biopsy tissue sampling prior to initiation of neoadjuvant systemic chemotherapy.
Availability of tissue blocks from initial core needle biopsy.
Signed informed consent.
Willing to discontinue use of all supplements containing Vitamin D for the duration of the study, and take only the Vitamin D provided by the study.

Exclusion criteria

Exclusion Criteria:

Presence of any Metastatic lesion.
History of parathyroid disease, hypercalcemia, or kidney stones.
History of Selective estrogen receptor modulator (SERM) or aromatase inhibitor therapy.
Receiving metformin.
History of renal failure requiring dialysis or kidney transplantation.
Women who are known to be pregnant or who are nursing. (As vitamin D does not have toxicity to the fetus, a negative pregnancy test is not a requirement to participate in the study.)
Patients planned for surgical therapy of their breast cancer or initiation of systemic chemotherapy, that would not allow for at least 7 days of vitamin D intervention
Any condition potentially interfering with subjects ability to comply with taking study medication.
Any medical condition that would potentially interfere with vitamin D absorption.
Current participation in another research study that would increase risk to subject, in the opinion of the investigators.
Patients currently taking more than 2000 IU of Vitamin D.

Study design

Phase: Phase 2
Primary purpose: Basic science
Allocation: Randomized
Intervention model: Parallel assignment
Masking: Double (Participant, Investigator)
Enrollment: 41 participants (actual)

Study arms

Experimental
Non-obese (Body Mass Index ≤ 25)
Non-obese participants receive Vitamin D at 400 or 10,000 IU/day
Drug: Vitamin D
Experimental
Obese (Body Mass Index > 25)
Obese participants receive Vitamin D at 400 or 10,000 IU/day
Drug: Vitamin D

Interventions

DrugVitamin D
Also known as: cholecalciferol

What researchers measure

Primary outcomes

Expression Level of Insulin-like Growth Factor-binding Protein 3 (IGFBP-3) Gene
To determine whether dietary vitamin D can reverse the negative effects of obesity and insulin resistance as reflected by changes in breast cancer gene expression patterns in obese and non-obese subjects diagnosed with breast cancer. IGFBP-3 is an endocrine factors. Insulin-like growth factor-binding protein 3 (IGFBP-3) gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.
Time frame: up to 6 weeks

Secondary outcomes

Expression Level of Cyclin-dependent Kinase Inhibitor 1 (CDKI1; p21) Gene
p21 \[aka p21Cip1; p21Waf1, cyclin-dependent kinase inhibitor 1 (CDKI1) or cyclin-dependent kinase (CDK)-interacting protein 1 (CDKIP1)\] gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.
Time frame: up to 6 weeks
Expression Level of Matrix Metalloproteinase-11 (MMP-11) Gene
Matrix metalloproteinase-11 (MMP-11), aka Stromelysin-3 (SL-3), gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.
Time frame: up to 6 weeks

Other outcomes

Expression Level of MKI67 Gene
Ki 67 gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.
Time frame: up to 6 weeks
Expression Level of ESR1 Gene
ESR1 gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.
Time frame: up to 6 weeks
Leptin to Adiponectin Ratio (Leptin:Adiponectin) in Blood
Levels in blood of leptin \& adiponectin were assessed at baseline \& after treatment in participants with body mass index ≤25 and \>25. By protocol design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day and 10,000 IU/day. For all serum protein levels, the outcome is reported as the ratio of the baseline to post-treatment values (baseline:post-treatment) of the ratio of the mean serum levels of leptin and adiponectin, (ie, lepton:adiponectin). As a ratio of the ratio of means, the outcome is reported as a number without dispersion. The outcome value expresses the treatment effect on both leptin and adiponectin collectively, with a value \<1.00 meaning that the effect on leptin levels was reduced relative to the effect on adiponectin levels, and a value \>1.00 that the effect on leptin levels was increased relative to the effect on adiponectin levels, with a larger difference from 1.00 indicating a greater effect (1.00 means no measure change).
Time frame: up to 6 weeks
HOMA-IR to Adiponectin Ratio (HOMA-IR:Adiponectin) in Blood
The Homeostasis Model of Assessment-Insulin Resistance (HOMA-IR) was used to assess fasting insulin \& glucose levels. HOMA-IR \& adiponectin were assessed at baseline \& after treatment in participants with body mass index ≤25 and \>25. By protocol design, the outcome is for non-obese vs obese participants stratified between 400 \& 10,000 IU/day. For all serum protein levels, the outcome is reported as the ratio of the baseline to post-treatment values (baseline:post-treatment) of the ratio of the mean serum levels of leptin \& adiponectin, (ie, lepton:adiponectin). As a ratio of the ratio of means, the outcome is reported as a number without dispersion. The outcome expresses the treatment effect on HOMA-IR \& adiponectin collectively, with \<1.00 meaning effect on HOMA-IR levels is reduced relative to the effect on adiponectin levels, \& \>1.00 meaning the effect is increased relative, with a greater difference meaning greater effect (1.00 represents no measure change).
Time frame: up to 6 weeks
cRP (C-reactive Protein) to Adiponectin Ratio (cRP:Adiponectin) in Blood
Levels in blood of cRP (C-reactive protein) \& adiponectin were assessed at baseline \& after treatment in participants with body mass index (BMI) ≤25 and \>25. By protocol design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day \& 10,000 IU/day. For all serum protein levels, the outcome is the ratio of the baseline to post-treatment values (baseline:post-treatment) of the ratio of the mean serum levels of leptin \& adiponectin, (ie, lepton:adiponectin). As a ratio of the ratio of means, the outcome is reported as a number without dispersion. The outcome value expresses the treatment effect on cRP and adiponectin collectively, with a value \< 1.00 meaning effect on cRP levels was reduced relative to the effect on adiponectin levels, and a value \> 1.00 meaning effect on cRP levels was increased relative to the effect on adiponectin levels, with a larger difference from 1.00 indicating a greater effect (1.00 represents no measure change).
Time frame: up to 6 weeks
Pharmacokinetics of Vitamin D Metabolite Calcitriol
Blood levels (pharmacokinetics) of Vitamin D were evaluated as the blood levels of Vitamin D metabolite calcitriol (also known as 1,25-dihydroxycholecalciferol or 1,25(OH)2D) in participants receiving 400 IU/day Vitamin D. The outcome is reported as the mean calcitriol level pre-treatment and post-treatment, with standard deviation.
Time frame: up to 6 weeks

Results

Posted Apr 19, 2019

Participant flow

Participant flow — Overall Study
Milestone	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Started	25	16
Completed	25	16
Not completed	0	0

Outcome measures

PrimaryExpression Level of Insulin-like Growth Factor-binding Protein 3 (IGFBP-3) Gene

To determine whether dietary vitamin D can reverse the negative effects of obesity and insulin resistance as reflected by changes in breast cancer gene expression patterns in obese and non-obese subjects diagnosed with breast cancer. IGFBP-3 is an endocrine factors. Insulin-like growth factor-binding protein 3 (IGFBP-3) gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.

Time frame:: up to 6 weeks
Reported as:: Mean · ratio baseline:post-treatment (slope)

Expression Level of Insulin-like Growth Factor-binding Protein 3 (IGFBP-3) Gene
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/day	0.02937 ± 0.03792	0.00941 ± 0.00680
Vitamin D 10,000 IU/day	0.0158 ± 0.03645	0.01443 ± 0.01828

SecondaryExpression Level of Cyclin-dependent Kinase Inhibitor 1 (CDKI1; p21) Gene

p21 \[aka p21Cip1; p21Waf1, cyclin-dependent kinase inhibitor 1 (CDKI1) or cyclin-dependent kinase (CDK)-interacting protein 1 (CDKIP1)\] gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.

Time frame:: up to 6 weeks
Reported as:: Mean · ratio baseline:post-treatment (slope)

Expression Level of Cyclin-dependent Kinase Inhibitor 1 (CDKI1; p21) Gene
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/day	0.04868 ± 0.07735	0.03465 ± 0.03755
Vitamin D 10,000 IU/day	0.02236 ± 0.04859	0.01854 ± 0.01700

SecondaryExpression Level of Matrix Metalloproteinase-11 (MMP-11) Gene

Matrix metalloproteinase-11 (MMP-11), aka Stromelysin-3 (SL-3), gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.

Time frame:: up to 6 weeks
Reported as:: Mean · ratio baseline:post-treatment (slope)

Expression Level of Matrix Metalloproteinase-11 (MMP-11) Gene
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/day	-0.03238 ± 0.04776	-0.00590 ± 0.02441
Vitamin D 10,000 IU/day	-0.00986 ± 0.05814	-0.02139 ± 0.01961

Other pre-specifiedExpression Level of MKI67 Gene

Ki 67 gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.

Time frame:: up to 6 weeks
Reported as:: Mean · ratio baseline:post-treatment (slope)

Expression Level of MKI67 Gene
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/day	-0.00958 ± 0.04108	-0.03809 ± 0.02416
Vitamin D 10,000 IU/day	-0.01318 ± 0.03231	0.00166 ± 0.01412

Other pre-specifiedExpression Level of ESR1 Gene

ESR1 gene expression was assessed at baseline and after treatment in participants with body mass index (BMI) ≤ 25 and \> 25. By design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day (control) and 10,000 IU/day (experimental), and is reported as the mean of the slope (a measure of magnitude of difference) between baseline and post-treatment, with standard deviation. A positive slope indicates increased expression, and a negative slope indicates decreasing values, with the larger values (positive or negative) indicating greater effect, and smaller values indicating lesser effect.

Time frame:: up to 6 weeks
Reported as:: Mean · ratio baseline:post-treatment (slope)

Expression Level of ESR1 Gene
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/day	0.00526 ± 0.14049	-0.02739 ± 0.02132
Vitamin D 10,000 IU/day	-0.05757 ± 0.0747	0.01225 ± 0.04041

Other pre-specifiedLeptin to Adiponectin Ratio (Leptin:Adiponectin) in Blood

Levels in blood of leptin \& adiponectin were assessed at baseline \& after treatment in participants with body mass index ≤25 and \>25. By protocol design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day and 10,000 IU/day. For all serum protein levels, the outcome is reported as the ratio of the baseline to post-treatment values (baseline:post-treatment) of the ratio of the mean serum levels of leptin and adiponectin, (ie, lepton:adiponectin). As a ratio of the ratio of means, the outcome is reported as a number without dispersion. The outcome value expresses the treatment effect on both leptin and adiponectin collectively, with a value \<1.00 meaning that the effect on leptin levels was reduced relative to the effect on adiponectin levels, and a value \>1.00 that the effect on leptin levels was increased relative to the effect on adiponectin levels, with a larger difference from 1.00 indicating a greater effect (1.00 means no measure change).

Time frame:: up to 6 weeks
Reported as:: Number · ratio baseline:post-treatment (slope)

Leptin to Adiponectin Ratio (Leptin:Adiponectin) in Blood
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/d	0.87	1.00
Vitamin D 10,000 IU/d	0.95	1.00

Other pre-specifiedHOMA-IR to Adiponectin Ratio (HOMA-IR:Adiponectin) in Blood

The Homeostasis Model of Assessment-Insulin Resistance (HOMA-IR) was used to assess fasting insulin \& glucose levels. HOMA-IR \& adiponectin were assessed at baseline \& after treatment in participants with body mass index ≤25 and \>25. By protocol design, the outcome is for non-obese vs obese participants stratified between 400 \& 10,000 IU/day. For all serum protein levels, the outcome is reported as the ratio of the baseline to post-treatment values (baseline:post-treatment) of the ratio of the mean serum levels of leptin \& adiponectin, (ie, lepton:adiponectin). As a ratio of the ratio of means, the outcome is reported as a number without dispersion. The outcome expresses the treatment effect on HOMA-IR \& adiponectin collectively, with \<1.00 meaning effect on HOMA-IR levels is reduced relative to the effect on adiponectin levels, \& \>1.00 meaning the effect is increased relative, with a greater difference meaning greater effect (1.00 represents no measure change).

Time frame:: up to 6 weeks
Reported as:: Number · ratio baseline:post-treatment (slope)

HOMA-IR to Adiponectin Ratio (HOMA-IR:Adiponectin) in Blood
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/day	0.96	0.52
Vitamin D 10,000 IU/day	1.35	0.99

Other pre-specifiedcRP (C-reactive Protein) to Adiponectin Ratio (cRP:Adiponectin) in Blood

Levels in blood of cRP (C-reactive protein) \& adiponectin were assessed at baseline \& after treatment in participants with body mass index (BMI) ≤25 and \>25. By protocol design, the outcome was determined for non-obese vs obese participants stratified between 400 IU/day \& 10,000 IU/day. For all serum protein levels, the outcome is the ratio of the baseline to post-treatment values (baseline:post-treatment) of the ratio of the mean serum levels of leptin \& adiponectin, (ie, lepton:adiponectin). As a ratio of the ratio of means, the outcome is reported as a number without dispersion. The outcome value expresses the treatment effect on cRP and adiponectin collectively, with a value \< 1.00 meaning effect on cRP levels was reduced relative to the effect on adiponectin levels, and a value \> 1.00 meaning effect on cRP levels was increased relative to the effect on adiponectin levels, with a larger difference from 1.00 indicating a greater effect (1.00 represents no measure change).

Time frame:: up to 6 weeks
Reported as:: Number · ratio baseline:post-treatment (slope)

cRP (C-reactive Protein) to Adiponectin Ratio (cRP:Adiponectin) in Blood
ratio baseline:post-treatment (slope)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Vitamin D 400 IU/day	0.80	0.83
Vitamin D 10,000 IU/day	1.33	1.00

Other pre-specifiedPharmacokinetics of Vitamin D Metabolite Calcitriol

Blood levels (pharmacokinetics) of Vitamin D were evaluated as the blood levels of Vitamin D metabolite calcitriol (also known as 1,25-dihydroxycholecalciferol or 1,25(OH)2D) in participants receiving 400 IU/day Vitamin D. The outcome is reported as the mean calcitriol level pre-treatment and post-treatment, with standard deviation.

Time frame:: up to 6 weeks
Reported as:: Mean · ng/mL

Pharmacokinetics of Vitamin D Metabolite Calcitriol
ng/mL	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Pre-treatment, 400 IU/day	30.44 ± 10.89	34.67 ± 4.62
Pre-treatment, 10,000 IU/day	30.75 ± 8.62	37.17 ± 12.51
Post-treatment, 400 IU/day	30.89 ± 7.52	31.67 ± 3.06
Post-treatment, 10,000 IU/day	53.75 ± 13.82	59.33 ± 27.74

Adverse events

Non-serious events are listed at a 0% frequency threshold.

Adverse event summary by group
Group	Deaths	Serious	Other
Non-obese (Body Mass Index ≤ 25)	0/25 (0%)	0/25 (0%)	0/25 (0%)
Obese (Body Mass Index > 25)	0/16 (0%)	1/16 (6.3%)	1/16 (6.3%)

Most frequent serious events

Most frequent serious events
Event	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
Primary hyperparathyroidism (HPT)Metabolism and nutrition disorders	0/25	1/16
Neuroendocrine cancer of the breast, metastaticNeoplasms benign, malignant and unspecified (incl cysts and polyps)	0/25	1/16

Most frequent other events

Most frequent other events
Event	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)
HypercalcemiaMetabolism and nutrition disorders	0/25	1/16
Plasma chromogranin A level, elevatedMetabolism and nutrition disorders	0/25	1/16

Baseline characteristics

All participants

Age, Categorical
Age, Categorical(Participants)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)	Total
<=18 years	0	0	0
Between 18 and 65 years	21	7	28
>=65 years	4	9	13

Age, Continuous
Age, Continuous(years)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)	Total
Mean	54.1 ± 11.6	62.1 ± 7.6	57.3 ± 10.8

Sex: Female, Male
Sex: Female, Male(Participants)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)	Total
Female	25	16	41
Male	0	0	0

Region of Enrollment
Region of Enrollment(participants)	Non-obese (Body Mass Index ≤ 25)	Obese (Body Mass Index > 25)	Total
United States	25	16	41

Study locations

1 site

Stanford University Cancer Institute
Stanford, California 94305, United States

References and documents

Individual participant data

Plan to share: No

No publications or documents are linked to this record.

Updates

Tracking since Sep 25, 2026

No changes since tracking began. The registry record was last updated on Apr 23, 2026, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗

Registry details

Key details

Study ID: NCT01472445
Lead sponsor: Melinda Telli
Responsible party: Melinda Telli (Assistant Professor of Medicine, Stanford University) — Sponsor-investigator
First posted: Nov 16, 2011
Start date: Nov 2011
Primary completion: Oct 2014
Completion: Oct 2015
Results posted: Apr 19, 2019
Last update: Apr 23, 2026

Study contacts

Melinda Telli, MD

principal investigator · Stanford University

Oversight

Data monitoring committee: Yes
FDA-regulated drug: Yes
FDA-regulated device: No

View the source record on ClinicalTrials.gov ↗

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