Obesity is a chronic condition of nutrients accumulation [1, 2] in which excess energy aggregates in the form of fat mass [3]. Based on the thrifty genotype hypothesis [4], since metabolic efficiency is raised in negative energy states, important interactions between gene and obesogenic environment (including food abundance and low physical activity [5]) result in improper metabolic programming and epigenic change in utero; hence in this condition obesity is an inevitable outcome [6]. 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 [1].

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 [17].

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 [22]. 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 [24]. Contrarily, high serum 1,25(OH)2 D concentrations may increase lipogenesis by stimulating of FAS [25].

Alterations in the vitamin D endocrine system are causally associated with augmented adiposity or result from augmented fat mass storage of vitamin D [17]. Accumulating evidence for involvement of vitamin D in fat mass metabolism [25] 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.

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 [34] and inhibit the development of adipocytes. These effects of vitamin D may be mediated by 1,25(OH)2D3 or via suppression of PTH [35].

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 [32] 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 [36] 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 [37] 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 [38] 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 [39] 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 [25]. According to this hypothesis, 1α, 25dihydroxyvitamin D is known as a key factor that provokes triglyceride accumulation in adiposities [18] a finding not confirmed by others [39]. 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 [42]. Meanwhile, with increasing of [Ca + 2], induction of fatty acid synthase is strengthened, which facilitates de novo lipogenesis [43]. 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.