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Adipocyte Insulin Resistance In PCOS: Relationship With GLUT-4 Expression, Whole-Body Glucose Disposal, β-Cell Function.

CONTEXT
Impaired sensitivity to the antilipolytic action of insulin in adipose tissue (AT) may play a role in determining metabolic dysfunction in Polycystic Ovary Syndrome (PCOS).


OBJECTIVES
To test the hypothesis that insulin resistance (IR) in AT is associated with whole-body insulin sensitivity and β-cell function in PCOS.


RESEARCH DESIGN AND SETTING
Prospective cross-sectional study.


METHODS
Eighteen PCOS and 18 matched controls underwent a modified frequently sampled intravenous glucose tolerance test (mFSIVGTT); subgroups underwent single-slice CT scans determining AT distribution, and adipocyte GLUT-4 expression.


MAIN OUTCOME MEASURES
IR in AT in basal (by the Adipose Insulin Resistance Index [Adipo-IR]) and dynamic (mFSIVGTT-derived indices of insulin-mediated non-esterified fatty acids (NEFA) suppression [NEFAnadir, TIMEnadir, and %NEFAsupp]) state; whole body insulin-mediated glucose uptake and insulin secretion in basal (by HOMA-IR and HOMA-β%) and dynamic (mFSIVGTT-derived insulin sensitivity index (Si), acute insulin response to glucose (AIRg), and disposition index (Di) state.


RESULTS
PCOS women had higher HOMA-IR and HOMA-β%, lower Si and Di, higher longer TIMEnadir, higher Adipo-IR and NEFAnadir and a trend towards lower GLUT-4, than controls. Adipo-IR was associated with dynamic state IR in AT (NEFAnadir TIMEnadir, and %NEFAsupp), but only in PCOS, and with HOMA-IR and HOMA-β% in both groups. NEFAnadir and TIMEnadir were negatively, and %NEFAsupp positively, associated with Si only in PCOS, but not with AIRg and Di, or GLUT-4 expression.


CONCLUSION
PCOS women demonstrate increased IR in AT, which is closely associated with whole-body IR, but not with dynamic state β-cell function or adipocyte GLUT-4 gene expression.