Inflammation in response to glucose ingestion is independent of excess abdominal adiposity in normal-weight women with polycystic ovary syndrome.
BACKGROUND
Inflammation and excess abdominal adiposity (AA) are often present in normal-weight women with polycystic ovary syndrome (PCOS).


OBJECTIVE
We determined the effects of hyperglycemia on nuclear factor-κB (NFκB) activation in mononuclear cells (MNC) of normal-weight women with PCOS with and without excess AA.


METHODS
This was a prospective controlled study.


METHODS
The study was conducted at an academic medical center.


METHODS
Fifteen normal-weight, reproductive-age women with PCOS (seven normal AA, eight excess AA) and 16 body composition-matched controls (eight normal AA, eight excess AA) participated in the study.


METHODS
Body composition was measured by dual-energy absorptiometry. Insulin sensitivity was derived from an oral glucose tolerance test (IS(OGTT)). Activated NFκB and the protein content of p65 and inhibitory-κB were quantified from MNC, and TNFα and C-reactive protein (CRP) were measured in plasma obtained from blood drawn while fasting and 2 h after glucose ingestion.


RESULTS
Compared with controls, both PCOS groups exhibited lower IS(OGTT), increases in activated NFκB and p65 protein, and decreases in inhibitory-κB protein. Compared with women with PCOS with excess AA, those with normal AA exhibited higher testosterone levels and lower TNFα and CRP levels. For the combined groups, the percent change in NFκB activation was negatively correlated with IS(OGTT) and positively correlated with androgens. TNFα and CRP were positively correlated with abdominal fat.


CONCLUSIONS
In normal-weight women with PCOS, the inflammatory response to glucose ingestion is independent of excess AA. Circulating MNC and excess AA are separate and unique sources of inflammation in this population.
Indiana University School of Medicine, Department of Obstetrics and Gynecology, AOC Room 6046, 550 North University Boulevard, Indianapolis, Indiana 46202, USA. gonzalef@iupui.edu
Frank
F
González
Chang Ling
CL
Sia
Marguerite K
MK
Shepard
Neal S
NS
Rote
Judi
J
Minium
D050153:Abdominal Fat / Q000378:metabolism*; D050154:Adiposity / Q000502:physiology*; D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D005951:Glucose Tolerance Test; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism*; D011085:Polycystic Ovary Syndrome / Q000378:metabolism*; D011446:Prospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D015415:Biomarkers; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D005947:Glucose