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REVIEW ARTICLE
Year : 2016  |  Volume : 5  |  Issue : 1  |  Page : 1-5

Is Vitamin D deficiency a cause or result of childhood obesity?


Department of Pediatrics, Taibah University, Tayba, Medina, Saudi Arabia

Date of Web Publication23-May-2016

Correspondence Address:
Abdul Hadi H Almazroea
Department of Pediatrics, Taibah University, Tayba, Medina
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-0521.182857

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  Abstract 

Obesity is increasing worldwide. Obese individuals are at higher risk of Vitamin D deficiency, which is highly prevalent in infants, children, and adolescents. In addition to causing rickets, there is a known association between obesity and Vitamin D status in both adults and children. Serum 25-hydroxy Vitamin D, a Vitamin D biomarker used in clinical diagnostics, is inversely associated with body mass index, waist circumference, and total body fat in both adults and adolescents. This association between low Vitamin D levels and high body weight suggests that Vitamin D deficiency may be causative for obesity; however, the opposite might also be true. Here, we review the relationship between Vitamin D deficiency and obesity, in particular, the genetics and biochemical pathways thought to link the two, with particular reference to the pediatric population. Regardless of etiology, pediatricians must be aware of Vitamin D deficiency in obese children and recommend healthy lifestyle choices.

Keywords: Adolescents, children, obesity, Vitamin D


How to cite this article:
Almazroea AH. Is Vitamin D deficiency a cause or result of childhood obesity?. Saudi J Health Sci 2016;5:1-5

How to cite this URL:
Almazroea AH. Is Vitamin D deficiency a cause or result of childhood obesity?. Saudi J Health Sci [serial online] 2016 [cited 2021 Dec 3];5:1-5. Available from: https://www.saudijhealthsci.org/text.asp?2016/5/1/1/182857


  Introduction Top


Obesity is increasing worldwide: Approximately one-third of the population is now obese. Obesity is defined as a body mass index (BMI, an indicator of body fat calculated by dividing a person's weight in kilograms by their height in meters squared) of over 30 kg/m 2 . Although there is a known genetic component to obesity, people generally become obese by consuming more energy from food and drink than needed for their daily activities. Thus, maintaining a healthy diet and exercising regularly can prevent obesity. Obese individuals are at increased risk diabetes, heart disease, and stroke and as a consequence, live shorter lives. They are also at higher risk of Vitamin D deficiency.

Vitamin D deficiency is highly prevalent in infants, children, and adolescents around the world. In Saudi Arabia, the overall prevalence of obesity is about 35.5%. [1] In addition to causing rickets, there is growing evidence to suggest that Vitamin D deficiency may place individuals at increased risk of serious chronic disease including autoimmunity, cardiovascular disease, and cancer. [2]

There is a known association between obesity and Vitamin D status in both adults and children. [3],[4],[5],[6],[7],[8] The association between low Vitamin D levels and high body weight has caused speculation that Vitamin D deficiency may be causative for obesity [9] while other studies have shown that the opposite might be true, i.e., obesity is a potential cause of Vitamin D deficiency. [10] Serum 25-hydroxy Vitamin D (25(OH)D), a Vitamin D biomarker used in clinical diagnostics, is inversely associated with BMI, waist circumference, and total body fat in both adults and adolescents. [11],[12],[13],[14] Sequestration of Vitamin D in body fat stores and consequently reduced bioavailability might explain this association. [7],[15] Here, we review the relationship between Vitamin D deficiency and obesity, in particular, the genetics and biochemical pathways thought to link the two, with particular reference to the pediatric population.


  Vitamin d metabolism Top


Exposure of the skin to sunlight is the main source of Vitamin D production. [16],[17] Over 80% of systemic Vitamin D 3 is derived from the epidermis, with the remaining 20% obtained from the diet from animal-derived cholecalciferol (D 3 ), plant-derived ergocalciferol (D 2 ), or drug supplementation. [18]

Production of Vitamin D 3 in the skin relies on a photochemical process in which epidermal 7-dehydrocholesterol (provitamin D 3 ) is converted to pre-Vitamin D 3 (pre-D 3 ) by ultraviolet radiation. [19] Pre-D 3 then isomerizes to D 3 via a thermosensitive but noncatalytic process. [20] This reaction requires specific UVB wavelengths between 290 and 315 nm, which are only emitted during certain parts of the day at specific latitudes and certain seasons. Therefore, the optimal formation of pre-D 3 is multifactorial, being dependent on genetic and environmental factors such as skin pigmentation, clothing, and sunscreen use. [16]

Dietary Vitamin D is fat-soluble and therefore transported via the lymphatics in chylomicrons and subsequently into the venous circulation. Although adipose tissue and muscle consume some dietary Vitamin D, the remainder is transported to the liver where it is metabolized by the Vitamin D 25-hydroxylase cytochrome P450 enzymes (CYP2R1 and CYP27A1) to (25(OH)D). [21] 25(OH)D is then converted to the biologically active form of Vitamin D, 1,25(OH) 2 D, in the proximal renal tubules. [21],[22]


  Storage, Circulation, and Excretion Top


25(OH)D is the major stored and circulating form of Vitamin D and is used clinically as a biomarker of Vitamin D status. Circulating 25(OH)D levels are usually high in the plasma, but in reality 25(OH)D is sequestered in adipose tissue and muscle. [23],[24] Although 25(OH)D's circulating half-life is approximately 10-15 days, [25],[26] tissue release results in an actual half-life of 2-3 months. [27] Vitamin D's distribution in humans has been demonstrated by injecting radiolabeled Vitamin D3 and monitoring biological activity and radioactivity in fat tissue. [28]

In contrast, biologically active 1,25(OH) 2 D circulates at the picomolar range. 1α-hydroxylation is under strict, rate-limiting regulation by serum parathyroid hormone (PTH) and fibroblast growth factor 23 in response to calcium and phosphate levels.

Vitamin D pathway metabolites mainly circulate bound to Vitamin D-binding protein (DBP, 85-90%) and albumin (about 10-15%); only about 1% circulates freely. [29] DBP and albumin have a similar structure, [30] DBP circulates at concentrations of 0.6-11 μmol/L, [29] showing high affinity for 25(OH)D but not Vitamin D or 1,25(OH) 2 D. [31],[32] Therefore, 1,25(OH) 2 D is not an accurate measure of total Vitamin D due to its tight metabolic regulation and short half-life, with its use limited to altered 1α-hydroxylation states. For instance, it is reduced in chronic kidney disease and increased in granulomatous disease.

Ultimately, 25(OH)D and 1,25(OH) 2 D undergo urinary and biliary excretion after conversion to water-soluble calcitroic acid via a multistep pathway. [33],[34]


  Vitamin d and adipose tissue Top


As noted above, Vitamin D insufficiency may be causally related to obesity, [35],[36] and Vitamin D receptor (VDR) gene polymorphisms are associated with obesity. [37] In Saudi Arabia, a high prevalence of Vitamin D deficiency was detected in children in Jeddah: Over 58% of children had relative 25(OH)D deficiency while over 27% had severe deficiency. [38] Vitamin D deficiency was also highly common in older age groups, for instance, in healthy Saudi medical students in the eastern province of Saudi Arabia [39] and in individuals in the Madinah Region. [40] Further afield, two studies in New York and North Texas reported high rates of Vitamin D deficiency in the obese pediatric population. [3],[41]

Hyppönen and Boucher recommended that pregnant women should receive daily Vitamin D supplementation because low Vitamin D levels in pregnancy are associated with insulin resistance and muscle loss, [42] and a high prevalence of Vitamin D deficiency in young pregnant women may increase childhood obesity rates in offspring. [43] Furthermore, other population studies have found that people with lower levels of Vitamin D are more likely to be obese than those with higher levels of Vitamin D [44] although the opposite might also be true. [45]


  Genetic factors related to vitamin d and obesity Top


Given these epidemiological and biological data, a number of genetic studies have attempted to establish links between Vitamin D and obesity. Vitamin D is immunoregulatory and antiproliferative in disease via the VDR. The VDR is expressed in adipose tissue and may, therefore, mediate Vitamin D's action in fat cells. Calcitriol binds to preadipocyte cells but not mature adipocytes [46] consistent with the hypothesis that Vitamin D is only likely to play a role in adipose tissue during preadipocyte to adipocyte transition. However, mechanisms of adipogenesis via the VDR vary depending on calcitriol binding. Although the VDR is expressed early in adipogenesis, functional activation of adipocytes results in high but transient VDR expression. [47],[48]

A number of in vivo studies support a causative role for Vitamin D signaling in adipose metabolism. The murine Insig-2 promoter contains a functional Vitamin D response element that might mediate preadipocyte differentiation. [49] VDR-knockout mice show adipose tissue atrophy around the prostate and mammary glands [50],[51] and overall lower body fat and plasma triglyceride and cholesterol levels compared to wild-type mice. VDR-null mice on high-fat diets grow slower and accumulate less fat than wild-type mice, [52],[53] and human VDR-overexpressing mice develop obesity due to reduced energy expenditure. [54]

In human gene association studies, VDR polymorphisms have been associated with several disease states and also to the risk of Vitamin D deficiency in children and adolescents. [55] The VDR TaqI allele is associated with obesity, [56],[57] and VDR BsmI and ApaI polymorphisms are also significantly associated with increased BMI. [58],[59] These observations suggested that altered VDR function might play a role in obesity.


  Vitamin d status and parathyroid hormone in obesity Top


It has become increasingly clear that low 25(OH)D and high PTH levels are associated with obesity. This appears to occur as a consequence of PTH stimulating renal hydroxylation of 25(OH)D to 1,25(OH) 2 D and calcium influx into adipocytes. Intracellular calcium enhances lipogenesis by activating fatty acid synthase and inhibiting lipolysis, [60],[61] the net effect being enhanced lipid storage. [61]

Vitamin D is also an important cofactor for insulin secretion, [62] with Vitamin D improving insulin sensitivity and secretion, at least in animal models. [63] In human studies, Thomas et al. found that fasting PTH levels were increased and 25(OH)D concentrations were decreased in obese children, [61] with these alterations normalizing after weight reduction, suggesting reversible weight loss.


  The beneficial role of calcium and vitamin d in obesity Top


As noted above, dietary calcium plays a pivotal role energy metabolism. High calcium diets prevent lipid accumulation in fat cells and weight gain from energy-dense diets and increase lipolysis during calorie restriction, thereby speeding up weight loss. [64] Lipid metabolism and triglyceride storage in adipocytes are regulated by intracellular calcium, which stimulates lipogenic gene expression and lipogenesis, suppresses lipolysis, and increases adipose tissue. In an indirect pathway, calcitriol released in response to low calcium diets stimulates calcium influx in human adipocytes and promotes adiposity. Calcitriol suppression via increased dietary calcium may, therefore, be an attractive strategy to prevent and manage obesity: In a transgenic mouse model of obesity, low calcium diets caused accelerated weight gain and fat accumulation while high calcium diets markedly inhibited lipogenesis, accelerated lipolysis, and suppressed fat accumulation. In clinical studies, increased dietary calcium is associated with a reduced risk of obesity, with calcium from dairy products exerting a greater anti-obesity effect than supplements.


  Exploiting The Vitamin D-Endocrine Axis for Therapeutic Benefit Top


The prevalence of being overweight and obese is increasing in both children and adults and is an important public health issue. [65] The Vitamin D-endocrine system appears to be dysregulated in obese individuals, and Vitamin D deficiency is common in obese patients. Many studies have demonstrated the significant effect of calcitriol and calcium on adipocytes while human and animal genetics studies have provided insights into causative links between Vitamin D and obesity. Although we have focused on the VDR, other signaling pathways such as receptor tyrosine kinase and toll-like receptor signaling may also play a role.

In terms of clinical control of obesity, calcitriol, the active form of the Vitamin D 3 metabolite, is likely to be most beneficial since its receptors are present in adipocytes and it modulates inflammatory cytokine expression, thereby possibly overcoming both genetic and nongenetic pathways. [61] Calcitriol modulates adipokine expression, inhibits anti-inflammatory cytokine expression, reduces monocyte recruitment by human preadipocytes, and restores glucose uptake in adipocytes. [66],[67],[68] Furthermore, serum monitoring of 25(OH)D after calcitriol intake is unnecessary because calcitriol inhibits 25(OH)D synthesis in the liver. [69],[70] There is, therefore, compelling evidence that calcitriol is active in obesity. However, it should be noted that some studies have demonstrated little or no effect of Vitamin D on weight, [71],[72] and cholecalciferol supplementation has been shown to have no effect on inflammatory markers in obese subjects. [73]


  Conclusions Top


Obesity is an emerging health problem of growing importance. Vitamin D deficiency is common in pediatric populations. There is evidence that the Vitamin D-endocrine system is dysregulated in obese subjects. Since Vitamin D deficiency is largely undertreated in children and even adults worldwide, this may be a significant contributor to the obesity epidemic. Furthermore, obese children often consume high-calorie foods that are low in minerals and vitamins, are more likely to be sedentary, and have reduced sunlight exposure, further compounding the problem and setting up a vicious cycle in which higher body fat mass and decreased Vitamin D bioavailability further increase the risk of Vitamin D deficiency in obese children.

As the number of obese children increases, pediatricians must be aware of Vitamin D deficiency in obese children and recommend healthy lifestyle choices. We recommend Vitamin D deficiency screening and treatment of obese and overweight children although further studies are required to determine the sequelae of low levels of Vitamin D, the amount and duration of treatment necessary to avoid complications, and the effects of Vitamin D supplementation on the obese pediatric population.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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Abstract
Introduction
Vitamin d metabolism
Vitamin d and ad...
Genetic factors ...
Vitamin d status...
The beneficial r...
Conclusions
Storage, Circula...
Exploiting The V...
References

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