Division of Endocrinology and Human Reproduction, Second Department of Obstetrics and Gynecology, Aristotle University of Thessaloniki, Greece
1 To whom correspondence should be addressed. e-mail: argic{at}med.auth.gr
Dear Sir,
We read the letter to the Editor by Orio et al. (2003b) with much interest, and would like to thank the authors for addressing some issues of significant importance. However, we do not consider our data and analyses to be weak in any case, and we fail to see how our conclusions (Panidis et al., 2003
) differ significantly from those reported recently by Orio et al. (2003a)
.
First of all, we recognize that group I of our study included overweight women with polycystic ovary syndrome (PCOS) as well as obese women; therefore, we tried to refer to this group throughout the text as group I or PCOS + BMI >25 kg/m2. However, at some points the terms obese women with PCOS or obesity were used, instead of the more accurate obese and overweight and increased adiposity, respectively. We apologize for the confusion this might have caused. Nevertheless, we by no means implied that obese and overweight women with PCOS have reduced adiponectin levels as a result of the syndrome rather than increased adiposity, and the wrong choice of words certainly does not make our results inconsistent with those of Orio et al. (2003a). On the contrary, we both seem to agree on the key thesis that the reduction of adiponectin levels in obese and overweight women with PCOS is most probably caused by adiposity and does not play a major role in the pathogenesis of the syndrome.
It is interesting, however, that Orio et al. (2003a) came to this conclusion, although a significant correlation between adiponectin levels and HOMA values is reported in their paper. Certainly, the fact that serum adiponectin levels in women with PCOS were comparable to those of control women matched for age and body mass index (BMI) implies that the observed correlation between adiponectin and insulin resistance is, most probably, adiposity dependent. Nevertheless, this is a finding that needs to be further analysed by means of multiple regression analysis controlling for BMI and/or waist:hip ratio, a simple step in most statistical packages. We believe that the results would certainly be of methodological importance, since there are, indeed, significant data linking adiponectin with insulin sensitivity, independent of increased adiposity (Spranger et al., 2003
; Tschritter et al., 2003
).
In conclusion, we believe that the findings reported in our paper are essentially in accordance with those by Orio et al., and await further evidence regarding any possible relationship between adiponectin or other lipocytokines and the complex metabolic state of PCOS.
References
Orio F Jr, Palomba S, Cascella T, Milan G, Mioni R, Pagano C, Zullo F, Colao A, Lombardi G and Vettor R (2003a) Adiponectin levels in women with polycystic ovary sindrome. J Clin Endocrinol Metab 88,26192623.
Orio F Jr, Palomba S, Zullo F, Colao A and Lombardi G (2003b) Are serum adiponectin levels really reduced in obese women with polycystic ovary syndrome? Hum Reprod 19,215.
Panidis D, Kourtis A, Farmakiotis D, Mouslech T, Rousso D and Koliakos G (2003) Serum adiponectin levels in women with polycystic ovary syndrome. Hum Reprod 18,17901796.
Spranger J, Kroke A, Mohlig M, Bergmann MM, Ritsow M, Boeing H and Pfeiffer AFH (2003) Adiponectin and protection against type 2 diabetes mellitus. Lancet 361,226228.[CrossRef][ISI][Medline]
Tschritter O, Fritsche A, Thamer C, Haap M, Shirkavand F, Rahe S, Staiger H, Maerker E, Haring H and Stumvoll M (2003) Plasma adiponectin concentrations predict insulin sensitivity of both glucose and lipid metabolism. Diabetes 52,239243.