The polycystic ovary syndrome per se is not associated with increased chronic inflammation.
OBJECTIVE
The syndrome of polycystic ovaries (PCOS) is a known risk factor for type 2 diabetes. It is not known, however, whether the increase in diabetes risk is related to endocrine abnormalities associated with PCOS such as hyperandrogenemia, or whether it is a consequence of the anthropometric or metabolic alterations frequently observed in PCOS women.


METHODS
Since markers of inflammation are supposed to predict type 2 diabetes, interleukin-6 (IL-6) and C-reactive protein (CRP) in combination with parameters of obesity, insulin resistance and hyperandrogenism were determined in 57 PCOS women and in 20 age-matched healthy controls. In addition, the C-174G IL-6 promoter polymorphism was analyzed as a determinant in influencing IL-6, obesity, and androgen levels in women.


RESULTS
Neither CRP nor IL-6 were significantly elevated in lean or obese PCOS women compared with age-matched lean or obese controls. In PCOS patients, variables of body composition (body mass index (BMI), waist to hip ratio, dual-energy X-ray-absorptiometry fat mass) and of insulin resistance were correlated with IL-6 or CRP, while parameters of hyperandogenism were not. Multivariate linear regression analysis revealed that obesity is the dominant force, thus explaining 18% and 24% of the IL-6 or CRP levels, respectively, in PCOS women. No association of IL-6 or BMI to a certain genotype at C-174G could be demonstrated in 50 PCOS patients. The heterozygous GC genotype, however, was associated with lower androstendione levels. Metformin treatment of 9 obese, insulin-resistant PCOS patients over a period of 6 months caused a significant decrease in body weight, body fat mass and total testosterone, but showed no significant decline in IL-6 or CRP concentrations.


CONCLUSIONS
In PCOS women, plasma levels of IL-6 and CRP were not increased when compared with age- and BMI-matched controls. BMI was, however, the parameter most strongly related to IL-6 and CRP in PCOS; thus PCOS-related endocrine abnormalities do not appear to activate inflammatory parameters thereby enhancing the risk of diabetes. In PCOS, the type 2 diabetes risk may, therefore, be confined to those with obesity and/or metabolic alterations rather than affecting all women suffering from the syndrome.
Möhlig
Matthias
M
Department of Clinical Nutrition, German Institute of Human Nutrition, 14558 Potsdam-Rehbruecke, Germany.
Spranger
Joachim
J
Osterhoff
Martin
M
Ristow
Michael
M
Pfeiffer
Andreas F H
AF
Schill
Thilo
T
Schlösser
Hans W
HW
Brabant
Georg
G
Schöfl
Christof
C
D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D002908:Chronic Disease; D003920:Diabetes Mellitus / Q000453:epidemiology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000453:epidemiology* / Q000235:genetics; D007333:Insulin Resistance / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D009765:Obesity; D011085:Polycystic Ovary Syndrome / Q000453:epidemiology* / Q000235:genetics / Q000276:immunology*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D012307:Risk Factors
D015850:Interleukin-6; D002097:C-Reactive Protein