AIMS/HYPOTHESIS: Polycystic ovary syndrome (PCOS) is an insulin resistant (IR) state. Increased skeletal muscle lipid content and impaired mitochondrial biogenesis have been implicated in the pathogenesis of IR. We investigated whether differences in these variables explain the IR of women affected by PCOS and whether improvements in IR with exercise are reflected by changes in these variables. METHODS: Sixteen PCOS and 13 non-PCOS overweight women were assessed, and eight PCOS and seven non-PCOS women were reassessed after 12 weeks of moderate and vigorous exercise training. Outcomes included insulin sensitivity (glucose infusion rate [GIR]), skeletal muscle gene expression and protein abundance, enzyme activity of selected mitochondrial components, and computed tomography (CT) attenuation-estimated muscle lipid. RESULTS: GIR was lower in women with PCOS versus those without (p = 0.01) and increased with exercise in both groups. Baseline CT muscle attenuation suggested a trend to less muscle lipid in PCOS, which increased with exercise training, with a difference in the change in muscle lipid (p = 0.01, age-corrected), compared with non-PCOS women. GIR correlated with PGC1A gene expression across the whole group; skeletal muscle expression of mitochondrial biogenesis markers was not different between groups at baseline, or after training. Neither lipid changes nor mitochondrial changes correlated with changes in GIR. CONCLUSIONS/ INTERPRETATION: Differences in IR in women with and without PCOS were not explained by differences in skeletal muscle lipid or mitochondrial parameters. Improvements in IR with exercise were dissociated from mitochondrial parameters. CT muscle attenuation suggested a differential capacity of PCOS muscle to store lipid compared with non-PCOS. TRIAL REGISTRATION: Clinicaltrials.gov ISRCTN84763265. FUNDING: National Health & Medical Research Council (Grant number 606553), Monash University and The Jean Hailes Foundation.
AIMS/HYPOTHESIS: Polycystic ovary syndrome (PCOS) is an insulin resistant (IR) state. Increased skeletal muscle lipid content and impaired mitochondrial biogenesis have been implicated in the pathogenesis of IR. We investigated whether differences in these variables explain the IR of women affected by PCOS and whether improvements in IR with exercise are reflected by changes in these variables. METHODS: Sixteen PCOS and 13 non-PCOS overweight women were assessed, and eight PCOS and seven non-PCOSwomen were reassessed after 12 weeks of moderate and vigorous exercise training. Outcomes included insulin sensitivity (glucose infusion rate [GIR]), skeletal muscle gene expression and protein abundance, enzyme activity of selected mitochondrial components, and computed tomography (CT) attenuation-estimated muscle lipid. RESULTS: GIR was lower in women with PCOS versus those without (p = 0.01) and increased with exercise in both groups. Baseline CT muscle attenuation suggested a trend to less muscle lipid in PCOS, which increased with exercise training, with a difference in the change in muscle lipid (p = 0.01, age-corrected), compared with non-PCOSwomen. GIR correlated with PGC1A gene expression across the whole group; skeletal muscle expression of mitochondrial biogenesis markers was not different between groups at baseline, or after training. Neither lipid changes nor mitochondrial changes correlated with changes in GIR. CONCLUSIONS/ INTERPRETATION: Differences in IR in women with and without PCOS were not explained by differences in skeletal muscle lipid or mitochondrial parameters. Improvements in IR with exercise were dissociated from mitochondrial parameters. CT muscle attenuation suggested a differential capacity of PCOS muscle to store lipid compared with non-PCOS. TRIAL REGISTRATION: Clinicaltrials.gov ISRCTN84763265. FUNDING: National Health & Medical Research Council (Grant number 606553), Monash University and The Jean Hailes Foundation.
Authors: Nigel K Stepto; Vernon G Coffey; Andrew L Carey; Anna P Ponnampalam; Benedict J Canny; David Powell; John A Hawley Journal: Med Sci Sports Exerc Date: 2009-03 Impact factor: 5.411
Authors: Vera B Schrauwen-Hinderling; Marco Mensink; Matthijs K C Hesselink; Jean-Pierre Sels; M Eline Kooi; Patrick Schrauwen Journal: J Clin Endocrinol Metab Date: 2008-05-06 Impact factor: 5.958
Authors: John J Dubé; Francesca Amati; Maja Stefanovic-Racic; Frederico G S Toledo; Sarah E Sauers; Bret H Goodpaster Journal: Am J Physiol Endocrinol Metab Date: 2008-03-04 Impact factor: 4.310
Authors: Melanie Cree-Green; Bradley R Newcomer; Gregory Coe; Lindsey Newnes; Amy Baumgartner; Mark S Brown; Laura Pyle; Jane E Reusch; Kristen J Nadeau Journal: Am J Physiol Endocrinol Metab Date: 2015-02-24 Impact factor: 4.310
Authors: Cheehoon Ahn; Benjamin J Ryan; Michael W Schleh; Pallavi Varshney; Alison C Ludzki; Jenna B Gillen; Douglas W Van Pelt; Lisa M Pitchford; Suzette M Howton; Thomas Rode; Scott L Hummel; Charles F Burant; Jonathan P Little; Jeffrey F Horowitz Journal: J Physiol Date: 2022-03-20 Impact factor: 6.228
Authors: SoJung Lee; Anthony R Deldin; David White; YoonMyung Kim; Ingrid Libman; Michelle Rivera-Vega; Jennifer L Kuk; Sandra Sandoval; Chris Boesch; Silva Arslanian Journal: Am J Physiol Endocrinol Metab Date: 2013-09-17 Impact factor: 4.310
Authors: Siew S Lim; Samantha K Hutchison; Emer Van Ryswyk; Robert J Norman; Helena J Teede; Lisa J Moran Journal: Cochrane Database Syst Rev Date: 2019-03-28
Authors: Adam R Konopka; Albert Asante; Ian R Lanza; Matthew M Robinson; Matthew L Johnson; Chiara Dalla Man; Claudio Cobelli; Mark H Amols; Brian A Irving; K S Nair Journal: Diabetes Date: 2015-01-20 Impact factor: 9.461