Plasma monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha are increased in patients with polycystic ovary syndrome (PCOS) and associated with adiposity, but unaffected by pioglitazone treatment.
OBJECTIVE
Hirsutism is most often caused by polycystic ovary syndrome (PCOS). PCOS patients are characterized by insulin resistance, abdominal obesity and low-grade inflammation. Insulin sensitizing treatment reduces the inflammatory state, but the effect on serum levels of migration inhibitor factor (MIF), monocyte chemoattractant protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha have not been evaluated before in PCOS.


METHODS
Plasma chemokine levels (MCP-1, MIP-1alpha and MIF) were measured in two study designs. (i) 51 hirsute patients and 63 matched controls and (ii) 30 PCOS patients before and after randomized treatment with 30 mg pioglitazone/placebo for 16 weeks. Clinical evaluations and whole body DXA-scans were performed in all participants.


RESULTS
Hirsute patients (n = 51) had significantly increased MCP-1 [121 (15-950) vs. 81 (18-365) pg/ml; P < 0.05] and MIP-1alpha[179 (8-4202) vs. 103 (4-1598) pg/ml; P < 0.05] than controls of matched body composition [geometric mean (-2SD to +2SD)]. In PCOS (n = 30), MCP-1, MIP-1alpha and MIF correlated positively with central fat mass. A BMI independent positive association was found between MIF and free testosterone (r = 0.49, P = 0.01) in PCOS. Pioglitazone treatment significantly improved insulin sensitivity without affecting testosterone, body composition, MCP-1, MIP-1alpha and MIF levels.


CONCLUSIONS
Chemokine levels were significantly increased and showed close associations with measures of adiposity in PCOS patients, but were unchanged during insulin sensitizing treatment with pioglitazone. Our data suggests a fat mass independent association between testosterone and MIF levels in PCOS and the effect of anti-androgen treatment on chemokine levels needs to be examined.
Glintborg
Dorte
D
Department of Endocrinology and Metabolism, Odense University Hospital, Kløvervaenget 6, Odense C, Denmark. dorte.glintborg@dadlnet.dk
Andersen
Marianne
M
Richelsen
Bjørn
B
Bruun
Jens M
JM
D050154:Adiposity / Q000502:physiology*; D018932:Chemokine CCL2 / Q000097:blood*; D054405:Chemokine CCL3 / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D019746:Intramolecular Oxidoreductases / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D008263:Macrophage Migration-Inhibitory Factors / Q000097:blood; D000077205:Pioglitazone; D011085:Polycystic Ovary Syndrome / Q000097:blood* / Q000188:drug therapy*; D011863:Radioimmunoassay; D013739:Testosterone / Q000097:blood; D045162:Thiazolidinediones / Q000627:therapeutic use*; D014280:Triglycerides / Q000097:blood
D018932:Chemokine CCL2; D054405:Chemokine CCL3; D007004:Hypoglycemic Agents; D008075:Lipoproteins, HDL; D008263:Macrophage Migration-Inhibitory Factors; D045162:Thiazolidinediones; D014280:Triglycerides; D013739:Testosterone; D002784:Cholesterol; D019746:Intramolecular Oxidoreductases; C515598:MIF protein, human; D000077205:Pioglitazone