Obesity and Polycystic Ovary Syndrome

The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major external triggers promote androgen overproduction in the ovaries: the increased secretion of luteinizing hormone, a consequence of aberrant hypotha...

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Published inJournal of Obesity & Metabolic Syndrome Vol. 33; no. 4; pp. 289 - 301
Main Author Kim, Jin Ju
Format Journal Article
LanguageEnglish
Published Korea (South) Korean Society for the Study of Obesity 01.12.2024
대한비만학회
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ISSN2508-6235
2508-7576
2508-7576
DOI10.7570/jomes24035

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Abstract The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major external triggers promote androgen overproduction in the ovaries: the increased secretion of luteinizing hormone, a consequence of aberrant hypothalamic gonadotropin-releasing hormone secretion dynamics, and compensatory hyperinsulinemia resulting from insulin resistance. Obesity interacts with polycystic ovary syndrome in multiple ways, but a major role of obesity in its pathophysiology is the exacerbation of insulin resistance. Additionally, obesity contributes to polycystic ovary syndrome by facilitating the conversion of precursor hormones to testosterone within adipose cells. Moreover, obesity can lead to relative hyperandrogenemia, which is marked by lower levels of sex hormone binding globulin and increased availability of free testosterone to target tissues. Also, obesity affects the secretion of gonadotropins, resulting in heightened luteinizing hormone secretion or increased sensitivity of thecal cells to luteinizing hormone. Obesity-related insulin resistance might be amplified by alterations in adipokine and inflammatory cytokine production. Ultimately, obesity and polycystic ovary syndrome might share a common genetic predisposition. The cornerstone of managing polycystic ovary syndrome is to address individual symptoms such as hyperandrogenism (hirsutism, acne, and female type boldness), menstrual irregularities, and infertility stemming from anovulation. However, obesity is integral to the pathophysiology of polycystic ovary syndrome and exacerbates all of its features. Therefore, lifestyle modifications aimed at weight reduction should be the primary strategy in overweight or obese women with polycystic ovary syndrome.
AbstractList The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major external triggers promote androgen overproduction in the ovaries: the increased secretion of luteinizing hormone, a consequence of aberrant hypothalamic gonadotropin-releasing hormone secretion dynamics, and compensatory hyperinsulinemia resulting from insulin resistance. Obesity interacts with polycystic ovary syndrome in multiple ways, but a major role of obesity in its pathophysiology is the exacerbation of insulin resistance. Additionally, obesity contributes to polycystic ovary syndrome by facilitating the conversion of precursor hormones to testosterone within adipose cells. Moreover, obesity can lead to relative hyperandrogenemia, which is marked by lower levels of sex hormone binding globulin and increased availability of free testosterone to target tissues. Also, obesity affects the secretion of gonadotropins, resulting in heightened luteinizing hormone secretion or increased sensitivity of thecal cells to luteinizing hormone. Obesity-related insulin resistance might be amplified by alterations in adipokine and inflammatory cytokine production. Ultimately, obesity and polycystic ovary syndrome might share a common genetic predisposition. The cornerstone of managing polycystic ovary syndrome is to address individual symptoms such as hyperandrogenism (hirsutism, acne, and female type boldness), menstrual irregularities, and infertility stemming from anovulation. However, obesity is integral to the pathophysiology of polycystic ovary syndrome and exacerbates all of its features. Therefore, lifestyle modifications aimed at weight reduction should be the primary strategy in overweight or obese women with polycystic ovary syndrome.
The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major external triggers promote androgen overproduction in the ovaries: the increased secretion of luteinizing hormone, a consequence of aberrant hypothalamic gonadotropin-releasing hormone secretion dynamics, and compensatory hyperinsulinemia resulting from insulin resistance. Obesity interacts with polycystic ovary syndrome in multiple ways, but a major role of obesity in its pathophysiology is the exacerbation of insulin resistance. Additionally, obesity contributes to polycystic ovary syndrome by facilitating the conversion of precursor hormones to testosterone within adipose cells. Moreover, obesity can lead to relative hyperandrogenemia, which is marked by lower levels of sex hormone binding globulin and increased availability of free testosterone to target tissues. Also, obesity affects the secretion of gonadotropins, resulting in heightened luteinizing hormone secretion or increased sensitivity of thecal cells to luteinizing hormone. Obesity-related insulin resistance might be amplified by alterations in adipokine and inflammatory cytokine production. Ultimately, obesity and polycystic ovary syndrome might share a common genetic predisposition. The cornerstone of managing polycystic ovary syndrome is to address individual symptoms such as hyperandrogenism (hirsutism, acne, and female type boldness), menstrual irregularities, and infertility stemming from anovulation. However, obesity is integral to the pathophysiology of polycystic ovary syndrome and exacerbates all of its features. Therefore, lifestyle modifications aimed at weight reduction should be the primary strategy in overweight or obese women with polycystic ovary syndrome. KCI Citation Count: 0
The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major external triggers promote androgen overproduction in the ovaries: the increased secretion of luteinizing hormone, a consequence of aberrant hypothalamic gonadotropin-releasing hormone secretion dynamics, and compensatory hyperinsulinemia resulting from insulin resistance. Obesity interacts with polycystic ovary syndrome in multiple ways, but a major role of obesity in its pathophysiology is the exacerbation of insulin resistance. Additionally, obesity contributes to polycystic ovary syndrome by facilitating the conversion of precursor hormones to testosterone within adipose cells. Moreover, obesity can lead to relative hyperandrogenemia, which is marked by lower levels of sex hormone binding globulin and increased availability of free testosterone to target tissues. Also, obesity affects the secretion of gonadotropins, resulting in heightened luteinizing hormone secretion or increased sensitivity of thecal cells to luteinizing hormone. Obesity-related insulin resistance might be amplified by alterations in adipokine and inflammatory cytokine production. Ultimately, obesity and polycystic ovary syndrome might share a common genetic predisposition. The cornerstone of managing polycystic ovary syndrome is to address individual symptoms such as hyperandrogenism (hirsutism, acne, and female type boldness), menstrual irregularities, and infertility stemming from anovulation. However, obesity is integral to the pathophysiology of polycystic ovary syndrome and exacerbates all of its features. Therefore, lifestyle modifications aimed at weight reduction should be the primary strategy in overweight or obese women with polycystic ovary syndrome.The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major external triggers promote androgen overproduction in the ovaries: the increased secretion of luteinizing hormone, a consequence of aberrant hypothalamic gonadotropin-releasing hormone secretion dynamics, and compensatory hyperinsulinemia resulting from insulin resistance. Obesity interacts with polycystic ovary syndrome in multiple ways, but a major role of obesity in its pathophysiology is the exacerbation of insulin resistance. Additionally, obesity contributes to polycystic ovary syndrome by facilitating the conversion of precursor hormones to testosterone within adipose cells. Moreover, obesity can lead to relative hyperandrogenemia, which is marked by lower levels of sex hormone binding globulin and increased availability of free testosterone to target tissues. Also, obesity affects the secretion of gonadotropins, resulting in heightened luteinizing hormone secretion or increased sensitivity of thecal cells to luteinizing hormone. Obesity-related insulin resistance might be amplified by alterations in adipokine and inflammatory cytokine production. Ultimately, obesity and polycystic ovary syndrome might share a common genetic predisposition. The cornerstone of managing polycystic ovary syndrome is to address individual symptoms such as hyperandrogenism (hirsutism, acne, and female type boldness), menstrual irregularities, and infertility stemming from anovulation. However, obesity is integral to the pathophysiology of polycystic ovary syndrome and exacerbates all of its features. Therefore, lifestyle modifications aimed at weight reduction should be the primary strategy in overweight or obese women with polycystic ovary syndrome.
Author Kim, Jin Ju
AuthorAffiliation 2 Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea
1 Department of Obstetrics and Gynecology, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Korea
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Cites_doi 10.1210/jc.82.7.2343
10.1210/jcem.85.8.6738
10.1007/s00125-008-1028-6
10.1016/j.fertnstert.2006.05.038
10.1210/endo-126-5-2711
10.2337/db11-1360
10.1677/joe.1.05762
10.1210/jc.2005-1852
10.1093/humupd/dmp024
10.1210/jc.2002-020363
10.1111/ijpo.12110
10.1210/jcem.83.10.5205
10.1093/humrep/deg367
10.1152/ajpendo.2001.281.2.E392
10.1210/jc.2017-02426
10.3389/fendo.2018.00375
10.1210/clinem/dgad463
10.1046/j.1365-2265.1999.00886.x
10.1093/humrep/den089
10.1038/sj.ijo.0801994
10.1210/jc.83.7.2361
10.1016/j.fertnstert.2016.07.1121
10.1111/cen.12784
10.1210/jc.2004-1860
10.1210/jc.2007-1834
10.1210/jc.2005-1457
10.1200/JCO.2016.69.4638
10.1016/j.nut.2012.07.003
10.1210/jc.2005-0691
10.1210/jc.83.6.2001
10.1111/j.1365-2265.2006.02587.x
10.1093/humupd/dml036
10.1210/jcem.79.5.7962325
10.1210/jc.85.7.2434
10.1371/journal.pone.0016390
10.2337/dc07-2190
10.1046/j.1365-2265.2001.01375.x
10.1111/j.1365-2265.1995.tb02665.x
10.1210/jc.2002-020815
10.1186/s12916-020-01861-x
10.1210/jcem-68-1-173
10.1016/S1472-6483(10)61182-0
10.1093/oxfordjournals.humrep.a136243
10.1210/jc.2003-031848
10.1136/adc.2004.053959
10.1111/jog.14132
10.1055/s-2002-38249
10.1210/jc.2003-032046
10.1016/j.jpag.2011.03.002
10.1093/humupd/dmac005
10.1210/jcem-68-6-1027
10.1056/NEJMra041536
10.1210/jc.2009-1908
10.1210/er.2015-1104
10.1177/1179558119874042
10.1210/jc.83.7.2317
10.1210/jc.2012-2937
10.1016/S0039-128X(96)00223-1
10.1016/S0015-0282(16)59293-0
10.1007/s00431-003-1358-9
10.1210/jendso/bvac150.1404
10.1001/jama.2009.2014
10.1530/EJE-20-0862
10.1097/00006254-199906000-00019
10.1007/978-0-387-69248-7_4
10.3109/09513590.2010.508543
10.1210/jc.2005-1329
10.1210/er.2004-0004
10.1186/1741-7015-8-41
10.1038/nrdp.2016.57
10.1530/EJE-21-0287
10.1210/jc.2005-2757
10.1210/jc.2008-0477
10.1111/j.1471-0528.2006.00990.x
10.1111/cen.12441
10.1056/NEJM198903023200904
10.1093/humrep/deq028
10.1111/j.1467-789X.2012.01053.x
10.1038/s41598-023-50650-y
10.1210/jc.2006-2725
10.1093/humrep/der291
10.1007/BF03345743
10.1093/humupd/dmp006
10.1210/jcem.84.11.6148
10.1055/s-2002-38265
10.1172/JCI118126
10.1016/0002-9378(92)91779-A
10.1055/s-2007-1009245
10.4103/jhrs.JHRS_77_17
10.1016/j.molmed.2023.02.006
10.1016/S0303-7207(98)00177-4
10.1016/j.fertnstert.2014.07.004
10.1046/j.1365-2265.1997.2321049.x
10.1093/humrep/deh098
10.1210/me.2004-0178
10.1016/S0889-8529(18)30245-7
10.1210/jc.2003-031122
10.1016/j.jsbmb.2014.06.003
10.1210/jc.84.4.1470
10.1016/j.mce.2008.01.007
10.1111/j.1749-6632.2000.tb06230.x
10.1016/S0015-0282(03)00265-6
10.1016/S2213-8587(22)00339-4
10.1111/j.1365-2265.1992.tb02909.x
10.1210/jc.2009-0545
10.1210/jcem.77.6.8263159
10.1016/j.fertnstert.2014.01.049
10.1093/humrep/den211
10.1095/biolreprod61.4.993
10.1016/j.bbrc.2008.06.039
10.1016/j.molmed.2006.05.006
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Issue 4
Keywords Obesity
Polycystic ovary syndrome
Insulin resistance
Anovulation
Language English
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References ref57
ref56
ref59
ref58
ref53
ref52
ref55
ref54
ref51
ref50
ref46
ref45
ref48
ref47
ref42
ref41
ref44
ref43
ref49
ref8
ref7
ref9
ref4
ref3
ref6
ref5
ref100
ref101
ref40
ref35
ref34
ref37
ref36
ref31
ref30
ref33
ref32
ref39
ref38
ref24
ref23
ref26
ref25
ref20
ref22
ref21
ref28
ref27
ref29
ref13
ref12
ref15
ref14
ref97
ref96
ref11
ref99
ref10
ref98
ref17
ref16
ref19
ref18
ref93
ref92
ref95
ref94
ref91
ref90
ref89
ref86
ref85
ref88
ref87
ref82
ref81
ref84
ref83
ref80
ref79
ref108
ref78
ref109
ref106
ref107
ref75
ref104
ref74
ref105
ref77
ref102
ref76
ref103
ref2
ref1
ref71
ref111
ref70
ref112
ref73
ref72
ref110
ref68
ref67
ref69
ref64
ref63
ref66
ref65
ref60
ref62
ref61
References_xml – ident: ref75
  doi: 10.1210/jc.82.7.2343
– ident: ref108
  doi: 10.1210/jcem.85.8.6738
– ident: ref80
  doi: 10.1007/s00125-008-1028-6
– ident: ref98
  doi: 10.1016/j.fertnstert.2006.05.038
– ident: ref72
  doi: 10.1210/endo-126-5-2711
– ident: ref43
  doi: 10.2337/db11-1360
– ident: ref65
  doi: 10.1677/joe.1.05762
– ident: ref95
  doi: 10.1210/jc.2005-1852
– ident: ref46
  doi: 10.1093/humupd/dmp024
– ident: ref25
  doi: 10.1210/jc.2002-020363
– ident: ref93
  doi: 10.1111/ijpo.12110
– ident: ref86
  doi: 10.1210/jcem.83.10.5205
– ident: ref36
– ident: ref109
  doi: 10.1093/humrep/deg367
– ident: ref24
  doi: 10.1152/ajpendo.2001.281.2.E392
– ident: ref10
  doi: 10.1210/jc.2017-02426
– ident: ref90
  doi: 10.3389/fendo.2018.00375
– ident: ref4
  doi: 10.1210/clinem/dgad463
– ident: ref50
  doi: 10.1046/j.1365-2265.1999.00886.x
– ident: ref101
  doi: 10.1093/humrep/den089
– ident: ref61
  doi: 10.1038/sj.ijo.0801994
– ident: ref100
  doi: 10.1210/jc.83.7.2361
– ident: ref45
  doi: 10.1016/j.fertnstert.2016.07.1121
– ident: ref44
  doi: 10.1111/cen.12784
– ident: ref14
  doi: 10.1210/jc.2004-1860
– ident: ref54
  doi: 10.1210/jc.2007-1834
– ident: ref38
  doi: 10.1210/jc.2005-1457
– ident: ref112
  doi: 10.1200/JCO.2016.69.4638
– ident: ref68
  doi: 10.1016/j.nut.2012.07.003
– ident: ref16
  doi: 10.1210/jc.2005-0691
– ident: ref20
  doi: 10.1210/jc.83.6.2001
– ident: ref96
  doi: 10.1111/j.1365-2265.2006.02587.x
– ident: ref97
  doi: 10.1093/humupd/dml036
– ident: ref15
  doi: 10.1210/jcem.79.5.7962325
– ident: ref51
  doi: 10.1210/jc.85.7.2434
– ident: ref81
  doi: 10.1371/journal.pone.0016390
– ident: ref78
  doi: 10.2337/dc07-2190
– ident: ref56
  doi: 10.1046/j.1365-2265.2001.01375.x
– ident: ref28
  doi: 10.1111/j.1365-2265.1995.tb02665.x
– ident: ref110
  doi: 10.1210/jc.2002-020815
– ident: ref103
  doi: 10.1186/s12916-020-01861-x
– ident: ref105
  doi: 10.1210/jcem-68-1-173
– ident: ref111
  doi: 10.1016/S1472-6483(10)61182-0
– ident: ref33
  doi: 10.1093/oxfordjournals.humrep.a136243
– ident: ref88
  doi: 10.1210/jc.2003-031848
– ident: ref89
  doi: 10.1136/adc.2004.053959
– ident: ref39
  doi: 10.1111/jog.14132
– ident: ref64
  doi: 10.1055/s-2002-38249
– ident: ref52
  doi: 10.1210/jc.2003-032046
– ident: ref42
  doi: 10.1016/j.jpag.2011.03.002
– ident: ref84
  doi: 10.1093/humupd/dmac005
– ident: ref22
  doi: 10.1210/jcem-68-6-1027
– ident: ref53
  doi: 10.1056/NEJMra041536
– ident: ref66
  doi: 10.1210/jc.2009-1908
– ident: ref9
  doi: 10.1210/er.2015-1104
– ident: ref104
  doi: 10.1177/1179558119874042
– ident: ref6
  doi: 10.1210/jc.83.7.2317
– ident: ref48
  doi: 10.1210/jc.2012-2937
– ident: ref5
  doi: 10.1016/S0039-128X(96)00223-1
– ident: ref21
  doi: 10.1016/S0015-0282(16)59293-0
– ident: ref87
  doi: 10.1007/s00431-003-1358-9
– ident: ref94
  doi: 10.1210/jendso/bvac150.1404
– ident: ref31
  doi: 10.1001/jama.2009.2014
– ident: ref91
  doi: 10.1530/EJE-20-0862
– ident: ref18
  doi: 10.1097/00006254-199906000-00019
– ident: ref19
  doi: 10.1007/978-0-387-69248-7_4
– ident: ref71
  doi: 10.3109/09513590.2010.508543
– ident: ref59
  doi: 10.1210/jc.2005-1329
– ident: ref76
  doi: 10.1210/er.2004-0004
– ident: ref1
  doi: 10.1186/1741-7015-8-41
– ident: ref2
  doi: 10.1038/nrdp.2016.57
– ident: ref92
  doi: 10.1530/EJE-21-0287
– ident: ref17
  doi: 10.1210/jc.2005-2757
– ident: ref77
  doi: 10.1210/jc.2008-0477
– ident: ref62
  doi: 10.1111/j.1471-0528.2006.00990.x
– ident: ref67
  doi: 10.1111/cen.12441
– ident: ref11
  doi: 10.1056/NEJM198903023200904
– ident: ref41
  doi: 10.1093/humrep/deq028
– ident: ref99
  doi: 10.1111/j.1467-789X.2012.01053.x
– ident: ref37
  doi: 10.1038/s41598-023-50650-y
– ident: ref47
  doi: 10.1210/jc.2006-2725
– ident: ref7
  doi: 10.1093/humrep/der291
– ident: ref34
  doi: 10.1007/BF03345743
– ident: ref69
  doi: 10.1093/humupd/dmp006
– ident: ref49
  doi: 10.1210/jcem.84.11.6148
– ident: ref63
  doi: 10.1055/s-2002-38265
– ident: ref23
  doi: 10.1172/JCI118126
– ident: ref40
  doi: 10.1016/0002-9378(92)91779-A
– ident: ref55
  doi: 10.1055/s-2007-1009245
– ident: ref60
  doi: 10.4103/jhrs.JHRS_77_17
– ident: ref83
  doi: 10.1016/j.molmed.2023.02.006
– ident: ref29
  doi: 10.1016/S0303-7207(98)00177-4
– ident: ref82
  doi: 10.1016/j.fertnstert.2014.07.004
– ident: ref12
  doi: 10.1046/j.1365-2265.1997.2321049.x
– ident: ref3
  doi: 10.1093/humrep/deh098
– ident: ref13
  doi: 10.1210/me.2004-0178
– ident: ref27
  doi: 10.1016/S0889-8529(18)30245-7
– ident: ref30
  doi: 10.1210/jc.2003-031122
– ident: ref8
  doi: 10.1016/j.jsbmb.2014.06.003
– ident: ref107
  doi: 10.1210/jc.84.4.1470
– ident: ref70
  doi: 10.1016/j.mce.2008.01.007
– ident: ref32
  doi: 10.1111/j.1749-6632.2000.tb06230.x
– ident: ref57
  doi: 10.1016/S0015-0282(03)00265-6
– ident: ref85
  doi: 10.1016/S2213-8587(22)00339-4
– ident: ref106
  doi: 10.1111/j.1365-2265.1992.tb02909.x
– ident: ref102
  doi: 10.1210/jc.2009-0545
– ident: ref74
  doi: 10.1210/jcem.77.6.8263159
– ident: ref35
  doi: 10.1016/j.fertnstert.2014.01.049
– ident: ref58
  doi: 10.1093/humrep/den211
– ident: ref73
  doi: 10.1095/biolreprod61.4.993
– ident: ref79
  doi: 10.1016/j.bbrc.2008.06.039
– ident: ref26
  doi: 10.1016/j.molmed.2006.05.006
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Snippet The core pathophysiology of polycystic ovary syndrome involves an overproduction of androgens primarily originating from ovarian thecal cells. Two major...
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SubjectTerms anovulation
insulin resistance
obesity
polycystic ovary syndrome
Review
가정의학
Title Obesity and Polycystic Ovary Syndrome
URI https://www.ncbi.nlm.nih.gov/pubmed/39701598
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Volume 33
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