Metabolic Disturbance in PCOS: Clinical and Molecular Effects on Skeletal Muscle Tissue

Show simple item record

dc.contributor Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP DANTAS, Wagner Silva
ROCHA, Michele Patrocinio
BARCELLOS, Cristiano Roberto Grimaldi
YANCE, Viviane dos Reis Vieira FMUSP-HC
MARCONDES, Jose Antonio Miguel FMUSP-HC 2013
dc.identifier.citation SCIENTIFIC WORLD JOURNAL, article ID 178364, 7p, 2013
dc.identifier.issn 1537-744X
dc.description.abstract Polycystic ovary syndrome is a complex hormonal disorder affecting the reproductive and metabolic systems with signs and symptoms related to anovulation, infertility, menstrual irregularity and hirsutism. Skeletal muscle plays a vital role in the peripheral glucose uptake. Since PCOS is associated with defects in the activation and pancreatic dysfunction of beta-cell insulin, it is important to understand the molecular mechanisms of insulin resistance in PCOS. Studies of muscle tissue in patients with PCOS reveal defects in insulin signaling. Muscle biopsies performed during euglycemic hyperinsulinemic clamp showed a significant reduction in glucose uptake, and insulin-mediated IRS-2 increased significantly in skeletal muscle. It is recognized that the etiology of insulin resistance in PCOS is likely to be as complicated as in type 2 diabetes and it has an important role in metabolic and reproductive phenotypes of this syndrome. Thus, further evidence regarding the effect of nonpharmacological approaches (e.g., physical exercise) in skeletal muscle of women with PCOS is required for a better therapeutic approach in the management of various metabolic and reproductive problems caused by this syndrome.
dc.description.sponsorship · Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2012/02827-7, 2012/14650-4]
dc.language.iso eng
dc.relation.ispartof Scientific World Journal
dc.rights openAccess
dc.subject.other polycystic-ovary-syndrome; impaired glucose-tolerance; insulin-resistance; pioglitazone treatment; androgen excess; adipose-tissue; women; prevalence; transport; health
dc.title Metabolic Disturbance in PCOS: Clinical and Molecular Effects on Skeletal Muscle Tissue
dc.type article
dc.identifier.doi 10.1155/2013/178364
dc.identifier.pmid 23844380
dc.type.category review
dc.type.version publishedVersion YANCE, Viviane dos Reis Vieira:FM: MARCONDES, Jose Antonio Miguel:HC:ICHC · DANTAS, Wagner Silva:Univ Sao Paulo, Sch Phys Educ & Sport, Lab Appl Nutr & Metab, BR-05508030 Sao Paulo, Brazil
· GUALANO, Bruno:Univ Sao Paulo, Sch Phys Educ & Sport, Lab Appl Nutr & Metab, BR-05508030 Sao Paulo, Brazil
· ROCHA, Michele Patrocinio:Univ Sao Paulo, Div Endocrinol, Sch Med, BR-05508030 Sao Paulo, Brazil
· BARCELLOS, Cristiano Roberto Grimaldi:Univ Sao Paulo, Div Endocrinol, Sch Med, BR-05508030 Sao Paulo, Brazil WOS:000320522800001 2-s2.0-84879330751 NEW YORK USA
hcfmusp.relation.reference · Abdul-Ghani MA, 2010, J BIOMED BIOTECHNOL, DOI 10.1155/2010/476279
· Apridonidze T, 2005, J CLIN ENDOCR METAB, V90, P1929, DOI 10.1210/jc.2004-1045
· Azziz R, 2006, J CLIN ENDOCR METAB, V91, P4237, DOI 10.1210/jc.2006-0178
· Azziz R, 2009, FERTIL STERIL, V91, P456, DOI 10.1016/j.fertnstert.2008.06.035
· Bandyopadhyay GK, 2006, DIABETES, V55, P2277, DOI 10.2337/db06-0062
· Barcellos CRG, 2007, ARQ BRAS ENDOCRINOL, V51, P601, DOI 10.1590/S0004-27302007000400015
· Bargiota Alexandra, 2012, Ther Adv Endocrinol Metab, V3, P27, DOI 10.1177/2042018812437355
· Blaak EE, 2005, BEST PRACT RES CL EN, V19, P391, DOI 10.1016/j.beem.2005.04.001
· Brettenthaler N, 2004, J CLIN ENDOCR METAB, V89, P3835, DOI 10.1210/jc.2003-031737
· Ciampelli M, 2005, J CLIN ENDOCR METAB, V90, P1398, DOI 10.1210/jc.2004-0410
· Ciaraldi TP, 2009, J CLIN ENDOCR METAB, V94, P157, DOI 10.1210/jc.2008-1492
· Cline GW, 1999, NEW ENGL J MED, V341, P240, DOI 10.1056/NEJM199907223410404
· Corbould A, 2008, PANMINERVA MED, V50, P279
· Corbould A, 2005, AM J PHYSIOL-ENDOC M, V288, pE1047, DOI 10.1152/ajpendo.00361.2004
· DeFronzo RA, 1997, DIABETES REV, V5, P177
· de Paula Martins W, 2007, EUR J OBSTET GYN R B, V133, P203, DOI 10.1016/j.ejogrb.2006.10.038
· Diamanti-Kandarakis E, 2006, TRENDS MOL MED, V12, P324, DOI 10.1016/j.molmed.2006.05.006
· Diamanti-Kandarakis E, 2012, ENDOCR REV, V33, P981, DOI 10.1210/er.2011-1034
· DOUEN AG, 1990, J BIOL CHEM, V265, P13427
· DUNAIF A, 1995, J CLIN INVEST, V96, P801, DOI 10.1172/JCI118126
· Dunaif A, 1997, ENDOCR REV, V18, P774, DOI 10.1210/er.18.6.774
· Dunaif A, 2001, AM J PHYSIOL-ENDOC M, V281, pE392
· DUNAIF A, 1989, DIABETES, V38, P1165, DOI 10.2337/diabetes.38.9.1165
· Ehrmann DA, 1999, DIABETES CARE, V22, P141, DOI 10.2337/diacare.22.1.141
· Fauser BCJM, 2012, FERTIL STERIL, V97, P28, DOI 10.1016/j.fertnstert.2011.09.024
· Fulghesu AM, 2006, FERTIL STERIL, V86, P398, DOI 10.1016/j.fertnstert.2006.01.024
· Geloneze Bruno, 2006, Arq Bras Endocrinol Metabol, V50, P208, DOI 10.1590/S0004-27302006000200007
· Glintborg D, 2008, J CLIN ENDOCR METAB, V93, P3618, DOI 10.1210/jc.2008-0760
· Goodarzi MO, 2005, FERTIL STERIL, V84, P766, DOI 10.1016/j.fertnstert.2005.03.051
· HIRSHMAN MF, 1990, J BIOL CHEM, V265, P987
· Hojlund K, 2008, DIABETES, V57, P357, DOI 10.2337/db07-0706
· Horakova O, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0043764
· Joost HG, 2002, AM J PHYSIOL-ENDOC M, V282, pE974, DOI 10.1152/ajpendo.00407.2001
· Karlsson HKR, 2007, CELL BIOCHEM BIOPHYS, V48, P103, DOI 10.1007/s12013-07-0030-9
· Knochenhauer ES, 1998, J CLIN ENDOCR METAB, V83, P3078, DOI 10.1210/jc.83.9.3078
· Kristiansen S, 1996, AM J PHYSIOL-ENDOC M, V270, pE197
· Legro RS, 1999, J CLIN ENDOCR METAB, V84, P165, DOI 10.1210/jc.84.1.165
· Loviscach M, 2000, DIABETOLOGIA, V43, P304, DOI 10.1007/s001250050048
· Marcondes J. A. M., 2007, ENDOCRINOLOGIA, P635
· Marcondes JAM, 2007, ARQ BRAS ENDOCRINOL, V51, P972, DOI 10.1590/S0004-27302007000600012
· Marcondes JAM, 2011, ARQ BRAS ENDOCRINOL, V55, P6, DOI 10.1590/S0004-27302011000100002
· Miyazaki Y, 2003, DIABETES, V52, P1943, DOI 10.2337/diabetes.52.8.1943
· Panidis D., 2012, CLIN ENDOCRINOLOGY
· Chang J, 2004, FERTIL STERIL, V81, P19, DOI 10.1016/j.fertnstert.2003.10.004
· Rocha MP, 2011, GYNECOL ENDOCRINOL, V27, P814, DOI 10.3109/09513590.2010.508852
· Sathyapalan T, 2012, EUR J ENDOCRINOL, V166, P575, DOI 10.1530/EJE-11-0755
· Shaw LJ, 2008, J CLIN ENDOCR METAB, V93, P1276, DOI 10.1210/jc.2007-0425
· Skov V., 2008, PLOS ONE, V3
· Skov V, 2007, DIABETES, V56, P2349, DOI 10.2337/db07-0275
· Solomon CG, 2002, J CLIN ENDOCR METAB, V87, P2013, DOI 10.1210/jc.87.5.2013
· Tfaylio H, 2008, ANN NY ACAD SCI, V1135, P85, DOI 10.1196/annals.1429.024
· The Rotterdam ESHRE/ASRM-Sponsored PCOS consensus workshop group, 2004, HUMAN REPROD, V19, P41, DOI 10.1093/HUMREP/DEH098
· Vigil P, 2007, HUM REPROD, V22, P2974, DOI 10.1093/humrep/dem302
· Vigorito C, 2007, J CLIN ENDOCR METAB, V92, P1379, DOI 10.1210/jc.2006-2794
· Vrbikova J, 2005, HUM REPROD, V20, P3328, DOI 10.1093/humrep/dei221
· Wild RA, 2010, J CLIN ENDOCR METAB, V95, P2038, DOI 10.1210/jc.2009-2724
· Zawadzki JK, 1992, POLYCYSTIC OVARY SYN, P377
dc.description.index MEDLINE
hcfmusp.citation.scopus 9
hcfmusp.citation.wos 8 Brasil

Files in this item

This item appears in the following Collection(s)

Show simple item record

Search DSpace


My Account