In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
240
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
Re iew A icle
A Sys ema ic Re iew on Li es yle and Nu i ional Managemen o
Polycys ic O a y Synd ome
D . Anamika Dixi 1*, Du gesh Kuma Sha ma 2
1 Assis an P o esso , Depa men o Human Nu i ion, Uni e si y Ins i u e o Heal h Science
C.S.J.M Uni e si y, Kanpu , U a P adesh, India
2 S uden , Depa men o Human Nu i ion, Uni e si y Ins i u e o Heal h Science,
C.S.J.M Uni e si y, Kanpu , U a P adesh, India
Co esponding Au ho : * D . Anamika Dixi DOI: h ps://doi.o g/10.5281/zenodo.17678623
Abs ac
Manusc ip In o ma ion
He e, we p esen a na a i e e iew o he widely unde s ood changes o he nu i ion and
li es yles o women and gi ls wi h polycys ic o a y synd ome (PCOS). The da abase was
analysed, combining PCOS en ies wi h causes, diseases, die supplemen a ion, li es yle,
physical ac i i y, and use o he bs. This s udy explains how di e en biochemical ou es
con ibu e o imbalances in lipid, ca bohyd a e, and ho mone egula ion among a ec ed
indi iduals. I also explo es links wi h sleep p oblems, physiological and psychological
shi s, and s ess- ela ed in lamma ion. These condi ions consis en ly lead o he occu ence
o se e e diseases in pa ien s su e ing om diabe es, he a y degene a ion o in e nal
o gans, in e ili y, a he oscle osis, ca dio ascula diseases and cance . Change in li es yles,
die pa e ns and p ope selec ion o nu ien s, pha macological and na u al
supplemen a ion in he o m o he bs, and physical ac i i y ha e been p oposed. The
p og ess and consequences o PCOS a e la gely modi iable and depend on he pa ien ’s
e o , al hough we ha e o ake in o accoun he gene ic de e minan s.
▪ ISSN No: 2583-7397
▪ Recei ed: 05-011-2024
▪ Accep ed: 11-12-2024
▪ Published: 30-12-2024
▪ IJCRM:3(6); 2024: 240-253
▪ ©2024, All Righ s Rese ed
▪ Plagia ism Checked: Yes
▪ Pee Re iew P ocess: Yes
How o Ci e his Manusc ip
Dixi A, Sha ma DK. A Sys ema ic
Re iew on Li es yle and Nu i ional
Managemen o Polycys ic O a y
Synd ome. In e na ional Jou nal o
Con empo a y Resea ch in
Mul idisciplina y.2024; 3(6): 240-253.
KEYWORDS: Nu i ion, li es yle, PCOS; ep oduc ion; die ; sleep; supplemen a ion; he bs suppo ing
INTRODUCTION
Polycys ic o a y synd ome (PCOS) is a p e alen ho monal
diso de ha a ec s a signi ican po ion o women du ing hei
ep oduc i e yea s, es ima ed a oughly one- i h o his
popula ion [1]. In 2003, in e na ional ep oduc i e medicine
expe s mee ing in Ro e dam e ised he diagnos ic s anda ds,
leading o b oade ecogni ion o he synd ome’s di e se clinical
o ms [2]. This di e si y p esen s challenges o managemen , ye
many pa ien s show o e lapping me abolic cha ac e is ics ha
a e impo an o bo h e alua ion and he apy [3].
Many s udies ha e shown ha highe ho mone le els, gu
mic obiome composi ion, and plasma me abolomics a e new
pa ame e s ela ed o he PCOS pheno ypes [4]. The clinical
pheno ypes can change o e he li e span wi h highe weigh
gain, and can ound in he same pa ien . Indi idualised ea men
emains he main app oach, bu g ouping he pheno ypes and
ollowing The apeu ic guidance may also ha e clinical alue.
Ea ly adop ion o well-de ined managemen s a egies is
essen ial, pa icula ly o emales wi h PCOS, who ace an
ele a ed isk o de eloping endome ial o o a ian malignancies.
[5,6]. The e o e, he apeu ic s a egies ha inco po a e an i-
in lamma o y agen s as adjunc s o an icance ea men a e
impo an . Such app oaches can dis up ha m ul signalling
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
241
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
pa hways, con ibu ing o imp o ed su i al a es, quicke
eco e y, and enhanced quali y o li e o pa ien s.
1.1.
Physiological Basis
The ou main causes o he physiological basis o PCOS include:
• diso de s o gonado opin ho monal syn hesis;
• he appea ance o insulin esis ance;
• he in luence o he p esen excessi e body a ; and inally,
• he me abolic pa hways in ol ed in PCOS ( he sec e ion and
ac i i y o insulin, encoding o s e oidogenesis, and o he
me abolic and ho monal pa hways) (Figu e 1) [7].
Figu e 1. Main pa hophysiological basis o polycys ic o a y synd ome (PCOS)-
diso de s o gonado opin ho monal syn hesis, he appea ance o insulin
esis ance, he in luence o he p esen excessi e body a and oblique me abolic
pa hways in ol ed in PCOS.
App op ia e unc ioning o he mechanisms esponsible o he
ma u a ion o he o a ian ollicle and i s o ula ion depends on
he p ope physiological ac i i y o h ee o gans: he
hypo halamus, pi ui a y gland, and o a ies.
Ho monal con ol wi hin he hypo halamic–pi ui a y–o a ian
(HPO) axis ope a es h ough long, sho , and ul asho nega i e
eedback mechanisms. Neu ons in he hypo halamic
sup achiasma ic egion syn hesise gonado opin- eleasing
ho mone (GnRH), which en e s he pi ui a y po al ci cula ion
ia he median eminence. I s elease depends on neu onal
ne wo k ac i i y and occu s in pulses ha de e mine
gonado opin ou pu . Slowe GnRH pulses a ou sec e ion o
ollicle-s imula ing ho mone (FSH), whe eas as e pulses
p omo e lu einizing ho mone (LH) elease om he an e io
pi ui a y. LH d i es co pus lu eum o ma ion and p oges e one
syn hesis, while FSH suppo s ollicula ma u a ion and es ogen
p oduc ion by ac i a ing a oma ase in g anulosa cells. When LH
p edomina es o e FSH, and ogen syn hesis inc eases, a pa e n
o en obse ed in polycys ic o a y synd ome (PCOS) [8].
Insulin also con ibu es o PCOS pa hophysiology by ac ing wi h
LH o ele a e and ogen ou pu and by educing hepa ic
p oduc ion o sex ho mone-binding globulin (SHBG), he eby
inc easing ee es os e one le els [8]. Excess adipose issue
u he agg a a es hese p ocesses because adipocy es elease
ho mones such as lep in and esis in and p oduce in lamma o y
media o s, including in e leukin-1β and umou nec osis ac o -
α [9]. The ac i i y o lep in a ec s he unc ion o he
hypo halamus–pi ui a y gland–o a y axis by modi ying he
sec e ion o GnRH, LH, and FSH. Lep in ac s on he
hypo halamus o in luence he elease o gonado opins,
indi ec ly s imula ing lu einizing ho mone (LH) sec e ion and
p omo ing gonado opin- eleasing ho mone (GnRH) ac i i y.
This mechanism may enhance and ogen p oduc ion. Adipose
issue also eleases in lamma o y cy okines ha sus ain oxida i e
s ess and in lamma ion in PCOS, condi ions in ensi ied by
hype glycemia, excess a mass, and ele a ed and ogens [8].
The clinical di e si y o PCOS e lec s he in ol emen o
nume ous me abolic pa hways. These include insulin signaling
and i s ela ed genes—such as hose coding o he insulin
ecep o (IR), insulin (INS), and insulin-like g ow h ac o (IGF)
and i s ecep o —as well as genes linked o s e oid ho mone
syn hesis, cy och ome P450 ac i i y (CYP17, CYP11A1), and
ho mone ecep o unc ion, including and ogen ecep o (AR),
LH ecep o , lep in, and ollis a in [10]. Die a y habi s
emphasising an i-in lamma o y oods and low glycemic index o
educed- a in ake appea o lowe he isk o PCOS de elopmen
[11,12].
1.2.
Imp o emen in Me abolic Pa hways
1.2.1.
Insulin Resis ance
Weigh gain media es mos o i s di ec medical sequelae h ough
wo sening insulin sensi i i y.
Insulin esis ance (IR) is cen al o he onse o me abolic
diso de s such as hype ension, impai ed glucose con ol, and
abno mal lipid p o iles. Resea ch indica es ha mi ochond ial
impai men con ibu es o IR, o en igge ed by excess lipid
accumula ion in non-adipose issues. The esul ing oxida i e
s ess in skele al muscle inc eases eac i e oxygen species (ROS)
gene a ion, u he dis up ing mi ochond ial unc ion and insulin
signalling [13]. This mechanism links IR o obesi y-associa ed
condi ions, including polycys ic o a y synd ome (PCOS). The
cellula e ec s o insulin occu h ough wo main pos - ecep o
pa hways: he phospha idylinosi ol 3-kinase (PI3K) and he
mi ogen-ac i a ed p o ein kinase (MAPK) pa hways [14]. The
PI3K pa hway egula es cellula in e media y me abolism,
whe eas he MAPK pa hway con ols g ow h p ocesses and
mi oses [14]. AKR1C3 exp ession in adipocy es leads o he
occu ence o insulin esis ance and hype insulinemia, hen
d i es a icious ci cle o in a-adipose and ogen ac i a ion, lipid
accumula ion, and hy- hype insulinemia [15]. Kau man e al.
sugges ed ha e hnici y has an addi i e e ec on insulin
esis ance in PCOS. Mexican Ame ican women showed
signi ican ly highe insulin le els. Resis ance compa ed wi h
Caucasian Ame ican women [16].
1.2.2 Oxida i e S ess and Ch onic In lamma ion
The associa ion be ween body weigh and IR is media ed h ough
in lamma o y pa hways [17]. Obesi y causes changes in he elease
o key cy okines and adipokines, which in u n mani es in
pa ac ine and endoc ine e ec s. The inc eased le els o lep in
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
242
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
and plasminogen ac i a o inhibi o -1 and he educed elease o
adiponec in esul in a gene alised low-g ade in lamma o y
esponse. This p ocess is media ed by mac ophages and o he
immune cells.
Ele a ed oxida i e s ess ma ke s—such as eac i e oxygen
species (ROS), p47phox exp ession, and hioba bi u ic acid-
eac i e subs ances (TBARS)—ha e been obse ed in women
wi h PCOS ollowing consump ion o sa u a ed a s, e en when
obesi y is no p esen . Die s high in e ined suga s and sa u a ed
a y acids u he in ensi y ROS o ma ion h ough se e al
pa hways, including al e a ions in gu mic obio a composi ion
[18]. Bo h ci cula ing immune cells and excess adipose issue
con ibu e independen ly o he oxida i e imbalance
cha ac e is ic o PCOS [19]. Lipid-d i en oxida i e s ess appea s
o play a cen al ole in he onse o insulin esis ance and
hype and ogenism, wi h adipose issue ac ing as an addi ional
p o-oxidan sou ce and modula o o insulin signalling [19].
Ch onic and ogen exposu e also inc eases oxida i e s ess in
panc ea ic isle cells, leading o mi ochond ial impai men [20,21].
Supe oxide is a ROS p oduced when NADPH is oxidised by
memb ane-bound NADPH oxidase [22]. Abno mal gene a ion o
eac i e oxygen species (ROS) by NADPH oxidase con ibu es
o ca dio ascula complica ions—such as endo helial
dys unc ion, a he oscle osis, and hype ension— ha a e
equen ly seen in women wi h PCOS [23]. Oxida i e s ess
igge ed by pe oxides ac i a es he nuclea ac o κB (NF-κB)
pa hway, a majo egula o o in lamma ion ha enhances he
ansc ip ion o he umou nec osis ac o -α (TNF-α) gene [24].
In ake o sa u a ed a s can u he in ensi y oxida i e esponses,
p omo ing TNF-α elease om leukocy es [19,25]. Ou indings
also indica e ele a ed TNF-α syn hesis in women wi h PCOS [4].
Those wi h no mal o low and ogen concen a ions, based on
o al es os e one and he ee and ogen index (FAI), appea
pa icula ly sensi i e o TNF-α–d i en oxida i e and
in lamma o y changes [26].
1.2.3 An icance P o ec ion
Many s udies ha e a ge ed he inac i a ion o he ansc ip ion
ac o (NRF2) as a he apeu ic app oach in a ious ypes o
cance [27]. NRF2 was i s ecognised in an icance esea ch as
an induce o se e al an ioxidan enzymes. I can p o ec cells
and issues agains many ypes o oxican s ha in e up
essen ial biochemical p ocesses and ca cinogens by inc easing
he exp ession o cy op o ec i e genes [28]. The ansc ip ion
ac o NRF2 exhibi s con ex -dependen beha iou , unc ioning
ei he as a umou supp esso o as a p omo e o umou
p og ession, depending on he biological se ing in which i is
ac i a ed [29]. Mode a e ac i a ion o NRF2 in heal hy cells can
limi oxida i e damage and genomic ins abili y, he eby
lowe ing cance isk. Con e sely, pe sis en o cons i u i e
NRF2 ac i i y in malignan cells can p omo e su i al
ad an ages, ea men esis ance, and poo clinical ou comes,
o en necessi a ing he apeu ic inhibi ion o he pa hway [29].
NRF2 s abili y is egula ed h ough a leas h ee dis inc
mechanisms. One in ol es he cy oplasmic ep esso KEAP1
[30]; ano he elies on β- ansducin epea -con aining p o ein (β-
T CP) [31]; and a hi d is media ed by he endoplasmic e iculum–
associa ed E3 ubiqui in ligase HRD1 [32].
The abno mal ac i a ion o he NRF2/KEAP1 pa hway p omo es
cance de elop- men [33], me as asis o ma ion [34], and e en
esis ance o o a ian cance he apy [35]. Mu a ions in he KEAP1
gene induce he hype ac i a ion o he NRF2/KEAP1 pa hway.
No ably, KEAP1 missense o nonsense mu a ions we e epo ed
in endome ial ca cinomas [36], as well as gall bladde [37], b eas
[38,39], ce ical [40], and o a ian [41,42]
cance s. Mic oRNA miR-141 was he i s -iden i ied miRNA o
di ec ly ep ess KEAP1 le els in o a ian ca cinoma cell lines [43].
1.3.
Gu Mic obio a Dysbiosis
The s uc u al and unc ional dysbiosis o he gu mic obio a in
high- a die (HFD)- induced obesi y was demons a ed in a
mouse model [44]. Gu mic oo ganisms and hei me aboli es
exe b oad in luences on appe i e egula ion, lipid and glucose
me abolism, and o e all body weigh con ol [44,45]. The
in es inal mic obiome can modula e oughly 10% o he hos
ansc ip ome, a ec ing immune, me abolic, and p oli e a i e
gene ne wo ks [46]. Die a y ib e, e men a ion p ocesses, and
p obio ic in ake ha e he e o e become majo esea ch a eas in
me abolic heal h [47]. E idence shows ha die a y ib e can
es o e mic obial balance in indi iduals wi h ype 2 diabe es [48].
G ow h o Bi idobac e ium species suppo s insulin elease,
enhances glucose ole ance, imp o es insulin sensi i i y, and
educes in lamma ion. Bene icial mic obes also gene a e sho -
chain a y acids (SCFAs), including ace a e and bu y a e, which
in luence blood glucose ia en e oendoc ine ho mones such as
glucagon-like pep ide-1 (GLP-1) and pep ide YY (PYY) [45,49].
PYY, ac ing locally in he gu and cen ally in he b ain,
con ibu es o appe i e egula ion. Because SCFAs a e in eg al o
lipid and ca bohyd a e me abolism, main aining a heal hy gu
mic obio a is an impo an he apeu ic aim o educing
in lamma ion and p e en ing u ogeni al ac in ec ions [50–52].
2.
Li es yle Changes
Li es yle modi ica ion emains he p ima y he apeu ic app oach
in he managemen o polycys ic o a y synd ome (PCOS),
hough i complemen s a he han eplaces pha macological
he apy [7]. Consis en physical ac i i y, main enance o heal hy
body weigh , balanced die a y habi s, and he a oidance o
smoking a e undamen al in he p e en ion and ea men o
me abolic complica ions. These elemen s a e inco po a ed in o
mos clinical guidelines add essing me abolic and ep oduc i e
heal h. A en ion o psychological well-being and s ess
educ ion is also essen ial, as sus ained beha iou al change
con ibu es o o e all quali y o li e. Nu i ional counselling has
long been a co ne s one o PCOS managemen . Howe e , s udies
indica e ha se e e calo ic es ic ion a ely achie es las ing
me abolic o ho monal imp o emen [53,54]. E en isocalo ic die s,
when pai ed wi h physical ac i i y, may no signi ican ly al e
biochemical o an h opome ic pa ame e s [55].
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
243
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
2.1. Die
Examina ion o mac onu ien composi ion— ela i e
p opo ions o p o ein, a , and ca bohyd a es—has e ealed no
majo di e ences in key me abolic indica o s. Ins ead, o al
calo ic educ ion and he adop ion o a die wi h a low glycemic
index (GI) a e he mos consis en p edic o s o clinical
imp o emen [56,57]. Low-GI (LGI) die s ha e been shown o
educe insulin esis ance (HOMA-IR), as ing insulin, o al and
LDL choles e ol, iglyce ides, wais ci cum e ence, and o al
es os e one compa ed wi h high-GI (HGI) die s, wi hou majo
changes in as ing glucose, HDL, body weigh , o he ee
and ogen index [58]. Combining an LGI die wi h mode a e
calo ic es ic ion, physical ac i i y, and omega-3 a y acid
supplemen a ion u he inc eases HDL le els, p omo es
syn hesis o sex ho mone–binding globulin (SHBG), and educes
adiposi y [8].
Die a y pa e ns ich in sa u a ed a y acids (SFA) can ele a e
ci cula ing umou nec osis ac o -α (TNF-α) and leukocy ic
supp esso o cy okine signalling-3 (SOCS-3) exp ession,
sugges ing ha limi ing SFA in ake is pa icula ly impo an o
PCOS managemen [25]. Sou ces o α-linolenic acid, such as
laxseed oil, ha e demons a ed a ou able e ec s on ho monal
and in lamma o y ma ke s in animal models, implying po en ial
bene i s in humans as well [59].
Soluble, e men able die a y ib e p omo es sho -chain a y
acid (SCFA) o ma ion, which suppo s a heal hy gu
mic obiome and imp o es me abolic ou comes [60]. Die s wi h a
low GI also modula e appe i e- egula ing ho mones, dec easing
gh elin and inc easing glucagon sec e ion in women wi h PCOS
[12,61]. Con e sely, excessi e uc ose in ake may exace ba e
endoc ine abno mali ies, wo sening ho monal imbalances
despi e limi ed me abolic changes [62]. Me a-analyses con i m
ha LGI die s a e sa e, p ac ical, and e ec i e o imp o ing
insulin esis ance, unde sco ing he need o indi idualised
die a y guidance in all PCOS pa ien s [63,64].
The ke ogenic die (KD) ep esen s ano he o m o ca bohyd a e
es ic ion ha eplaces a po ion o die a y ca bohyd a es wi h
plan -de i ed a s. In women wi h PCOS—especially hose wi h
obesi y o a y li e disease—KD has been associa ed wi h
imp o ed mens ual egula i y, educed body mass, lowe
glucose and insulin le els, and be e li e unc ion [65]. A 12-
week ial demons a ed signi ican educ ions in body weigh
(≈9.4 kg), BMI (≈3.3 uni s), and a mass (≈8.3 kg), along wi h
imp o ed lipid p o iles, educed iglyce ides and LDL
choles e ol, ele a ed HDL choles e ol, and no malisa ion o
ho monal a ios, including LH/FSH and and ogens [66]. Es adiol,
p oges e one, and SHBG le els inc eased, while he Fe iman–
Gallwey sco e showed a modes decline, indica ing pa ial
imp o emen in hi su ism. The absence o co ela ion be ween
hi su ism and he isce al adiposi y index (VAI) sugges s ha
hai g ow h diso de s a e no di ec ly d i en by isce al a
dys unc ion [67].
Fo women wi h obesi y o me abolic synd ome, a ke ogenic o
low-GI die may p oduce g ea e me abolic and ho monal
bene i s han s anda d die a y in e en ions. O e all, adhe ence
o a nu ien -balanced, calo ie-con olled ea ing plan emains key
o es o ing physiological equilib ium and p omo ing eco e y
in PCOS.
2.1.1 Physical Ac i i y
Exe cise aining in he managemen o PCOS is becoming mo e
ecognised and accep ed among p o essionals in he heal h sec o
and pa ien s. Physical aining po en ia es he e ec s caused by
insulin sensi i i y h ough he op imisa ion o glucose anspo
and me abolism [68].
Recen e idence indica es ha he in ensi y o physical ac i i y
has a s onge impac on heal h ou comes han o al exe cise
olume. Vigo ous-in ensi y ac i i y appea s o p oduce he
la ges imp o emen s in ca dio espi a o y capaci y, insulin
esis ance, and body composi ion among women wi h PCOS [69].
Signi ican educ ions in insulin esis ance, measu ed by
HOMA-IR, and in BMI ha e been obse ed ollowing mode a e-
and high-in ensi y p og ams (MD −0.57; 95% CI −0.98 o −0.16,
p = 0.01; and MD −1.90; 95% CI −3.37 o −0.42, p = 0.01,
espec i ely) [70]. Sys ema ic e iews ecommend inco po a ing
bo h ae obic and esis ance exe cise o op imise insulin
sensi i i y and and ogen balance in his popula ion [71]. A
minimum o app oxima ely 120 minu es o ae obic ac i i y pe
week is gene ally ad ised [69].
2.1.2. Sleep
Psychological dis u bances such as anxie y, dep ession, and
sleep abno mali ies occu mo e equen ly in women wi h PCOS
[72]. Sleep dys egula ion con ibu es o bo h he onse and
p og ession o me abolic and emo ional dis u bances; he e o e,
ea ing sleep issues is a c i ical componen o PCOS
managemen [72]. Insu icien o agmen ed sleep is linked o a
highe isk o insulin esis ance, obesi y, and ype 2 diabe es [73–
75]. The mechanisms appea o in ol e au onomic dys egula ion,
ho monal luc ua ions in lep in and gh elin, and in lamma o y
signalling. Expe imen al models show ha ch onic sleep
agmen a ion leads o in lamma ion in whi e adipose issue and
agg a a es insulin esis ance, pa ly h ough dis up ion o
in es inal ba ie unc ion and lipopolysaccha ide-media ed
in lamma ion (“gu leakage”) [51,76]. These indings sugges ha
mic obio a- a ge ed he apy may mi iga e some o he me abolic
e ec s o poo sleep [76].
Mela onin, he main ho mone sec e ed by he pineal gland,
egula es ci cadian hy hm and exhibi s s ong an ioxidan
p ope ies. In PCOS, educed mela onin concen a ions ha e
been epo ed in ollicula luid [77]. Mela onin ecep o s wi hin
o a ian issue in luence s e oidogenesis du ing ollicula
ma u a ion, and su icien mela onin le els help p o ec
de eloping oocy es om oxida i e damage [77]. O e all, sleep
diso de s may ep esen an ea ly con ibu o o diminished
physiological esilience and wo sening insulin esis ance in
PCOS.
2.1.3. Supplemen a ion
Die a y su eys e eal ha many women wi h PCOS consume
unbalanced die s lacking ib e, omega-3 a y acids, and key
mic onu ien s such as calcium, magnesium, zinc, ola e,
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
244
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
i amins C, B12, and D, while showing excessi e in ake o
suc ose, sodium, sa u a ed a , and choles e ol [8]. Calo ie-
con olled, low-glycemic-index die s can co ec some
de iciencies, especially o wa e -soluble i amins [78,79].
Imp o ed plasma concen a ions o mos B i amins ha e been
no ed a e die a y adjus men , hough i amin B3 esponses
emain subop imal [79]. Inadequa e niacin (B3) in ake has been
associa ed wi h in lamma ion and highe ca dio ascula isk
[80,81].
Me o min he apy, while bene icial o glycemic con ol, may
educe hiamine and cobalamin s o es, wa an ing
supplemen a ion [82]. Thiamine enhances anske olase ac i i y
and suppo s ascula p o ec ion, po en ially educing
ca dio ascula complica ions [83,84]. Coenzyme Q10 (CoQ10)
supplemen a ion o eigh weeks has been shown o imp o e
in lamma o y s a us and endo helial unc ion in o e weigh and
obese women wi h PCOS [85]. Vi amin D plays mul iple
me abolic oles, enhancing insulin syn hesis, ecep o
exp ession, and esponse o glucose [86]. I indi ec ly modula es
ca bohyd a e me abolism by main aining calcium–pa a hy oid
ho mone balance and by supp essing p o-in lamma o y cy okine
exp ession [87]. Weekly supplemen a ion wi h 20,000 IU
cholecalci e ol imp o ed as ing glucose, iglyce ides, es adiol
le els, and mens ual egula i y, al hough and ogen le els
emained unchanged [88].
Combined supplemen a ion wi h magnesium, zinc, calcium, and
i amin D p oduced educ ions in hi su ism and o al es os e one
bu did no a ec SHBG o he ee and ogen index [89]. Simila ly,
i amin D adminis e ed wi h ish oil educed se um C- eac i e
p o ein, down egula ed in e leukin-1 exp ession, lowe ed
es os e one le els, and imp o ed mood sco es in women wi h
PCOS [90]. O e all, nu i ional op imisa ion, a ge ed i amin and
mine al eplacemen , and an ioxidan suppo ep esen
impo an adjunc s o li es yle and pha macologic he apy in
PCOS.
Cu en e idence indica es ha myo-inosi ol p o ides me abolic
and ho monal imp o emen s in women wi h PCOS compa able
o hose achie ed wi h me o min, pa icula ly ega ding insulin
sensi i i y and glucose egula ion, bu wi hou he
gas oin es inal side e ec s o en associa ed wi h me o min
he apy [91,92]. Supplemen a ion wi h inosi ol enhances issue
esponsi eness o insulin, lowe s ci cula ing and ogen
concen a ions, imp o es glycemic con ol, and posi i ely
a ec s se e al ma ke s o me abolic synd ome [93,94]. In PCOS,
an excessi e con e sion o myo-inosi ol (MI) o D-chi o-inosi ol
(DCI) has been obse ed in he o a ies unde he in luence o
insulin, leading o a local sho age o MI and an excess o DCI.
This imbalance may impai ollicle-s imula ing ho mone (FSH)
signalling and comp omise oocy e ma u a ion and quali y [95].
Clinical s udies sugges ha using inosi ol isome s—ei he
indi idually o in combina ion—can es o e spon aneous
o ula ion, suppo olliculogenesis, and imp o e concep ion
a es in women wi h PCOS. Li e a u e e iews consis en ly
iden i y inosi ol supplemen a ion as a sa e and e ec i e
he apeu ic op ion ha enhances o a ian unc ion, oocy e
de elopmen , and p egnancy ou comes [96].
T adi ional and complemen a y medicine app oaches ha e also
explo ed he use o na u al compounds such as isoquinoline
alkaloids o egula e and ogen syn hesis and lipid and
ca bohyd a e me abolism. Be be ine, one such alkaloid, has
a ac ed a en ion o i s mul iple bene icial e ec s in PCOS
managemen [97–99]. I s me abolic ac ion esembles ha o
me o min, la gely h ough ac i a ion o adenosine
monophospha e-ac i a ed p o ein kinase (AMPK), leading o
imp o emen s in glucose and lipid p o iles, educ ion in body
mass, and inc eased insulin sensi i i y [100]. Be be ine
addi ionally in luences he hypo halamic–pi ui a y–o a ian axis
by educing he syn hesis o s e oid ho mones and
down egula ing o a ian a oma ase, which con ibu es o
imp o ed o ula o y unc ion, mens ual egula i y, and highe
p egnancy and li e-bi h a es. Long- e m use has been
associa ed mainly wi h mild and ansien ad e se e ec s such as
nausea o cons ipa ion, indica ing a a ou able sa e y p o ile
[98,101,102].
Ch omium, an elemen in ol ed in ca bohyd a e and lipid
me abolism, has long been included in die a y supplemen s
ma ke ed o me abolic heal h in he Uni ed S a es [103].
Al hough he essen iali y o ch omium emains deba ed, some
indings sugges i can enhance insulin signalling, p omo e
AMPK ac i i y, and inc ease cellula glucose up ake, he eby
bene i ing pa ien s wi h PCOS and ype 2 diabe es [104–106].
Fu he mo e, al e a ions in he exp ession o s e oidogenic
enzymes—speci ically 3β-hyd oxys e oid dehyd ogenase and
17β-hyd oxys e oid dehyd ogenase—in adipose issue ha e been
linked o dehyd oepiand os e one me abolism, sugges ing ha
ch omium may indi ec ly a ec and ogen balance [107].
E idence om clinical and expe imen al esea ch indica es ha
supplemen a ion wi h ace mine als such as zinc and selenium
may be bene icial o some women wi h PCOS. Zinc is in ol ed
in nume ous in acellula p ocesses, se ing bo h s uc u al and
signalling unc ions ha in luence glucose and lipid me abolism
as well as ep oduc i e heal h [108]. Insu icien zinc in ake,
pa icula ly among indi iduals wi h obesi y, has been linked o
hype insulinemia, ch onic low-g ade in lamma ion, and an
ad e se lipid p o ile. In adipose issue, zinc ions can ac simila ly
o insulin by p omo ing glucose up ake ia ansloca ion o he
glucose anspo e GLUT4 o he plasma memb ane and by
s imula ing lipogenesis [109]. Se e al s udies epo ha women
wi h PCOS ha e lowe se um zinc concen a ions han heal hy
con ols, and hose wi h impai ed glucose ole ance exhibi he
lowes le els [110]. Selenium, ano he essen ial mic onu ien ,
demons a es po en an i-in lamma o y and an ioxidan ac ions
and shows an in e se co ela ion wi h ci cula ing C- eac i e
p o ein (CRP) le els [111]. Main aining adequa e selenium and
zinc s a us may he e o e suppo me abolic equilib ium and
educe he in lamma o y bu den cha ac e is ic o PCOS.
Omega-3 a y acids a e also equen ly de icien in he die s o
women wi h PCOS. When an o e all balanced die is ollowed,
a ge ed omega-3 supplemen a ion may be equi ed only
seasonally o du ing pe iods o die a y imbalance [112].
Polyunsa u a ed a y acids (PUFAs) con ibu e o imp o ed
o a ian unc ion by enhancing he exp ession o s e oidogenic
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
245
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
enzymes—such as CYP51, CYP19, S AR, and 3β-HSD—which
egula e ho mone syn hesis and ep oduc i e pe o mance [113].
Supplemen a ion should always be indi idualised and moni o ed
by a quali ied die i ian o ensu e pa ien adhe ence and sa e y.
Ac i e pa icipa ion by he pa ien emains c ucial o achie ing
a las ing imp o emen in me abolic homeos asis. A nu i ionally
adequa e die , combined wi h egula exe cise and s ess con ol,
con inues o ep esen he co ne s one o PCOS he apy.
2.2. He bs Suppo ing T ea men
A nu i ionally balanced plan ha s abilises insulin esponse can
be e ec i ely complemen ed by selec ed medicinal he bs.
Bo anical p epa a ions such as Aloe e a, cinnamon
(Cinnamomum e um), g een ea (Camellia sinensis),
chamomile (Ma ica ia chamomilla), and whi e mulbe y (Mo us
alba) ha e demons a ed bene icial e ec s on glucose and lipid
me abolism and may also exe mild an i-in lamma o y ac i i y
[114,115]. Because o hese p ope ies, such he bal agen s can be
applied o di e en PCOS pheno ypes, especially whe e
me abolic dis u bances domina e. G een ea [116] and ma jo am
(Majo ana ho ensis) ha e been shown o imp o e insulin
sensi i i y, es o e ho monal balance, and enhance an ioxidan
and an i-in lamma o y pa ame e s in bo h clinical and p eclinical
s udies [117,118].
Fo women wi h ele a ed and ogen le els, speci ic
an iand ogenic he bs may be help ul. Spea min (Men ha spica a
L.) educes ci cula ing es os e one concen a ions and suppo s
ollicula de elopmen in o a ian issue [119,120]. Liquo ice
(Glycy hiza glab a), long used in adi ional medicine, con ains
phy oac i e molecules ha exe bo h es ogen-like and
an iand ogenic ac ions. Glycy he inic acid, one o i s p incipal
me aboli es, inhibi s 11β-hyd oxys e oid dehyd ogenase ype 2
and binds o mine aloco icoid ecep o s, he eby in luencing
s e oid me abolism [121,122]. Despi e i s he apeu ic po en ial,
liquo ice can inc ease blood p essu e and al e po assium
balance; indi iduals wi h high co isol le els o ca dio ascula
disease should he e o e use i cau iously [123]. O he bo anical
ex ac s possess 5-α- educ ase inhibi o y ac i i y and may
coun e ac and ogen-d i en hai loss. Se enoa epens, Camellia
sinensis, Rosma inus o icinalis, and Glycy hiza glab a ha e
demons a ed he capaci y o educe and ogen concen a ions and
slow he p og ession o and ogene ic alopecia [124].
Vi ex agnus-cas us emains one o he bes -s udied he bal agen s
o es o ing mens ual cyclici y and alle ia ing p emens ual
symp oms h ough dopamine gic and pi ui a y modula ion [125].
Phy oes ogen- ich sou ces such as laxseed (Linum
usi a issimum), abundan in lignans, may egula e a oma ase
ac i i y and in luence es ogen me abolism, he eby helping o
no malise sex ho mone a ios [126,127]. Tu me ic (Cu cuma longa)
and i s main polyphenolic cons i uen , cu cumin, ha e well-
documen ed an ioxidan and an i-in lamma o y e ec s. In
PCOS, cu cumin supplemen a ion has been associa ed wi h
educ ions in oxida i e s ess ma ke s and inhibi ion o NF-κB–
dependen in lamma o y signalling [128–132]. U ica dioica (ne le)
displays wide- anging pha macological ac i i ies, including
an ioxidan , an imu agenic, and an i-in lamma o y e ec s ha
may aid me abolic egula ion [133,134]. Plan -de i ed la onoids,
p esen in many o hese he bs, can neu alise eac i e oxygen
species such as pe oxides and hyd oxyl adicals, p o ec ing
issues om oxida i e damage and suppo ing cellula esilience
[135]. In mo e ad anced PCOS accompanied by me abolic
synd ome o non-alcoholic a y li e disease, hepa op o ec i e
plan s can be use ul adjunc s. Ex ac s om milk his le (Silybum
ma ianum), which con ain silyma in, ha e shown an ioxidan
and memb ane-s abilising e ec s ha p o ec hepa ocy es om
oxida i e inju y [136–138]. A ichoke (Cyna a ca dunculus)
p o ides sesqui e pene lac ones and phenolic acids wi h simila
hepa op o ec i e p ope ies [139,140]. Compounds om dandelion
(Ta axacum o icinale), pa icula ly a axas e ol, ac i a e
SIRT1-dependen pa hways ha sa egua d li e cells [141].
Nigella sa i a (black cumin) also exhibi s an ioxidan and an i-
in lamma o y ac ions, and may educe hepa ic s ea osis and
insulin esis ance in obese women wi h PCOS [142].
In summa y, he bal and mic onu ien supplemen a ion o e
nume ous complemen a y s a egies o PCOS managemen . The
combined ac ions o an ioxidan , an iand ogenic, and
hepa op o ec i e mechanisms con ibu e o es o ing me abolic
and ho monal equilib ium. Indi idualised selec ion o he bal
mix u es and nu i ional suppo —guided by clinical assessmen
and e idence-based p ac ice—can enhance he e icacy o
s anda d medical he apies and imp o e he o e all heal h
ou comes o women li ing wi h PCOS. Summa y in o ma ion
has been added in Table 1.
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
246
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
Table 1: O e iew o he bal in e en ions and hei epo ed ou comes in PCOS
SCFA—sho -chain a y acids;
GI—glycemic index;
SFA—sa u a ed a acids;
PUFA—Polyunsa u a ed a y acid.
A Symp om
Accompanying PCOS
Die
Physical
Ac i i y
Sleep
Supplemen a ion
Mic obio a
He bs
Hi su ism
Reduced Die
[26,44,45,54,58]
Daily
Physical
Ac i i y
[68–71]
Imp o ing
Sleep [72–
77]
Magnesium, Zinc, Calcium
[89,108–111], Vi amin D [86–90],
Myo-Inosi ol [93–96]
Mic obio a
And
Me aboli es
[46,47]
Gl Glycy hiza Glab a,
Se enoa Repens, Camellia
Sinensis [120,121], Rosma inus
O icinalis [122]
The and ogen le els
Die Wi h Reduced
GI And Calo ie
[26,44,45,54,58],
Ke ogenic Die [64]
Daily
Physical
Ac i i y
[68–71]
Imp o ing
Sleep [72–
77]
Magnesium, Zinc, Calcium
[89,108–111], Vi amin D [86–90],
Be be ine [97–102],
Ch omium [105–107], Zinc [110]
SCFA
[47,52],
Mic obio a
and
Me aboli es
[50]
Men ha Spica a [120,121],
Glycy hiza Glab a [122],
Se enoa Repens, Camellia
Sinensis, Rosma inus
O icinalis [124]
O ula ion diso de s
Die Wi h Reduced
GI And Calo ie
[26,44,45,54,58],
Ke ogenic Die [64]
Daily
Physical
Ac i i y
[71–74]
Imp o ing
Sleep
[72–77]
Vi amin D [86–90], Myo-
Inosi ol [97,98], Be be ine
[99], Zinc [108], Pu as
[112,113]
Bi idobac e ia
[45,50]
Glycy hiza Glab a [121],
Vi ex Agnus-Cas us [124],
Flaxseed (Linum
Usi a issimum) [59,125,126]
Fa mass educ ion
High-Fib e Die
wi h Reduced GI
And Calo ie
[28,46,47,56,60],
Ke ogenic Die [64],
Elimina ion O SFA
[22,58]
Daily
Physical
Ac i i y
[68–71]
Mela onin
[77]
Vi amin B1 [82–84],
Vi amin D [86–90], Myo-
Inosi ol [91–96], Be be ine
[97–102], Ch omium [105–
107], Zinc [109]
SCFA
[47,52];
Mic obio a
and
Me aboli es
[50]
Aloe Ve a, Cinnamomum
Ve um, Camellia Sinensis
[115], Ma ica ia
Chamomilla, Mo us Alba
[117]
Ca bohyd a e
me abolism diso de s
High-Fib e Die
Wi h Reduced GI
And Calo ie
[26,44,45,54,58],
Ke ogenic Die [64]
—
—
Vi amin D [86–90], Myo-
Inosi ol [91–96], Be be ine
[97–102]
—
Aloe Ve a, Cinnamon, G een
Tea [115], Chamomile,
Whi e Mulbe y [117]
Insulin esis ance
High-Fib e Die
Wi h Reduced GI
And Calo ie
[26,44,45,54,58],
Elimina ion SFA
[22,58]
In ensi y
Exe cise
[72]
—
Omega-3 [112,113],
Be be ine [97–102], Zinc
[110]
—
Milk This le [137,138],
A ichoke Ex ac [139,140],
Dandelion [141], Black
Cumin [142]
Lipids me abolism
diso de s
High-Fib e Die
Wi h Reduced GI
And Calo ie
[26,44,45,54,58],
Elimina ion O SFA
[25,60]
—
—
—
Bi idobac e ia
[45,50]
Milk This le [137,138],
A ichoke Ex ac [139,140],
Dandelion [141], Black
Cumin [142]
S ea osis o o gans – li e
p o ile
High-Fib e Die
Wi h Reduced GI
And Calo ie
[46,47,56,60]
—
—
Α-Linolenic Acid [59],
Vi amin B3 [80,81],
Vi amin B1 [82–84],
Coenzyme Q10 [85]
—
—
Ca dio ascula diseases
High-Fib e Die
Wi h Reduced GI
And Calo ie
[46,47,56,60]
—
—
—
—
—
In es inal dysbiosis
High-Fib e Die
[49,50]
—
—
—
—
—
A Symp om
Accompanying PCOS
Die
Physical
Ac i i y
Sleep
Supplemen a ion
Mic obio a
He bs
Ch onic in lamma ion
High-Fib e Die
Wi h Reduced GI
And Calo ie
[28,46,47,56,60]
Daily
Physical
Ac i i y
[71–74]
Mela onin
[79]
Α-Linolenic Acid [59],
Vi amin B3 [80,81],
Coenzyme Q10 [85],
Vi amin D [88,89],
Selenium [112], Fla onoids
[135]
Bi idobac e ia
[45,50]
Ma jo am [117–119],
Tu me ic [128–131], Ne le
[133,134], Milk This le
[137,138], A ichoke Ex ac
[139,140], Dandelion [141],
Black Cumin [142]
Limi ing p edisposi ion o
cance
Elimina ion SFA
[25,27]; High-Fibe
Die [49,50]
—
Imp o ing
Sleep [75]
Α-Linolenic Acid [59]
—
Tu me ic [128–131], Ne le
[133,134]
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
247
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
3. CONCLUSIONS
Me abolic dys egula ion associa ed wi h polycys ic o a y
synd ome (PCOS) equi es a mul i ace ed he apeu ic app oach
ha simul aneously add esses ho monal, ep oduc i e, and
me abolic dis u bances. These dis u bances s em om se e al
in e ac ing biochemical pa hways; he e o e, clinical
managemen should emphasize imp o ing e ili y ou comes,
minimizing and ogen- ela ed symp oms, and es o ing glucose–
lipid me abolism and insulin esponse. Li es yle modi ica ion
emains cen al o he apy, wi h e idence suppo ing he
bene i s o a calo ie-con olled, low-glycemic-index die ,
adequa e sleep, and consis en physical ac i i y in educing
ca diome abolic isk and enhancing o e all heal h in a ec ed
women.
Adjunc nu i ional and phy o he apeu ic s a egies ha e gained
a en ion as suppo i e in e en ions in PCOS. Bioac i e
compounds wi h an ioxidan and hepa op o ec i e p ope ies
may con ibu e o educed in lamma ion and imp o ed
me abolic s a us. Speci ic agen s—such as ex ac s om
Cu cuma longa o Silybum ma ianum and p obio ics aimed a
es o ing gu mic o lo a—ha e shown p elimina y bene i s in
clinical and expe imen al con ex s. In he p esen s udy,
nu ien -in ake pa e ns and supplemen a ion p ac ices we e
e alua ed o unde s and hei in luence on mic onu ien
balance among women wi h PCOS. Eme ging e idence also
highligh s po en ial oles o inosi ols, hiamine, coenzyme
Q10, i amin D, zinc, and selenium in op imizing me abolic and
ep oduc i e ou comes.
Al hough hese indings indica e encou aging ends, de ini i e
conclusions canno ye be d awn. La ge , well-designed ials
a e needed o alida e he e icacy, sa e y, and long- e m
clinical signi icance o hese nu i ional and he bal
in e en ions when combined wi h s anda d medical ca e..
4. Me hods o Sea ching
This e iew ocused on non-pha macological app oaches o he
managemen o PCOS. A comp ehensi e li e a u e sea ch was
ca ied ou in he PubMed and Embase (Else ie ) da abases,
co e ing esea ch published wi hin he pas wen y yea s.All
e ie ed eco ds we e sc eened a he abs ac le el.
Publica ions un ela ed o he p ima y opic, duplica ed be ween
he wo da abases, o limi ed o con e ence p oceedings we e
excluded. Only a icles w i en in English we e included o
ull- ex e iew.The discussion also d aws on he au ho s’
decade o clinical and esea ch expe ience wi h PCOS pa ien s.
F om his wo k, s udies co esponding o each s age o he
in e en ions discussed we e selec ed. The li e a u e sea ch
emphasized physiological mechanisms linking PCOS wi h
insulin esis ance, ch onic in lamma ion, endoc ine
dys unc ion, cance de elopmen , and gu mic obio a
al e a ions. Li es yle modi ica ion s udies we e analyzed i s ,
ollowed by hose in es iga ing die and supplemen a ion—
including inosi ol, be be ine, i amin D, ch omium, zinc,
selenium, and mela onin—along wi h epo s e alua ing he bal
adjunc he apies. In cases o o e lapping in o ma ion ac oss
publica ions, he mos comp ehensi e and ele an s udies we e
p io i ised o inclusion.
REFERENCES
1.
Fause , B.C.J.M.; Ta la zis, B.C.; Reba , R.W.; Leg o,
R.S.; Balen, A.H.; Lobo, R.; Ca mina, E.; Chang, J.;
Yildiz, B.O.; La en, J.S.E.; e al. Consensus on Women’s
Heal h Aspec s o Polycys ic O a y Synd ome (PCOS):
The Ams e dam ESHRE/ASRM-Sponso ed 3 d PCOS
Consensus Wo kshop G oup. Fe il. S e il. 2023 97, 28–
38.e25. [C ossRe ]
2.
Zuo, M.; Liao, G.; Zhang, W.; Xu, D.; Lu, J.; Tang, M.;
Yan, Y.; Hong, C.; Wang, Y. E ec s o Exogenous
Adiponec in Supple- men a ion in Ea ly P egnan PCOS
Mice on he Me abolic Synd ome o Adul Female
O sp ing. J. O a ian Res. 2018, 14, 15. [C ossRe ]
3.
Szczuko, M.; Zapałowska-Chwyc´, M.; Maciejewska, D.;
D ozd, A.; S a czewski, A.; S achowska, E. Signi ican
Imp o emen Selec ed Media o s o In lamma ion in
Pheno ypes o Women wi h PCOS a e Reduc ion and
Low GI Die . Media . In lamm. 2017, 2017, 5489523.
[C ossRe ]
4.
Ma, L.; Cao, Y.; Ma, Y.; Zhai, J. Associa ion be ween
hype and ogenism and ad e se p egnancy ou comes in
pa ien s wi h di e en polycys ic o a y synd ome
pheno ypes unde going in i o
e iliza ion/in acy oplasmic spe m injec ion: A
sys ema ic e iew and me a-analysis. Gynecol.
Endoc inol. 2017, 1–8. [C ossRe ] [PubMed]
5.
Ma ini, A.E.; Healy, M.W. Polycys ic O a ian
Synd ome: Impac on Adul and Fe al Heal h. Clin. Obs.
Gynecol. 2018, 64, 26–32. [C ossRe ]
6.
Hong, G.; Wu, H.; Ma, S.-T.; Su, Z. Ca echins om
Oolong Tea Imp o e U e ine De ec s by Inhibi ing
STAT3 Signaling in Polycys ic O a y Synd ome Mice.
Chin. Med. 2018, 15, 125. [C ossRe ]
7.
Del Pup, L.; Cagnacci, A. IMPROVE Li es yle in
Polycys ic O a y Synd ome: A Sys ema ic S a egy.
Gynecol. Endoc inol. 2018, 1–4. [C ossRe ]
8.
Szczuko, M.; Skow onek, M.; Zapałowska-Chwyc´, M.;
S a czewski, A. Quan i a i e Assessmen o Nu i ion in
Pa ien s wi h Polycys ic O a y Synd ome (PCOS). Rocz.
Pans w. Zakl. Hig. 2016, 67, 419–426. [PubMed]
9.
Makki, K.; F oguel, P.; Wolowczuk, I. Adipose Tissue in
Obesi y-Rela ed In lamma ion and Insulin Resis ance:
Cells, Cy okines, and Chemokines. ISRN In lamm. 2013,
2013, 139239. [C ossRe ] [PubMed]
10.
Dniak-Nikolajew, A. Zespół Policys ycznych Jajników
Jako P zyczyna Niepłodnos´ci Kobiecej [Polycys ic
O a y Synd ome as a Cause o Female In e ili y].
Połoz˙na Nauka I P ak . 2012, 17, 14–17.
11.
Panjeshahin, A.; Salehi-Aba gouei, A.; Ana i, A.G.;
Mohammadi, M.; Hosseinzadeh, M. Associa ion be ween
Empi ically De i ed Die a y Pa e ns and Polycys ic
O a y Synd ome: A Case-Con ol S udy. Nu i ion 218,
79–80, 110987. [C ossRe ]
In . J . o Con emp. Res. in Mul i. Volume 3 Issue 6 [No - Dec] Yea 2024
248
© 2024 D . Anamika Dixi , Du gesh Kuma Sha ma. This is an open-access a icle dis ibu ed unde he e ms o he C ea i e Commons A ibu ion 4.0
In e na ional License (CC BY NC ND). h ps://c ea i ecommons.o g/licenses/by/4.0/
12.
Szczuko, M.; Zapalowska-Chwyc´, M.; D ozd, R. A Low
Glycemic Index Dec eases In lamma ion by Inc easing
he Concen a ion o U ic Acid and he Ac i i y o
Glu a hione Pe oxidase (GPx3) in Pa ien s wi h Polycys ic
O a y Synd ome (PCOS). Molecules 2018, 24, 1508.
[C ossRe ]
13.
Di Meo, S.; Iossa, S.; Vendi i, P. Skele al Muscle Insulin
Resis ance: Role o Mi ochond ia and O he ROS Sou ces.
J. Endoc inol. 2017, 233, R15–R42. [C ossRe ]
14.
Ba be , T.M.; Ky ou, I.; Rande a, H.S.; Weicke , M.O.
Mechanisms o Insulin Resis ance a he C oss oad o
Obesi y wi h Associa ed Me abolic Abno mali ies and
Cogni i e Dys unc ion. In . J. Mol. Sci. 2021, 22, 546.
[C ossRe ]
15.
Kempegowda, P.; Melson, E.; Manolopoulos, K.N.; A l ,
W.; O’Reilly, M.W. Implica ing And ogen Excess in
P opaga ing Me abolic Disease in Polycys ic O a y
Synd ome. Ad . Endoc inol. Me ab. 2022, 11. [C ossRe ]
16.
Kau man, R.P.; Bake , V.M.; Dima ino, P.; Gimpel, T.;
Cas acane, V.D. Polycys ic O a ian Synd ome and
Insulin Resis ance in Whi e and Mexican Ame ican
Women: A Compa ison o Two Dis inc Popula ions. Am.
J. Obs. Gynecol. 2002, 187, 1362–1369. [C ossRe ]
[PubMed]
17.
Shoelson, S.E.; He e o, L.; Naaz, A. Obesi y,
In lamma ion, and Insulin Resis ance. Gas oen e ology
2007, 132, 2169–2180. [C ossRe ] [PubMed]
18.
Fajs o a, A.; Galano a, N.; Cou al, S.; Malko a, J.;
Kos o cik, M.; Ce mako a, M.; Pelan o a, H.; Kuzma,
M.; Sedi a, B.; Hudco ic, T.; e al. Die Rich in Simple
Suga s P omo es P o-In lamma o y Response ia Gu
Mic obio a Al e a ion and TLR4 Signaling. Cells 2018, 9,
2701. [C ossRe ]
19.
González, F.; Considine, R.V.; Abdelhadi, O.A.; Ac on,
A.J. Oxida i e S ess in Response o Sa u a ed Fa
Inges ion Is Linked o Insulin Resis ance and
Hype and ogenism in Polycys ic O a y Synd ome. J.
Clin. Endoc inol. Me ab. 2018, 104, 5360–5371.
[C ossRe ]
20.
Wang, H.; Wang, X.; Zhu, Y.; Chen, F.; Sun, Y.; Han, X.
Inc eased And ogen Le els in Ra s Impai Glucose-
S imula ed Insulin Sec e ion h ough Dis up ion o
Panc ea ic Be a Cell Mi ochond ial Func ion. J. S e oid
Biochem. Mol. Biol. 2015, 154, 254–266. [C ossRe ]
[PubMed]
21.
Liu, S.; Na a o, G.; Mau ais-Ja is, F. And ogen Excess
P oduces Sys emic Oxida i e S ess and P edisposes o
Be a-Cell Failu e in Female Mice. PLoS ONE 2010, 5,
e11302. [C ossRe ]
22.
Jiang, F.; Zhang, Y.; Dus ing, G.J. NADPH Oxidase-
Media ed Redox Signaling: Roles in Cellula S ess
Response, S ess Tole ance, and Tissue Repai . Pha m.
Re . 2011, 63, 218–242. [C ossRe ] [PubMed]
23.
Beda d, K.; K ause, K.-H. The NOX Family o ROS-
Gene a ing NADPH Oxidases: Physiology and
Pa hophysiology. Physiol. Re .2007, 87, 245–313.
[C ossRe ] [PubMed]
24.
E ans, J.L.; Gold ine, I.D.; Maddux, B.A.; G odsky, G.M.
Oxida i e S ess and S ess-Ac i a ed Signaling
Pa hways: A Uni ying Hypo hesis o Type 2 Diabe es.
Endoc . Re . 2002, 23, 599–622. [C ossRe ] [PubMed]
25.
González, F.; Considine, R.V.; Abdelhadi, O.A.; Ac on,
A.J. Sa u a ed Fa Inges ion P omo es
Lipopolysaccha ide-Media ed In lamma ion and Insulin
Resis ance in Polycys ic O a y Synd ome. J. Clin.
Endoc inol. Me ab. 2018, 104, 934–946. [C ossRe ]
[PubMed]
26.
Szczuko, M.; Zapałowska-Chwyc´, M.; Maciejewska, D.;
D ozd, A.; S a czewski, A.; S achowska, E. High
Glycemic Index Die in PCOS Pa ien s. The Analysis o
IGF I and TNF-α Pa hways in Me abolic Diso de s. Med.
Hypo heses 2016, 96, 42–47. [C ossRe ]
27.
Panie i, E.; Saso, L. Po en ial Applica ions o NRF2
Inhibi o s in Cance The apy. Oxida i e Med. Cell.
Longe . 2018, 2019, e8592348.[C ossRe ]
28.
Panie i, E.; Buha, A.; Telkopa an-Akillila , P.; Ce ik, D.;
Kou e as, D.; Veskoukis, A.; Skape da, Z.; Tsa sakis, A.;
Wallace, D.; Suzen, S.; e al. Po en ial Applica ions o
NRF2 Modula o s in Cance The apy. An ioxidan s 2018,
9, 193. [C ossRe ]
29.
Panie i, E.; Telkopa an-Akillila , P.; Suzen, S.; Saso, L.
The NRF2/KEAP1 Axis in he Regula ion o Tumo
Me abolism: Mecha- nisms and The apeu ic Pe spec i es.
Biomolecules 2018, 10, 791. [C ossRe ] [PubMed]
30.
Suzuki, T.; Yamamo o, M. S ess-Sensing Mechanisms
and he Physiological Roles o he Keap1-N 2 Sys em
du ing Cellula S ess. J. Biol. Chem. 2017, 292, 16817–
16824. [C ossRe ]
31.
Chowdh y, S.; Zhang, Y.; McMahon, M.; Su he land, C.;
Cuad ado, A.; Hayes, J.D. N 2 Is Con olled by Two
Dis inc β-T CP Recogni ion Mo i s in I s Neh6 Domain,
One o Which Can Be Modula ed by GSK-3 Ac i i y.
Oncogene 2013, 32, 3765–3781. [C ossRe ]
32.
Wu, T.; Zhao, F.; Gao, B.; Tan, C.; Yagishi a, N.;
Nakajima, T.; Wong, P.K.; Chapman, E.; Fang, D.; Zhang,
D.D. H d1 Supp esses N 2-Media ed Cellula P o ec ion
du ing Li e Ci hosis. Genes De . 2014, 28, 708–722.
[C ossRe ]
33.
Rojo, A.I.; Rada, P.; Mendiola, M.; O ega-Molina, A.;
Wojdyla, K.; Rogowska-W zesinska, A.; Ha disson, D.;
Se ano, M.; Cuad ado, A. The PTEN/NRF2 Axis
P omo es Human Ca cinogenesis. An ioxid. Redox.
Signal. 2014, 21, 2498–2514. [C ossRe ] [PubMed]
34.
Zhang, C.; Wang, H.-J.; Bao, Q.-C.; Wang, L.; Guo, T.-
K.; Chen, W.-L.; Xu, L.-L.; Zhou, H.-S.; Bian, J.-L.;
Yang, Y.-R.; e al. NRF2 P omo es B eas Cance Cell
P oli e a ion and Me as asis by Inc easing RhoA/ROCK
Pa hway Signal T ansduc ion. Onco a ge 2016, 7,
73593–73606. [C ossRe ] [PubMed]
35.
Bao, L.; Wu, J.; Dodson, M.; Rojo de la Vega, E.M.; Ning,
Y.; Zhang, Z.; Yao, M.; Zhang, D.D.; Xu, C.; Yi, X.
