A 12-week double-blind randomized clinical trial of vitamin D3supplementation on body fat mass in healthy overweight and obese women
© Salehpour et al.; licensee BioMed Central Ltd. 2012
Received: 23 April 2012
Accepted: 5 September 2012
Published: 22 September 2012
Vitamin D concentrations are linked to body composition indices, particularly body fat mass. Relationships between hypovitaminosis D and obesity, described by both BMI and waist circumference, have been mentioned. We have investigated the effect of a 12-week vitamin D3 supplementation on anthropometric indices in healthy overweight and obese women.
In a double-blind, randomized, placebo-controlled, parallel-group trial, seventy-seven participants (age 38±8.1 years, BMI 29.8±4.1 kg/m2) were randomly allocated into two groups: vitamin D (25 μg per day as cholecalciferol) and placebo (25 μg per day as lactose) for 12 weeks. Body weight, height, waist, hip, fat mass, 25(OH) D, iPTH, and dietary intakes were measured before and after the intervention.
Serum 25(OH)D significantly increased in the vitamin D group compared to the placebo group (38.2±32.7 nmol/L vs. 4.6±14.8 nmol/L; P<0.001) and serum iPTH concentrations were decreased by vitamin D3 supplementation (-0.26±0.57 pmol/L vs. 0.27±0.56 pmol/L; P<0.001). Supplementation with vitamin D3 caused a statistically significant decrease in body fat mass in the vitamin D group compared to the placebo group (-2.7±2.1 kg vs. -0.47±2.1 kg; P<0.001). However, body weight and waist circumference did not change significantly in both groups. A significant reverse correlation between changes in serum 25(OH) D concentrations and body fat mass was observed (r = -0.319, P = 0.005).
Among healthy overweight and obese women, increasing 25(OH) D concentrations by vitamin D3 supplementation led to body fat mass reduction.
This trial is registered at clinicaltrials.gov as NCT01344161.
KeywordsVitamin d3 Supplementation Body fat mass Obesity
Obesity is a chronic condition of nutrients accumulation [1, 2] in which excess energy aggregates in the form of fat mass . Based on the thrifty genotype hypothesis , since metabolic efficiency is raised in negative energy states, important interactions between gene and obesogenic environment (including food abundance and low physical activity ) result in improper metabolic programming and epigenic change in utero; hence in this condition obesity is an inevitable outcome . Fat mass distribution specifically visceral distribution, produces toxic milieu by initiating metabolic and inflammatory cascade, which is followed by endocrine, cardiovascular and malignant events. The risk of mortality rises synergistically with increase in BMI over than 30 kg/m2 .
Serum 25-hydroxyvitamin D concentrations are low in obese adults [7, 8] and linked to components of body composition, particularly body fat mass [9, 10]. Alterations in the vitamin D endocrine system have been reported in obesity [11, 12]. Lumb et al believed that vitamin D is stored in adipose and muscle tissues after absorption, and is slowly released into the blood stream [13, 14]. It was thought that vitamin D deficiency caused obesity, and is proposed that hypothalamus diagnoses low calcidiol concentrations in circulation and induces higher body set point by increase in appetite and decrease in energy consumption via stimulating Agouti Related Protein/Neuropeptide Y (AgRP/NPY) and suppressing pro-Opiomelanocortin/Cocaine- Amphetamine- Regulated Transcription (POMC/CART) pathway [15, 16]. Wortsman et al confirmed insufficiency of vitamin D in the obese people indicating that they need to higher doses of vitamin D .
Evidence implies that dairy product consumption, and high calcium and/or vitamin D intakes can repress fatty acid synthase enzyme (FAS) by decreasing intracellular Ca + 2 in adiposities [18–21]. Recent literature reveals that vitamin D receptor (VDR) gene polymorphisms are associated with adiposity phenotypes . It has been postulated that both 1,25(OH)2D and VDR have imperative roles in adipocyte differentiation [23, 24]. The differentiation of pre-adipocytes to mature adipocytes in vitro is halted by 1,25(OH)2D3 . Contrarily, high serum 1,25(OH)2 D concentrations may increase lipogenesis by stimulating of FAS .
Alterations in the vitamin D endocrine system are causally associated with augmented adiposity or result from augmented fat mass storage of vitamin D . Accumulating evidence for involvement of vitamin D in fat mass metabolism  was the impetus for this clinical trial in which we tested the effect of vitamin D3 supplementation on body composition in overweight and obese women.
We conducted the study between November 2009 and April 2010 in the Heart and Vascular Laboratory in Pharmacology Department of Tehran University of Medical Sciences, Tehran, Iran. Recruitment began in August 2009 by advertisements on university and ended in November 2009. The criteria for eligibility were age between 18-50 years old, a BMI ≥25 kg/m2, an apparently healthy status based on self-reports from the subjects, free from metabolic bone disease, gastrointestinal disease, diabetes mellitus, cardiovascular disease, renal disease, no medications, no vitamin supplements, none pregnant or lactating. We excluded individuals with changes in body weight more than 3 kg within last three months, following weight-loss programs, taking weight loss drugs, smoking and drinking alcohol. Of a total of 140 subjects initially selected, eighty five subjects who met the above inclusion criteria were recruited.
The present study was approved by the Ethics Committee of the Tehran University of Medical Sciences and Iranian Registry of Clinical Trial (registration no. IRCT138809092709N2) and written informed consent and subject assent were obtained.
Individuals were randomly allocated in a double-blind parallel manner from randomized number in an 85-person list; 42 women were assigned to the vitamin D group and 43 women to the placebo group. The vitamin D group had to take vitamin D3 supplement tablet of 25 μg/d as cholecalciferol; Merck Pharma GmbH, Germany, while the placebo group took tablet of 25 μg/d as lactose; Merck Pharma GmbH, Germany. The intervention was conducted for 90 days. To ensure and assess compliance, vitamin D supplements were issued at baseline, exchanged for a new package at both 4 wk and 8 wk, and returned to the research staff at post testing, and pills were counted later for compliance, which was 87.1% in the vitamin D and 87.4% in the placebo groups. To remain blinded, one research assistant who was not involved in data collection coordinated the supplement assignment schedule.
After a 12-h overnight fast, blood specimens were collected from the antecubital vein into the tubes. After centrifugation for 20 min (3000 g), the serum samples were frozen consecutively and stored at -80°C.
We assessed energy and nutrient intakes by 24 h food recall and validated food frequency questionnaires . A nutritionist completed questionnaires during monthly face to face interviews. Because the Iranian food composition table (FCT) is incomplete (limited to only raw materials and few nutrients) , each food and beverage was analyzed for nutrient intake using Nutritionist IV software (Version 4.1, First Databank Division, The Hearst Corporation, San Bruno, CA) to assess macronutrient and micronutrient contents of foods. The Iranian FCT was used as an alternative for traditional Iranian food items, such as kashk, which are not included in the Food Composition Tables for USA (USDA FCT) . The average of MET-minutes/week was calculated by multiplying the time of exercise by the respective metabolic equivalent task (MET) using the International Physical Activity Questionnaires (IPAQ) .
We measured body weight to the nearest 0.1 kg and height in light indoor clothes using a digital scale (model 763; Seca GmbH & Co, KG, Hamburg, Germany). Waist and hip circumference were measured on a horizontal plane at the level of the iliac crest by an Ergonomic Circumference Measuring Tape (model 201; Seca GmbH & Co, KG, Hamburg, Germany). Body mass index was calculated as weight in kilograms divided by the square of the height in meters. We assessed body fat mass and fat free mass by Bioelectrical Impedance Analysis (model 4000; Body Stat Quad Scan, Douglas Isle of Man, British Isles) after five minutes resting, with standard errors of estimate (accuracy) of 4.1%. All anthropometric indices were obtained using the WHO standard procedures .
Intact PTH was measured by immunoenzymo-metric assay (IEMA) (Immunodiagnostic Systems Ltd, Boldon, UK). Intra- and interassay CVs for intact PTH were 5.5%, and 8.3%, respectively. Serum 25(OH) D was measured by enzyme immunoassay (EIA) (Immunodiagnostic Systems Ltd, Boldon, UK). Intra- and interassay CVs for 25(OH) D were 6.9%, and 8.1%, respectively. Calcium was measured by colorimetric enzymatic (Pars Azmoon, Tehran, Iran), the kit expected range was 2.15-2.57 mmol/L. The assay sensitivity was 0.05 mmol/L, and intra- and interassay coefficients of variation were 2.4% and 3%, respectively. Phosphorus was measured by enzymatic photometric UV test (Pars Azmoon Co., Tehran, Iran); the kit expected range was 0.83-1.45 mmol/L. The assay sensitivity was 0.22 mmol/L, and intra- and interassay coefficients of variation were 3.2% and 4.1%, respectively.
Descriptive statistics are presented as mean ± SD. We examined the normality of data by Kolmogorov-Smirnov and Shapiro-Wilk tests. All data had been normally distributed. For the primary analysis, we used an analysis of covariance (ANCOVA) to adjust mean differences on biochemical variables. Simple Pearson correlations were computed between changes in 25(OH) D and iPTH concentrations and body fat mass. All statistical analyses were performed using SPSS (version 16; SPSS Inc, Chicago, IL). All tests were two-sided and P values <0.05 were considered statistically significant.
Baseline characteristics of subject groups who received vitamin D3 supplements (25 μ/d) or placebo before the intervention
Vitamin D group
Body weight (kg)
Waist circumference (cm)
Hip circumference (cm)
Fat mass (kg)
Fat free mass (kg)
Physical activity (MET-minutes/week)
Energy intake (kcal/d)
Carbohydrate intake (g/d)
Fiber intake (g/d)
Protein intake (g/d)
Fat intake (g/d)
Dietary calcium intake (mg/d)
Dietary vitamin D intake (μg/d)
25(OH) D (nmol/L)2
Anthropometric, dietary and serum variables in the subject groups after vitamin D3 supplementation and changes in variables between measurement periods
Vitamin D group
Body weight (kg)
Waist circumference (cm)
Hip circumference (cm)
Fat free mass (kg)
Physical activity (METminutes/week)
Energy intake (kcal/d)
Carbohydrate intake (g/d)
Fiber intake (g/d)
Protein intake (g/d)
Fat intake (g/d)
Dietary calcium intake (mg/d)
Dietary vitamin D intake (μg/d)
25(OH) D (nmol/L)
The present study shows that a 12 week supplementation with 25 μg vitamin D3 in overweight and obese women with mean serum 25(OH)D concentrations of 41.8±31.4 nmol/L decreases body fat mass, but does not affect body weight and waist circumference.
There is a large body of growing evidence showing that dairy products, and calcium and vitamin D intake play a role in the regulation of body fat mass [31–33]. Data also indicates that vitamin D may increase lean body mass  and inhibit the development of adipocytes. These effects of vitamin D may be mediated by 1,25(OH)2D3 or via suppression of PTH .
However, there are few clinical trials of vitamin D supplementation on body composition and most of them have assessed effects of combined calcium and vitamin D supplementation. Moreover, these studies are heterogeneous with regard to doses and types of vitamin D, lengths of follow up, outcome ascertainment methods, prevalence of vitamin D deficiency and other characteristics in studied subjects, which have led to inconsistent results. Our study is one of the few clinical trials which have investigated the effect of vitamin D3 supplementation in overweight or obese women with low 25(OH)D concentrations on body compositions. The 12 week vitamin D3 supplementation did not significantly affect body weight, waist or hip circumference. However, a modest fat mass reduction of 7% was associated with a significant increase of 25OHD levels by 103% and a significant decrease of PTH levels by 14%. The initial serum 25(OH)D concentrations were low in both groups.
Recently, in a double-blind, placebo-controlled trial in overweight and obese participants, Rosenblum et al  reported that after a 16 week calcium and vitamin D supplementation with either regular or reduced energy (lite) orange juice (three 240 mL glasses of orange juice fortified with 350 mg Ca and 100 IU vitamin D per serving), the average weight loss did not differ significantly between groups, but in the regular orange juice trial, the reduction of visceral adipose tissue (VAT) was significantly greater in the CaD group than in controls (−12.7 ± 25.0 cm2 vs. −1.3 ± 13.6 cm2; P = 0.024, respectively) and in the lite orange juice trial, the reduction of VAT was significantly greater in the CaD group than in controls (−13.1 ± 18.4 cm2 vs. − 6.4 ± 17.5 cm2; P = 0.039, respectively) after control for baseline VAT. They suggested that calcium and vitamin D supplementation contributes to a beneficial reduction of VAT. Dong et al  in a 16 week randomized, blinded, controlled clinical trial of 2000 IU vitamin D3 supplementation in forty nine black youth, evaluated the relation between 25(OH)D concentrations and total body fat mass by dual-energy x-ray absorptiometry. The experimental group compared with the controls reached significantly higher 25(OH)D concentrations at 16 wk (85.7±30.1 nmol/liter vs. 59.8±18.2 nmol/liter,P<0.001, respectively) and partial correlation analyses indicated that total body fat mass at baseline was significantly and inversely associated with 25(OH)D concentrations in response to the 2000 IU supplement (R = -0.46; P = 0.03). Zhou et al  in a large-scale, placebo controlled, double-blind, 4-year longitudinal clinical trial, investigated the effect of calcium and vitamin D supplementation on obesity in postmenopausal women, randomly assigned into one of three groups: 1) supplemental calcium (1400 mg/d or 1500 mg/d) plus vitamin D placebo (Ca-only group); 2) supplemental calcium (1400 mg/d or 1500 mg/d) plus supplemental vitamin D3 (1100 IU/d) (Ca + D group); or, 3) two placebos. No significant difference was observed for body mass index between groups, but changes in trunk fat (for Ca-only and Ca + D groups compared to the placebo group preserved lower trunk fat 2.4%, 1.4% vs. 5.4%, P = 0.015 at year 3) and trunk lean (for Ca-only and Ca + D groups preserved more trunk lean compared to the placebo group, -0.6%, -1.0% vs. -2.1%, P = 0.004 at year 4), were significantly different between groups. Major et al  conducted a randomized, double-blind, placebo-controlled study to compare the effects of a 15 week weight-reducing program (-700 kcal/d) coupled with a calcium plus vitamin D supplementation (600 mg elemental calcium and 5 mg vitamin D, twice a day or placebo), on the body fat of sixty-three overweight or obese women. The calcium + D supplementation did not induce statistically significant increase in fat mass loss. However, when analyses were limited to very low-calcium consumers only (initial calcium intake ≤600 mg/d), significant time × treatment interaction were observed in body weight (P<0·009), BMI (P<0·008) and fat mass (P<0.02). Waist circumference decreased in both groups and there were significant treatment effects (P = 0.03). Zittermann et al  investigated the effect of vitamin D (83 μg/d) on weight loss in overweight subjects with a mean 25(OH)D concentration of 30 nmol/L in a double-blind manner for 12 months while participating in a weight-reduction program. Their results showed that although weight loss was not affected significantly by vitamin D supplementation, waist circumference however decreased in both groups and there were significant treatment effects (P = 0.022). Body fat mass did not alter after the intervention.
It has been suggested that high levels of calcitrophic hormones such as 1α,25,dihydroxyvitamin D and iPTH can modulate intracellular Ca + 2 concentrations, so increasing Ca + 2 flux to adiposities, which stimulate fatty acid synthase enzyme, may increase lipogenesis and inhibit lipolysis . According to this hypothesis, 1α, 25dihydroxyvitamin D is known as a key factor that provokes triglyceride accumulation in adiposities  a finding not confirmed by others . Vitamin D insufficiency and secondary hyperparathyroidism lead to PTH related phospholipase C activation in adiposities, a process, which is followed by increase in intracellular calcium [40, 41]. Chronic increase in [Ca + 2] may attenuate the ability of catecholamines in activating of lipolysis by increasing the activity of Ca + 2 related cAMP phosphodiesterase . Meanwhile, with increasing of [Ca + 2], induction of fatty acid synthase is strengthened, which facilitates de novo lipogenesis . Thus hyperparathyroidism can affect weight gain [44, 45].
The primary limitation of our study is that we could not assess body composition by Dual X-Ray Absorptiometry (DXA) as a gold standard method. However, Bioelectrical Impedance Analysis is a validated and reliable method to assess body composition. A second limitation is that Resting Metabolic Rate (RMR) was not determined in subjects. Although our main goal was to examine the effect of vitamin D3 supplementation on body composition. A third potential limitation is not evaluating sun exposure, a confounding factor, which can not be completely ruled out. However, the subjects were requested not to use sunscreen during the intervention.
To summarize, based on result of the 12 week vitamin D3 supplementation, we concluded body fat mass decreased in healthy overweight and obese women via increase in serum 25(OH) D and decrease in iPTH concentrations. Further investigation into whether vitamin D may play a role in regulation of body composition is warranted.
We thank Ghazaleh Shimi, Saeedeh Nasiri, and Majid Goharinejad for specimen processing, anthropometric, and dietary data collection. Dr. Mehdi Hedayati and colleagues are acknowledged for biochemical analyses. We acknowledge Ms. Nilufar Shiva for language editing of the manuscript. This clinical trial was supported by grants from Tehran University of Medical Sciences (grant no. 852) and the Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences (grant no. 293).
- Welborn TA, Dhaliwal SS, Bennett SA: Waist-hip ratio is the dominant risk factor predicting cardiovascular death in australia. Med J Aust. 2003, 179: 580-585.
- Welborn TA, Dhaliwal SS: Preferred clinical measures of central obesity for predicting mortality. Eur J Clin Nutr. 2007, 61: 1373-1379. 10.1038/sj.ejcn.1602656.View Article
- Marieke B, Snijder MB, van Dam RM, Visser M, Deeg DJH, Dekker JM, Bouter LM, Seidell JC, Lips P: Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women. J Clin Endocrinol Metab. 2005, 90: 4119-4123. 10.1210/jc.2005-0216.View Article
- Neel JV: Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”?. Am J Hum Genet. 1962, 14: 353-362.
- Wareham N: Physical activity and obesity prevention. Obes Rev. 2007, 8 (Suppl): 109-114.View Article
- Buffington C, Walker B, Cowan GS, Scruggs D: Vitamin D deficiency in morbidly obese. Obes Surg. 1993, 3: 421-424. 10.1381/096089293765559142.View Article
- Zamboni G, Soffiati M, Giavarina D, Tato L: Mineral metabolism in obese children. Acta Paediatr Scand. 1988, 77: 741-746. 10.1111/j.1651-2227.1988.tb10740.x.View Article
- Yanoff LB, Parikh SJ, Spitalnik A, Denkinger B, Sebring NG, Slaughter P, McHugh T, Remaley AT, Yanovski JA: The prevalence of hypovitaminosis d and secondary hyperparathyroidism in obese black americans. Clin Endocrinol. 2006, 64: s23-s29.View Article
- Liel Y, Ulmer E, Shary J, Hollis BW, Bell NH: Low circulating vitamin d in obesity. Calcif Tissue Int. 1988, 43: 199-201. 10.1007/BF02555135.View Article
- Danescu LG, Levy S, Levy J: Vitamin d and diabetes mellitus. Endocrine. 2009, 35: 11-7. 10.1007/s12020-008-9115-5.View Article
- Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ, Shaw S: Evidence for alteration of the vitamin d endocrine system in obese subjects. J Clin Invest. 1985, 76: 370-373. 10.1172/JCI111971.View Article
- Sutherland ER, Goleva E, Jackson LP, Stevens AD, Leung DY: Vitamin d levels, lung function, and steroid response in adult asthma. Am J Respir Crit Care Med. 2010, 181: 699-704. 10.1164/rccm.200911-1710OC.View Article
- Cowley MA, Pronchuk N, Fan W, Dinulescu DM, Colmers WF, Cone RD: Integration of npy, agrp, and melanocortin signals in the hypothalamic paraventricular nucleus: evidence of a cellular basis for the adipostat. Neuron. 1999, 24 (Suppl 1): 155-163.View Article
- Bays HE, Gonzalez-Campoy JM, Bray GA, Kitabchi AE, Bergman DA, Schorr AB, Rodbard HW, Henry RR: Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hypertrophy and increased visceral adiposity. Expert Rev Cardio Ther. 2008, 6: 343-368. 10.1586/14779072.6.3.343.View Article
- Schwartz MW, Niswender KD: Adiposity signaling and biological defense against weight gain: absence of protection or central hormone resistance?. J Clin Endocrinol Metab. 2004, 89 (Suppl 12): 5889-5897.View Article
- Posey KA, Clegg DJ, Printz RL, Byun J, Morton GJ, Vivekanandan-Giri A, Pennathur S, Baskin DG, Heinecke JW, Woods SC, Schwartz MW, Niswender KD: Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet. Am J Physiol Endocrinol Metab. 2009, 296: E1003-E1012. 10.1152/ajpendo.90377.2008.View Article
- Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF: Decreased bioavailability of vitamin d in obesity. Am J Clin Nutr. 2000, 72: 690-693.
- Zemel MB, Shi H, Greer B, Dirienzo D, Zemel PC: Regulation of adiposity by dietary calcium. FASEB J. 2000, 14: 1132-1138.
- Teegarden D: Calcium intake and reduction of fat mass. J Nutr. 2003, 133: 249S-251S.
- Zemel MB: Proposed role of calcium and dairy food components in weight management and metabolic health. Physician Sport Med. 2009, 37: 29-39.View Article
- Spence LA, Cifelli CJ, Miller GD: The role of dairy products in healthy weight and body composition in children and adolescents. Curr Nutr Food Sci. 2011, 7 (Suppl 1): 40-49(10).View Article
- Ochs-Balcom HM, Chennamaneni R, Millen AE, Shields PG, Marian C, Trevisan M, Freudenheim JL: Vitamin d receptor gene polymorphisms are associated with adiposity phenotypes. Am J Clin Nutr. 2011, 93: 5-10. 10.3945/ajcn.2010.29986.View Article
- Wood RJ: Vitamin d and adipogenesis: new molecular insights. Nutr Rev. 2008, 66: 40-46. 10.1111/j.1753-4887.2007.00004.x.View Article
- Kong J, Li YC: Molecular mechanism of 1,25-dihydroxyvitamin d3 inhibition of adipogenesis in 3 T3-L1 cells. Am J Physiol Endocrinol Metab. 2006, 290: E916-E924. 10.1152/ajpendo.00410.2005.View Article
- Zemel MB: Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications. J Am Coll Nutr. 2002, 21: 146S-151S.View Article
- Hosseini Esfahani F, Asghari G, Mirmiran P, Azizi F: Reproducibility and relative validity of food group intake in a food frequency questionnaire developed for the tehran lipid and glucose study. J Epidemiol. 2010, 20: 150-158. 10.2188/jea.JE20090083.View Article
- Azar M, Sarkisian E: Food Composition Table of Iran. 1980, National Nutrition and Food Research Institute, Shaheed Beheshti University, Tehran
- Ars.usda.gov. http://www.nal.usda.gov/fnic/foodcomp/
- Craig CL, Marshall AL, Sjostrom M, Bauman AE, Booth ML, Ainsworth BE: International physical activity questionnaire: 12-country reliability and validity. Med Sci Sports Exercise. 2003, 35: 1381-1395. 10.1249/01.MSS.0000078924.61453.FB.View Article
- World Health Organization Physical Status: The Use 478 and Interpretation of Anthropometry. Technical Report 479 Series no. 854. 1995, WHO, Geneva
- Siddiqui SM, Chang E, Li J, Burlage C, Zou M, Buhman KK, Koser S, Donkin SS, Teegarden D: Dietary intervention with vitamin d, calcium, and whey protein reduced fat mass and increased lean mass in rats. Nutr Res. 2008, 28: 783-790. 10.1016/j.nutres.2008.08.004.View Article
- Rosenblum JL, Castro VM, Moore CE, Kaplan LM: Calcium and vitamin d supplementation is associated with decreased abdominal visceral adipose tissue in overweight and obese adults. Am J Clin Nutr. 2012, 95 (Suppl 1): 101-108.View Article
- Adams JS, Hewison M: Update in vitamin d. J Clin Endocrinol Metab. 2010, 95: 471-478. 10.1210/jc.2009-1773.View Article
- Reid IR: Relationships between fat and bone. Osteoporos Int. 2008, 19: 595-606. 10.1007/s00198-007-0492-z.View Article
- Ward KA, Das G, Berry JL, Roberts SA, Rawer R, Adams JE, Mughal Z: Vitamin d status and muscle function in post-menarchal adolescent girls. J Clin Endocrinol Metab. 2009, 9: 559-563.View Article
- Dong Y, Stallmann-Jorgensen IS, Pollock NK, Harris RA, Keeton D, Huang Y, Li K, Bassali R, Guo D, Thomas J, Pierce GL, White J, Holick MF, Zhu H: A 16-week randomized clinical trial of 2000 international units daily vitamin d3 supplementation in black youth: 25-hydroxyvitamin d, adiposity, and arterial stiffness. J Clin Endocrinol Metab. 2010, 95: 4584-4591. 10.1210/jc.2010-0606.View Article
- Zhou J, Zhao LJ, Watson P, Zhang Q, Lappe JM: The effect of calcium and vitamin d supplementation on obesity in postmenopausal women: secondary analysis for a large-scale, placebo controlled, double-blind, 4-year longitudinal clinical trial. Nutr Metab. 2010, 7: 62-70. 10.1186/1743-7075-7-62.View Article
- Major GC, Alarie FP, Dore J, Tremblay A: Calcium plus vitamin d supplementation and fat mass loss in female very low-calcium consumers: potential link with a calcium-specific appetite control. Brit J Nutr. 2009, 101: 659-663. 10.1017/S0007114508030808.View Article
- Zittermann A, Frisch S, Berthold HK, Götting C, Kuhn J, Kleesiek K, Stehle P, Koertke H, Koerfer R: Vitamin d supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers. Am J Clin Nutr. 2009, 89: 1321-1327. 10.3945/ajcn.2008.27004.View Article
- Begum N, Sussman KE, Draznin B: Calcium-induced inhibition of phosphoserine phosphatase in insulin target cells is mediated by the phosphorylation and activation of inhibitor 1. J Biol Chem. 1992, 267: 5959-5963.
- Ni Z, Smogorzewski M, Massry SG: Effects of parathyroid hormone on cytosolic calcium of rat adipocytes. Endocrinology. 1994, 135: 1837-1844. 10.1210/en.135.5.1837.
- Xue B, Greenberg AG, Kraemer FB, Zemel MB: Mechanism of intracellular calcium ([ca2+]i) inhibition of lipolysis in human adipocytes. FASEB J. 2001, 15: 2527-2529.
- Kim JH, Mynatt RL, Moore JW, Woychik RP, Moustaid N, Zemel MB: The effects of calcium channel blockade on agouti-induced obesity. FASEB J. 1996, 10: 1646-1652.
- Shrago E, Spennetta T: The carbon pathway for lipogenesis in isolated adipocytes from rat, guinea pig, and human adipose tissue. Am J Clin Nutr. 1976, 29: 540-545.
- Guo ZK, Cella LK, Baum C, Ravussin E, Schoeller DA: De novo lipogenesis in adipose tissue of lean and obese women: application of deuterated water and isotope ratio mass spectrometry. Int J Obes Relat Metab Disord. 2000, 24: 932-937. 10.1038/sj.ijo.0801256.View Article
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