High-molecular-weight adiponectin is selectively reduced in women with polycystic ovary syndrome independent of body mass index and severity of insulin resistance.
BACKGROUND
High-molecular-weight (HMW) adiponectin contributes to insulin resistance (IR), which is closely associated with the pathophysiology of polycystic ovary syndrome (PCOS). Abnormalities in adipocyte function have been identified in PCOS and potentially contribute to lower adiponectin concentrations.


OBJECTIVE
Our objective was to determine which variables in plasma and adipose tissue influence HMW adiponectin in a well characterized cohort of women with PCOS.


METHODS
This was a cross-sectional study.


METHODS
A teaching hospital. Women with PCOS (n = 98) and body mass index (BMI)-matched controls (n = 103) (including 68 age-, BMI-, and IR-matched pairs).


METHODS
A standard 75-g oral glucose tolerance test was performed for each participant. Subcutaneous adipose tissue samples were taken by needle biopsy for a subset of PCOS women (n = 9) and controls (n = 8).


METHODS
Serum levels of HMW adiponectin and their relation to indices of insulin sensitivity, body composition, and circulating androgens as well as adipose tissue expression levels of ADIPOQ, TNFalpha, PPARgamma, and AR were assessed.


RESULTS
HMW adiponectin was significantly lower in women with PCOS compared with both BMI- and BMI- and IR-matched controls (P = 0.009 and P = 0.027, respectively). Although BMI and IR were the main predictors of HMW adiponectin, an interaction between waist to hip ratio and plasma testosterone contributed to its variance (P = 0.026). Adipose tissue gene expression analysis demonstrated that AR and TNFalpha (P = 0.008 and P = 0.035, respectively) but not ADIPOQ mRNA levels were increased in PCOS compared with controls.


CONCLUSIONS
HMW adiponectin is selectively reduced in women with PCOS, independent of BMI and IR. Gene expression analysis suggests that posttranscriptional/translational modification contributes to reduced HMW adiponectin in PCOS.
O'Connor
A
A
Nutrigenomics Research Group, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
Phelan
N
N
Tun
T Kyaw
TK
Boran
G
G
Gibney
J
J
Roche
H M
HM
D052242:Adiponectin / Q000097:blood*; D000328:Adult; D000886:Anthropometry; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition / Q000502:physiology; D015992:Body Mass Index; D003430:Cross-Sectional Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D020738:Leptin / Q000097:blood; D011085:Polycystic Ovary Syndrome / Q000097:blood*; D052243:Resistin / Q000097:blood; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012720:Severity of Illness Index; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D018709:Statistics, Nonparametric
D052242:Adiponectin; D001786:Blood Glucose; D020738:Leptin; D052243:Resistin; D012738:Sex Hormone-Binding Globulin