1. IJGMP - Pediatric Obesity and Vitamin D Deficiency - Adilo.S.bahathiq - Saudi Arabia - OPaid

8/20/2019 1. IJGMP - Pediatric Obesity and Vitamin D Deficiency - Adilo.S.bahathiq - Saudi Arabia - OPaid

http://slidepdf.com/reader/full/1-ijgmp-pediatric-obesity-and-vitamin-d-deficiency-adilosbahathiq- 1/12

PEDIATRIC OBESITY AND VITAMIN D DEFICIENCY: A CONCEPT AND

UNDERSTANDING

ADILO S. BAHATHIQ

Vice-Dean, Public Health and Health Informatics, Associate Professor in Reproductive Endocrinology,

Department of Physiology, ollege of !edicine, "!!-A#$"RA "niversity, !a%%ah, &audi Arabia

ABSTRACT

Pediatrics obesity is a ma'or community health issues globally no( days) *he commonness of Pediatrics obesity

and vitamin D deficiency has increased over in several decades) It is caused by imbalance bet(een calories inta%e and

calories utili+ed in body) ne or more factors cause obesity in children that is Physical, psychological, and social health problems are caused due to childhood obesity) Effective active strategies can be used to prevent and control obesity in

children (hich is more effective) *he purpose of this paper is to address various factors influencing childhood obesity and

vitamin D deficiency) It is also addressing the sources of Vitamin D, classification, Ris% factors, the role of vitamin D on

adipose tissue, the genetic role in vitamin D and obesity, the role of inflammation on obesity and Vitamin D status in

!iddle East, etc)

KEYWORDS: hild besity, Pediatric besity, Vitamin D Deficiency

INTRODUCTION SYNTHESIS OF VITAMIN D

Vitamin D or sunshine vitamin, its main and ma'or source is obtained from the sun eposure and minor source is

obtained from diet .dairy products, oil fish, meat and eggs/ 01-123)

It consumed fe( steps to be synthesi+ed) In the s%in, "V-4 (avelengths in sunlight convert 5-dehydrocholesterol

to cholecalciferol .vitamin D6/, (hich has the ability to enter the circulation) In the liver, vitamin D6 by the 1sthydroylation

step it become 78.H/D) In the %idney, by the 7nd hydroylation step it converted to 1,78.H/7D6 (hich is the bioactive

form) #ater on, this final active form has the ability to bind to VDRs and act through it 01-123) VDRs are distributed

throughout the body in the endocrine glands, endothelial cells, vascular smooth muscle cells, cardiomyocytes and

hemolymphopoietic cells01,15,193)

CLASSIFICATION

:e can define vitamin D deficiency based on the follo(ing stratifications of 78.H/D serum

concentration01,12,1;,7<,713=

• Deficiency >8<)< nmol?# or >7<)< ng?m#

• Insufficiency @ 8<)<5B); nmol?# or 7<)<7;); ng?m#

• &ufficiency C58)< nmol?# or C6<)< ng?m#

:e can define obesity based on the follo(ing stratificationsof 4!I=

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• "nder(eight > 19)8

• Healthy @ 19)8 to 7B);

•

ver(eight @ 78 to 7;);

• bese C 6<

Fi=!$e: 2: S-&+esis #) Via,i& D

RISK FACTORS

Vitamin D deficiency is an independent ris% factor for obesity in (omen 06-6<3) In children it is associated (ith

gro(th retardation and s%eletal deformities) !oreover, ne( evidence providedan association bet(een the levels of

78.H/D and increasing age, obesity, reducing insulin sensitivity, hypertension, visceral obesity, hypertriglyceridemia,

metabolic syndrome, immune function, respiratory diseases, infection, allergy, cancers, and cardiovascular diseases06-673)

*here is an indication signs of deviation in the endocrine system of vitamin D in obese sub'ects063=

• Increase in serum P*H)

• Increase in cA!P)

• Increase in renal tubular reabsorption of a)








• Increase circulating 1,78.H/7D6)

• Decrease in serum level of 78.H/D)

•

Decrease in HD#)

• Increase in triglycerides and #D#)

*he ris% factors that lin% the deficiency of vitamin D (ith child obese sub'ects= decreased sunlight eposure,

season .(inter/, limited outdoor activity, clothes that limit cutaneous vitamin D synthesis0B-853) !oreover, lo( vitamin D

levels in the mother during pregnancy play a role on her childs levels and lo(er birth (eight but higher fat mass at B to 2

years old child, race .non-(hite/, age of puberty, lo( mil% consumption, female gander0173 and some mutations in VDR 0

16-5B3)

A study done by *homas et al ) provided an increase in P*H levels and a decrease in 78.H/D levels in obese

sub'ects) &ince these changes normali+ed after (eight loss so, these changes considered as a conseFuences rather than a

ris% factors05-9<3)

L#w C#&*e&$ai#& #) Via,i& D i& O;ese S!;>e*s C#!'" ;e a Res!' #) De)e$e& Me*+a&is,s

• G* genotype variation could affect vitamin D levels and (eight gain by decreasing the insulin effect in brain

tissues, affecting appetite, food choice, and dietary inta%e from an early age09-253)

• Direct relationship bet(een circulating adiponectin and vitamin D levels) Inverse relationship bet(een the

circulating adiponectin and 4!I07-783) Gurthermore, patients (ith insulin resistance, type 7 diabetes and

cardiovascular disease have lo(er concentration of adiponectin07-783)

• *he relationship bet(een 4!I and serum level of 78.H/D is inverse, each unit increase in 4!Ibeing associated

(ith 1)18lo(er concentration of 78.H/D0B-8B3)

• 4ody fats acts as a reservoir for vitamin D .lipid soluble vitamin/, so increasing the content of body fats (ill

increase its seFuestration, leading to decrease its bioavailability0B-883)

• &ome studies has been sho(n that 78.H/D (as stored 66 in fat and 7< in muscle) 4ased on these studies(e

can loo% at the muscles as another reservoir for vitamin D0B-823)

• In obese sub'ects and due to hepatic steatosis, the liver may lo(er the rate of 78.H/Dsynthesis0B-893)

• High levels of leptin and I#2 .secreted by adipose tissue/ may inhabit 1,78.H/7D6 synthesis0B-8;3)

T+e R#'e #) Via,i& D #& A"i<#se Tiss!e

Recently, ne( studies classified the adipose tissues as one of the ma'or endocrine organs0B-2<3) Divided into t(o

types (hite and bro(n, each type has a different cell origin, structure and function01<3) *he bro(n one are present in

children only, it has an average life span of 1< years, so most of them disappears in adulthood01<3) At that time, they

replaced by the (hite one01<3) 4ro(n adipose tissues (or% as thermogenesis0B3, (hile the (hite adipose tissues serve

mainly as energy reserves, secrete hormones, mechanical protection and insulation to the body01<3)In response to high body (eight there (ill be an increase in both fat mass and lean body mass .subtracting body


http://en.wikipedia.org/wiki/Body_fat







6 A"i'# S. Ba+a+i?

fat (eight from total body (eight/0113) *hat is ho( (e eplain the increase in fat mass the adipose tissues are structurally

plastic, so they have the ability to epand and become larger in si+e and number0B-213)

&ome studies have sho(n that vitamin D has no direct effect on body (eight, but it may have an effect on the fat

mass and its distribution) *his effect (as seen only in sub'ects (ith 78.H/D levels less than 8<)< nmol?#0B,27,26 3)

T+e Ge&ei* R#'e i& Via,i& D a&" O;esi-

A study in 4ra+ilian Ama+on area, (as found a significant relationship bet(een an A allele of G* rs;;6;2<; and

being obese during childhood) Ho(ever, the study provided a pivotal role of vitamin D levels on altering the genotype

effects on 4!I) Deficient children presented larger increases in 4!I for each A allele compared (ith normal children093)

*he variation at the G* locus affects 4!I in childhood by accelerating adiposity rebound and fat mass deposits09-293,

(hich may play a role in metabolic disease ris%09-2;3) *a%en together, (e detect an important interaction bet(een G*

and vitamin D levels in relation to childhood obesity, but the mechanisms of this interaction still remain unclear093)

Gurthermore, G* gene is epressed in the human brain, and there is evidence of a relation bet(een its ris% allele and

decreased cerebrocortical insulin sensitivity09-5<3) &ome studies have mentioned a functional role for insulin in the

regulation of energy homeostasis and body (eight in the J&09-513) &ubseFuently, a possible mechanism for the

association bet(een G* genotype and vitamin D levels may involve insulin action at a central level09,57,563)

T+e R#'e #) A"i<#&e*i& #& Via,i& D a&" O;esi-

Adiponectin is a protein produced by adipose tissues and secreted to adipocytes07-7;3) It is located (ithin one of

the susceptibility gene loci for obesity07-7B3) linical trials has been confirmed a difference in the plasma concentration of

adiponectin in obese pediatric sub'ects bet(een sub'ects (ith vitamin D deficiency and sub'ects (ith vitamin D

sufficiency073) Adiponectin circulates in plasma in different forms= trimmers-.#!:/, heamers-.!!:/ and heamers-

.H!:/07-7B3) H!: is identified as the most bioactive form07-7B3) *he concentration of adiponectin in pediatric obese

sub'ects (ith vitamin D deficiency (as significantly lo(er than in pediatric obese sub'ects (ith vitamin D sufficiency073)

!oreover, the greatest difference (as observed in heamers-H!:) It has been proved to have insulin sensiti+ing effects07-

783, regulates centrally food inta%e and body (eight07-723, cardioprotective07-753, anti inflammatory and antioidant

properties07-793, demonstrating that it has a clear clinical important role (ith respect to obesity and its comorbid

conditions073)

Ma$i@ Mea''#<$#ei&ases MMPs/ E&-,es

!!Ps en+ymes play a role in tissue remodeling, migration of leucocytes, inflammation, infection and obesity)

*hese en+ymes are produced by different cell types, including lymphocytes, granulocytes, astrocytes, activated

macrophages and adipose tissue063)

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http://en.wikipedia.org/wiki/Body_weight

http://en.wikipedia.org/wiki/Body_weight




Pe"ia$i* O;esi- a&" Via,i& D De)i*ie&*-: A C#&*e< a&" U&"e$sa&"i&=

Evidence and reports provided a remar%able increase in the levels of some en+ymes .!!P-7, !!P-9 and !!P-

;/ in obese children06,66,6B,683) Also, it has been sho(n a correlation bet(een !!P-; and 4!I06-623) *he study that

provided an increase in !!P-9 levels, it also proved a decrease in *I!P-1 levels at the same time in obese sub'ects more

than non-obese06-653)

!!P-7 promoter haplotype play a role in the percentage of body fat in obese children06-693) Gunctional !!P-;

gene polymorphism is strongly associated (ith obesity06-6;3, and !!P-; genotypes and haplotypes affect !!P-; levels

in obese sub'ects06-B<3)

VDR-K mice play a role in some of these en+ymes .!!P-7, !!P-; and !!P-17/ by up regulating their

epression, reduce body (eight, lo(er serum lept in concentrations and it also enhance the influ of inflammatory cells

andphospho-acetylation of JG-L4 in lungs06-B13) !oreover, VDR *aFI polymorphism play a role in decreasing the

production of *I!P-106-B73)1,78.H/7D6do(n regulated !!P-; levels in %eratinocytes, and may reduce the harmful

effects of ecessive *JG-M-induced proteolytic activity, (hich play a role in cutaneous inflammation06-B63) It also inhibits

both the basal levels and the staphylococcus-stimulated production of !!P-; in human blood monocytes and alveolar

macrophages06-BB3) In addition, some reports provided a beneficial role of vitamin D analog in reducing the epression of

!!P-7, !!P-;, VENG and P*H-related peptide in #e(is lung carcinoma cells06-B83) *a%en together,1,78.H/ 7D6 may

play an important role in obesity by do(n regulating !!Ps levels and regulating *I!Ps levels063)

T+e R#'e #) I&)'a,,ai#& #& O;esi-

Inflammatory processes play apivotalrole in obesity) PNs play a role in inflammation) Os play a role in

converting the arachidonic acid into PNs) &ome of PNs= PNE 7, PNG7M PND7 and PN7 has been reported to induce obesity

by different (ays,either by inducing adipogenesis or inhabiting lipolysis06,B2,B53) PNE7 (or% as enhancer to lipid

accumulation in hepatocytes and participated in the development of hepatic steatosis06-8<3) PNG7M is a potent inhibitor of

adipocyte differentiation06,B9,B;3) O-7 play a role in activation of PNE706-813, so increase the O-7 levels (ill

increase the activation rate of PNE7 (hich (ill lead to obesityand vise versa) Interestingly, there is an inverse relationship







8 A"i'# S. Ba+a+i?

bet(een PNs levels and fat mass) !oreover, vitamin D may play a role in modulating the inflammatory process in obese

sub'ects, 1,78.H/7D6and its analogs has been reported that it has a role in do(n regulating PNs synthesis by inhibiting

selectively the activity of O-706,87,863)

Via,i& D Sa!s i& Mi""'e Eas

Vitamin D deficiency and its comorbid conditions are a pandemic health problem, especially in the !iddle East,in

particular in &audi Arabia because of limited outdoor activities and the prevalence of (earing dar% s%in covering clothes

for cultural and religious reasons016-1B3) As a matter of fact, 6<-8< of children and adults in "AE, Australia, *ur%ey,

India and #ebanon have been found to have vitamin D deficiency016,58,523) Although, &audi Arabia is one of the sunniest

countries, vitamin D deficiency has long been reported as prevalent in &audi population018,55,593) A study done by

Arda(iet al ) reported an approimately 9< prevalence of vitamin D deficiency in 1157 &audi (omen from the (estern

region of &audi Arabia018-5;3)

D#si&= C#&si"e$ai#&s #) Via,i& D

Jo(adays, ne( studies proved that the optimum dose of vitamin D6 supplements is depend on body (eight 0

B,28,223, so (e suggest that obese sub'ects have to receive t(o to three times vitamin D more than non-obese to satisfy

their bodyQs vitamin D reFuirements0B-2B3)

Ho(ever, if the target of vitamin D supplementation in obese (as to affect one of comorbidities associated (ith

obesity, the dose (ill be various for each comorbid condition 0B3)

CONCLUSIONS

*he function of adipose tissues is not only as nutritive storage083) Recently, it classified as a ma'or endocrineorgan) Vitamin D is a fat soluble prohormone) It is easily stored and seFuestered in adipose tissue) Also, it can be stored in

muscles) *he deficiency of vitamin D is common in obese sub'ects) !any efforts have been made in the understanding of

vitamin D metabolism and functions) Interestingly, several studies provided the interrelationship bet(een vitamin D and

adipose tissue, it may both regulate and be regulated by vitaminD023) It is able to act via numerous genomic and non-

genomic mechanisms= including protein epression, inflammation, and cellular metabolism) *here is a clear relationship

bet(een G* rs;;6;2<; and being obese in childhood in 4ra+ilian Ama+on) !oreover, some evidence proved an

association bet(een genetic effects of G* and vitamin D levels) #i%e(ise, it has been proved a relationship bet(een

pediatric obesity, adiponectin and vitamin D levels) *he decrease in vitamin D levels (ill lead to decrease in circulating

adiponectin and as a result there (ill be an increase in the total body (eight) In fact, vitamin D deficiency and its comorbid

conditions are a pandemic health problem,particularly in &audi Arabia in the (estern region due to their food lifestyle,

limited outdoor activities and the prevalence of (earing dar% s%in covering clothes for cultural and religious reasons)

ABBREVIATIONS

P*H,Parathyroid hormonecA!P,"rinary cyclic adenosine 6,8-monophosphate 1,78.H/7D6, 1M, 78-

hydroyvitamin D6 78.H/D, 78-hydroyvitamin D6 I#, Interleu%in VDR, Vitamin D receptor"V-4, "ltraviolet 4

4!I, 4ody mass inde!!Ps, !atri metalloproteinases *I!P-1, *issue inhibitor of metalloproteinase-1 VDR-K,

Vitamin D receptor-%noc%-out PNs, Prostaglandins O, yclooygenase#!:, #o( molecular (eight !!:,

!edium molecular (eight H!:, High molecular (eight J&, entral nervous system)

I,<a* Fa*#$ (CC/: 1.063 NAAS Rai&=: 1.6



Pe"ia$i* O;esi- a&" Via,i& D De)i*ie&*-: A C#&*e< a&" U&"e$sa&"i&=

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http://en.wikipedia.org/wiki/Lean_body_mass





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Documents

1. IJGMP - Pediatric Obesity and Vitamin D Deficiency - Adilo.S.bahathiq - Saudi Arabia - OPaid