• Users Online: 672
  • Print this page
  • Email this page


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 4  |  Issue : 2  |  Page : 162-165

Vitamin D status among overweight and obese adolescents


1 Department of Biochemistry, Govind Ballabh Pant Institute of Postgraduate Medical Education and Research, Rohini, New Delhi, India
2 Department of Laboratory Medicine, Shree Aggarsain International Hospital, Rohini, New Delhi, India
3 Department of Biochemistry, Pt. B.D. Sharma PGIMS, Rohtak, Haryana, India

Date of Submission10-Feb-2020
Date of Acceptance25-Feb-2020
Date of Web Publication17-Jun-2020

Correspondence Address:
Dr. Jyoti Bala
217, RPS, DDA Flats, Mansarovar Park, Shahdara, New Delhi
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bbrj.bbrj_11_20

Rights and Permissions
  Abstract 


Introduction: Deficiency of vitamin D is pandemic and has been associated with a wide variety of disease states such as cardiovascular disease risk factors and impaired glucose homeostasis and are more common in overweight and obese children. Both endocrine and metabolic disorders occur with obesity and it has been suggested that obesity is a risk factor for vitamin D deficiency. The inverse association between higher body fat and lower vitamin D levels has been attributed to sequestration of the fat soluble vitamins within the plentiful adipose tissue. Aim and Objective: This study aims to determine the status of vitamin D levels in overweight and obese adolescent children and to compare them with age and sex matched healthy controls. Materials and Methods: This observational study was conducted in the Department of Biochemistry in collaboration with Department of Pediatrics, Pt. B.D. Sharma, PGIMS, Rohtak. Twenty-five overweight and obese adolescents based on BMI were recruited in study group (Group II) and twenty-five age and sex matched healthy controls were included in group I (Control group). Study samples were drawn and serum vitamin D levels were analyzed by radioimmunoassay. Results: Out of 25 cases 12(48%) were overweight and 13(52%) were obese adolescents. Mean BMI in group I was 17.36±3.67 kg/m2 and in group II was 31.90±1.01 kg/m2. 14 (56%) had vitamin D levels <20 ng/mL that is in the deficiency range. 7 (28%) had in the insufficiency range (21-30 ng/mL), 4 (16%) had in the sufficient range. Mean serum vitamin D levels in group I (Controls) were 28.41±8.83 and group II (Cases) were 21.6 ±5.65. The serum vitamin D levels were significantly decreased in group II as compared to group I (p = 0.002). Conclusion: The findings of present study concluded that, vitamin D deficiency is common problem obese and overweight adolescents, this may help to explain the relationship between obesity and several chronic diseases that are associated with poor Vitamin D status. However, there is a need for more randomized controlled trials, involving larger sample sizes, focusing on obese adolescents with documented vitamin D deficiency and careful selection of the dose, dosing regimen, and achievement of vitamin D concentrations.

Keywords: Adolescent, body mass index, obesity, Vitamin D


How to cite this article:
Saurabh K, Bala J, Hemang. Vitamin D status among overweight and obese adolescents. Biomed Biotechnol Res J 2020;4:162-5

How to cite this URL:
Saurabh K, Bala J, Hemang. Vitamin D status among overweight and obese adolescents. Biomed Biotechnol Res J [serial online] 2020 [cited 2020 Jul 7];4:162-5. Available from: http://www.bmbtrj.org/text.asp?2020/4/2/162/286835




  Introduction Top


Vitamin D is also called “sunshine vitamin” is a fat-soluble vitamin which also serves as a hormone in the body. It is obtained from sun exposure, food, and supplements and must two hydroxylation reactions to be converted into the active form. The first hydroxylation occurs in the liver and converts Vitamin D to 25-hydroxyvitamin D [25(OH)D], also known as calcidiol. This is followed by further hydroxylation in the kidney and forms the physiologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol.[1]

Vitamin D maintains normal mineralization of bone by promoting calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations and to prevent hypocalcemic tetany. It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts.[2],[3] Insufficient Vitamin D results in thin and brittle bones. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults.[2] Other important roles of Vitamin D in the body are the modulation of cell growth, neuromuscular and immune function, and reduction of inflammation. Deficiency of Vitamin D often associates with weight gain, deficient immune function, decreased muscle strength and bone disorders, mood disorders, and cognitive impairments.[2],[4],[5] Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated by Vitamin D.[2]

Nutrient deficiencies are usually the result of dietary inadequacy, impaired absorption and use, increased requirement, or increased excretion. A Vitamin D deficiency can occur when usual intake is lower than recommended levels, limited sun exposure, the kidneys cannot convert 25(OH)D to its active form, or inadequate absorption of Vitamin D from the digestive tract. Vitamin D-deficient diets are associated with milk allergy, lactose intolerance, ovo vegetarianism, and veganism.[2] The Endocrine Society has suggested that 25(OH)D levels of 75–250 nmol/l (30–100 ng/ml) are “sufficient,” 52–72 nmol/l (21–29 ng/ml) are “insufficient” and <50 nmol/l (20 ng/ml) are “deficient.”[6]

Obesity is a condition of excess adiposity, and the most common measurement used in its diagnosis is body mass index (BMI) (BMI; weight in kilograms divided by the square of height in meters). Obesity, defined by the World Health Organization as a BMI of 30 kg/m2 or more.[7]

Deficiency of Vitamin D is pandemic and has been implicated in a wide variety of disease states. Vitamin D deficiency is associated with cardiovascular disease risk factors and impaired glucose homeostasis and is more common in overweight and obese children. Both endocrine and metabolic disorders occur with obesity, and it has been suggested that obesity is a risk factor for Vitamin D deficiency. The inverse association between higher body fat and lower Vitamin D levels has been attributed to sequestration of the fat-soluble vitamins with in the plentiful adipose tissue (AT).[8] There are very few studies that examine the relationship between Vitamin D status and obesity in children and adolescents. Hence with this background, we analyzed Vitamin D status in this age group.

Aim and objective

The aim of the present study is to determine the status of Vitamin D levels in overweight and obese adolescent children and to compare them with age- and sex-matched healthy controls.


  Methods Top


This study has been approved by the ethical committee of the institute in which study was carried out. This observational study was conducted in the Department of Biochemistry in collaboration with the Department of Pediatrics, Pt. B. D. Sharma, PGIMS, Rohtak. Twenty-five overweight and obese adolescents based on BMI were recruited in the study group (Group II) and twenty-five age and sex-matched healthy controls were included in Group I (Control group). Individuals on antiepileptic drugs, Vitamin D intake, chronic disease (renal, hepatic disease, endocrine, and malignancy), gastric or bowel resection, and malabsorption were excluded from the study. Study samples were drawn, and serum Vitamin D levels were analyzed by radioimmunoassay.[9]


  Results Top


Of 25 cases, 12 (48%) were overweight, and 13 (52%) were obese adolescents. Mean BMI in Group I was 17.36 ± 3.67 kg/m2, and in Group II was 31.90 ± 1.01 kg/m2. Fourteen (56%) had Vitamin D levels <20 ng/mL that is in the deficiency range. Seven (28%) had in the insufficiency range (21–30 ng/mL), 4 (16%) had in the sufficient range [Table 1]. The mean serum Vitamin D levels in Group I (controls) were 28.41 ± 8.83, and Group II (cases) were 21.6 ± 5.65. The serum Vitamin D levels were significantly decreased in Group II as compared to Group I (P = 0.002) [Figure 1] and [Table 2].
Table 1: Vitamin D status in cases and controls

Click here to view
Figure 1: Mean serum Vitamin D levels in cases and control

Click here to view
Table 2: Baseline characteristics in both the groups

Click here to view



  Discussion Top


Vitamin D deficiency is considered to be a worldwide problem in both adults and children.[10] National surveys across three different continents revealed that among youth, Vitamin D deficiency is more frequent in adolescents than younger children.[11] In the US, data collected from the National Health and Nutrition Examination Survey 2003–2006 show that approximately 27% of adolescents age 12–18 years are Vitamin D deficient,[12] while in Europe one study showed that over 90% of teenage girls had 25(OH)D concentrations <50 nmol/l during the winter months.[7]

The results of this study confirm that decreased Vitamin D levels are common in obese and overweight adolescents, and this may help to explain the relationship between obesity and several chronic diseases that are associated with poor Vitamin D status.

Recent studies from different countries have also demonstrated that Vitamin D deficiency is common in obese children,[13] possibly due to the low quality of diet.[14] 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 deficiency in obese children.[15]

Excess adiposity has long been associated with Vitamin D deficiency[16] and it is estimated that 34%–92% of obese children have suboptimal Vitamin D status.[12],[13] Epidemiological data also suggest that the prevalence of Vitamin D deficiency in obese children is directly related to the degree of adiposity, with overweight children at 29%, obese at 34%, and severely obese at 49%.[12]

The genomic responses to 1,25(OH)2D result from its stereospecific interactions with its nuclear Vitamin D receptor (VDR). This protein is a member of the superfamily of the steroid hormone zinc finger receptors. On binding to 1,25(OH)2D, VDR forms a heterodimer with the retinoid-X receptor and binds to Vitamin D response elements on DNA sequences resulting in expression or transrepression of specific gene products.[17] In humans, VDR is encoded by the VDR gene. VDR regulates the expression of numerous genes involved in calcium/phosphate homeostasis, cellular proliferation and differentiation, and immune response, largely in a ligand-dependent manner.[18] Germane to glucose tolerance and insulin sensitivity, VDR is present in pancreatic β cells[7],[18] and in the peripheral tissues of AT[19] and skeletal muscle.[7]

Early studies demonstrate that compared with lean controls, obese individuals are only about half as efficient in converting the vitamin, whether taken orally or through cutaneous synthesis following ultraviolet B exposure, to 25(OH)D.[20] However, some recent investigations challenge this hypothesis, concluding that the low Vitamin D status of obesity is simply a result of volumetric dilution in larger-sized individuals. These newer studies show that when 25(OH)D concentrations are corrected for body mass, Vitamin D bioavailability does not differ between normal weight and obese individuals.[16]

There are very few studies that examine the relationship between Vitamin D status and body fat indexes exclusively in adolescents. In a multivariate analysis of data collected on 58 obese adolescents, 25(OH)D decreased by 1.15 ± 0.55 nmol/l per 1% increment in total body fat mass, whereas it was not significantly associated with AO as determined by computed tomography measured visceral AT mass.[21]

In a weight intervention study of obese children, a reduction of 1 kg/m2 BMI was accompanied by an increase of ~12.5 nmol/l 25(OH)D serum concentration.[19] The beneficial effects of weight loss on Vitamin D status are likely to be transient; however, as 25(OH)D concentrations are found to fall when measured over time.[22]

AT in obese women expresses the enzymes for both the formation of 25D and its active metabolite, 1,25D, and for degradation of Vitamin D.[23] Subcutaneous AT has also been found to have lower expression of one of the enzymes responsible for 25-hydroxylation of Vitamin D (CYP2J2), as well as a tendency toward a decreased expression of the 1-α hydroxylase. These data suggest that both 25-hydroxylation and 1-α hydroxylation are impaired in obesity.In vitro studies have demonstrated that 1,25D inhibits adipogenesis and induces adipocyte apoptosis.[24],[25]


  Conclusion Top


The findings of the present study concluded that Vitamin D deficiency is a common problem obese and overweight adolescents, and this may help to explain the relationship between obesity and several chronic diseases that are associated with poor Vitamin D status. However, there is a need for more randomized controlled trials involving larger sample sizes, focusing on obese adolescents with documented Vitamin D deficiency and careful selection of the dose, dosing regimen, and achievement of Vitamin D concentrations.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Thacher TD, Clarke BL. Vitamin D insufficiency. Mayo Clin Proc 2011;86:50-60.  Back to cited text no. 1
    
2.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press; 2010.  Back to cited text no. 2
    
3.
Cranney C, Horsely T, O'Donnell S, Weiler H, Ooi D, Atkinson S, et al. Effectiveness and Safety of Vitamin D. Evidence Report/Technology Assessment No. 158 Prepared by the University of Ottawa Evidence-Based Practice Center under Contract No. 290-02.0021. AHRQ Publication No. 07-E013. Rockville, MD: Agency for Healthcare Research and Quality; 2007.  Back to cited text no. 3
    
4.
Holick MF. Vitamin D. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, editors. Modern Nutrition in Health and Disease. 10th ed. Philadelphia: Lippincott Williams and Wilkins; 2006.  Back to cited text no. 4
    
5.
Norman AW, Henry HH. Vitamin D. In: Bowman BA, Russell RM, editors. Present Knowledge in Nutrition. 9th ed. Washington DC: ILSI Press; 2006.  Back to cited text no. 5
    
6.
Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, et al. Evaluation, treatment, and prevention of Vitamin D deficiency: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2011;96:1911-30.  Back to cited text no. 6
    
7.
Peterson CA, Tosh AK, Belenchia AM. Vitamin D insufficiency and insulin resistance in obese adolescents. Ther Adv Endocrinol Metab 2014;5:166-89.  Back to cited text no. 7
    
8.
Hollis BW, Kamerud JQ, Selvaag SR, Lorenz JD, Napoli JL. Determination of Vitamin D status by radioimmunoassay with an 125I-labeled tracer. Clin Chem 1993;39:529-33.  Back to cited text no. 8
    
9.
Reddy TP, Reddy K, Reddy MS, Manjunathan GA. Levels of Vitamin D among overweight and obese adolescents: An observational study. Int J Contemp Pediatr 2017;4:1934-9.  Back to cited text no. 9
    
10.
van Schoor NM, Lips P. Worldwide Vitamin D status. Best Pract Res Clin Endocrinol Metab 2011;25:671-80.  Back to cited text no. 10
    
11.
Stoffman N, Gordon CM. Vitamin D and adolescents: What do we know? Curr Opin Pediatr 2009;21:465-71.  Back to cited text no. 11
    
12.
Turer CB, Lin H, Flores G. Prevalence of Vitamin D deficiency among overweight and obese US children. Pediatrics 2013;131:e152-61.  Back to cited text no. 12
    
13.
Olson ML, Maalouf NM, Oden JD, White PC, Hutchison MR. Vitamin D deficiency in obese children and its relationship to glucose homeostasis. J Clin Endocrinol Metab 2012;97:279-85.  Back to cited text no. 13
    
14.
Beydoun MA, Boueiz A, Shroff MR, Beydoun HA, Wang Y, Zonderman AB. Associations among 25-hydroxyvitamin D, diet quality, and metabolic disturbance differ by adiposity in adults in the United States. J Clin Endocrinol Metab 2010;95:3814-27.  Back to cited text no. 14
    
15.
Almazroea AH. Is Vitamin D deficiency a cause or result of childhood obesity? Saudi J Health Sci 2016;5:1-5.  Back to cited text no. 15
  [Full text]  
16.
Drincic AT, Armas LA, Van Diest EE, Heaney RP. Volumetric dilution, rather than sequestration best explains the low Vitamin D status of obesity. Obesity (Silver Spring) 2012;20:1444-8.  Back to cited text no. 16
    
17.
Haussler MR, Whitfield GK, Kaneko I, Haussler CA, Hsieh D, Hsieh JC, et al. Molecular mechanisms of Vitamin D action. Calcif Tissue Int 2013;92:77-98.  Back to cited text no. 17
    
18.
Wang Y, Zhu J, DeLuca HF. Where is the Vitamin D receptor? Arch Biochem Biophys 2012;523:123-33.  Back to cited text no. 18
    
19.
Ding C, Gao D, Wilding J, Trayhurn P, Bing C. Vitamin D signalling in adipose tissue. Br J Nutr 2012;108:1915-23.  Back to cited text no. 19
    
20.
Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of Vitamin D in obesity. Am J Clin Nutr 2000;72:690-3.  Back to cited text no. 20
    
21.
Lenders CM, Feldman HA, Von Scheven E, Merewood A, Sweeney C, Wilson DM, et al. Relation of body fat indexes to Vitamin D status and deficiency among obese adolescents. Am J Clin Nutr 2009;90:459-67.  Back to cited text no. 21
    
22.
Reinehr T, de Sousa G, Alexy U, Kersting M, Andler W. Vitamin D status and parathyroid hormone in obese children before and after weight loss. Eur J Endocrinol 2007;157:225-32.  Back to cited text no. 22
    
23.
Coupaye M, Breuil MC, Rivière P, Castel B, Bogard C, Dupré T, et al. Serum Vitamin D increases with weight loss in obese subjects 6 months after Roux-en-Y gastric bypass. Obes Surg 2013;23:486-93.  Back to cited text no. 23
    
24.
Kong J, Li YC. Molecular mechanism of 1,25-dihydroxyvitamin D3 inhibition of adipogenesis in 3T3-L1 cells. Am J Physiol Endocrinol Metab 2006;290:E916-24.  Back to cited text no. 24
    
25.
Sergeev IN. 1,25-Dihydroxyvitamin D3 induces Ca2+-mediated apoptosis in adipocytes via activation of calpain and caspase-12. Biochem Biophys Res Commun 2009;384:18-21.  Back to cited text no. 25
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed50    
    Printed1    
    Emailed0    
    PDF Downloaded13    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]