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Archives of Gynecology and Obstetrics
Published in: Archives of Gynecology and Obstetrics 4/2012

01-10-2012 | Reproductive Medicine

A macrophage activation marker chitotriosidase in women with PCOS: does low-grade chronic inflammation in PCOS relate to PCOS itself or obesity?

Authors: Ibrahim Alanbay, Cihangir Mutlu Ercan, Mehmet Sakinci, Hakan Coksuer, Mustafa Ozturk, Serkan Tapan

Published in: Archives of Gynecology and Obstetrics | Issue 4/2012

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Abstract

Objective

Polycystic ovary syndrome (PCOS) is described as a low-grade chronic inflammatory state where the macrophage infiltration increased in visceral fat play the major role. The aim of this study was to assess chitotriosidase (ChT) activity (an activated macrophage marker) in women with PCOS and controls and to evaluate its correlation with anthropometric and biochemical parameters.

Study design

Seventy-nine women with PCOS and 60 healthy controls were included in the study. PCOS and controls were divided into two subgroups according to body mass indexes (BMIs) as normoweight (<25 kg/m2) and overweight (≥25 kg/m2). ChT activity, biochemical (free testosterone, luteinizing hormone, insulin resistance index, etc.) and clinical parameters [BMI, waist-to-hip ratio, modified Ferriman–Gallwey scores (mFG)] were analyzed according to groups.

Results

Serum ChT activity was significantly (p < 0.001) higher in women with PCOS than controls (normoweight, 87.1 ± 90.1 vs. 18.4 ± 9.0 nmol/ml/h; overweight, 92.0 ± 96.7 vs. 17.9 ± 12.1 nmol/ml/h PCOS and controls, respectively). No statistically significant difference was noted between ChT activity of normoweight and overweight PCOS subgroups. A positive correlation was found between ChT activity and PCOS status (r 0.598, p < 0.001), mFG scores (r 0.525, p < 0.001), free testosterone (r 0.402, p 0.001) and total testosterone (r 0.168, p 0.048) for the combined groups (PCOS + controls). In multivariant linear regression analysis participants’ PCOS status (presence or absence) and LH levels were the main predictors of ChT activity in the whole study population (p 0.002 and p 0.041, respectively).

Conclusion

ChT activity elevates in PCOS independent of obesity. Our findings support the concept of PCOS is a state of low-grade chronic inflammation where the macrophages could play the major role. Hyperandrogenism might also be related to this inflammatory state and can be a subject of further trials.
Literature
1.
March WA, Moore VM, Wilson KJ, Phillips DIW, Norman RJ, Davies MJ (2010) The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Hum Reprod 25:544–551PubMedCrossRef
2.
Goodarzi MO, Dumesic DA, Chazenbalk G, Azziz R (2011) Polycystic ovary syndrome: etiology, pathogenesis and diagnosis. Nat Rev Endocrinol 7:219–231PubMedCrossRef
3.
Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, Janssen OE, Legro RS, Norman RJ, Taylor AE, Witchel SF (2009) The androgen excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 91:456–488PubMedCrossRef
4.
5.
Katsikis I, Karkanaki A, Misichronis G, Delkos D, Kandaraki EA, Panidis D (2011) Phenotype expression, body mass index and insulin resistance in relation to LH levels in women with polycystic ovary syndrome. Eur J Obstet Gynecol Reprod 156(2):181–185CrossRef
6.
Doi SAR, Towers PA, Scott CJ, Al-Shoumer KAS (2005) PCOS: an ovarian disorder that leads to dysregulation in the hypothalamic–pituitary–adrenal axis? Eur J Obstet Gynecol Reprod 118:4–16CrossRef
7.
Baptiste CG, Battista M-C, Trottier A, Baillargeon J-P (2010) Insulin and hyperandrogenism in women with polycystic ovary syndrome. J Steroid Biochem Mol Biol 122:42–52PubMedCrossRef
8.
Dunaif A (1997) Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis. Endocr Rev 18:774–800PubMedCrossRef
9.
Gilling-Smith C, Story H, Rogers S (1997) Evidence for a primary abnormality of theca cell steroidogenesis in the polycystic ovary syndrome. Clin Endocrinol 47:93–99CrossRef
10.
Kelly CJ, Lyall H, Petrie JR, Gould GW, Connell JM, Sattar N (2001) Low grade chronic inflammation in women with polycystic ovarian syndrome. J Clin Endocrinol Metab 86:2453–2455PubMedCrossRef
11.
Puder JJ, Varga S, Kraenzlin M, De Geyter C, Keller U, Muller B (2005) Central fat excess in polycystic ovary syndrome: relation to low-grade inflammation and insulin resistance. J Clin Endocrinol Metab 90:6014–6021PubMedCrossRef
12.
Repaci A, Gambineri A, Pasquali R (2011) The role of low-grade inflammation in the polycystic ovary syndrome. Mol Cell Endocrinol 335:30–41PubMedCrossRef
13.
Barber TM, McCarthy MI, Wass JAH, Franks S (2006) Obesity and polycystic ovary syndrome. Clin Endocrinol 65:137–145CrossRef
14.
Kirchengast S, Huber J (2001) Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome. Hum Reprod 16:1255–1260PubMedCrossRef
15.
Carmina E, Bucchieri S, Esposito A et al (2007) Abdominal fat quantity and distribution in women with polycystic ovary syndrome and extent of its relation to insulin resistance. J Clin Endocrinol Metab 92:2500–2505PubMedCrossRef
16.
Yildirim B, Sabir N, Kaleli B (2003) Relation of intra-abdominal fat distribution to metabolic disorders in nonobese patients with polycystic ovary syndrome. Fertil Steril 79(6):1358–1364PubMedCrossRef
17.
Glintborg D, Andersen M (2010) An update on the pathogenesis, inflammation, and metabolism in hirsutism and polycystic ovary syndrome. Gynecol Endocrinol 26:281–296PubMedCrossRef
18.
Cascella T, Palomba S, De Sio I, Manguso F, Giallauria F, De Simone B, Tafuri D, Lombardi G, Colao A, Orio F (2008) Visceral fat is associated with cardiovascular risk in women with polycystic ovary syndrome. Hum Reprod 23:153–159PubMedCrossRef
19.
Cancello R, Cle′ment K (2006) Is obesity an inflammatory illness? Role of low-grade inflammation and macrophage infiltration in human white adipose tissue. BJOG 113:1141–1147PubMedCrossRef
20.
21.
Strissel KJ, Stancheva Z, Miyoshi H et al (2007) Adipocyte death, adipose tissue remodeling, and obesity complications. Diabetes 56:2910–2918PubMedCrossRef
22.
Heilbronn LK, Campbell LV (2008) Adipose tissue macrophages. Low grade inflammation and insulin resistance in human obesity. Cur Pharm Des 14:1225–1230CrossRef
23.
Cinti S, Mitchell G, Barbatelli G, Murano I, Ceresi E, Faloia E, Wang S, Fortier M, Greenberg AS, Obin MS (2005) Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res 46:2347–2355PubMedCrossRef
24.
Hollak CE, van Weely S, van Oers MH, Aerts JM (1994) Marked elevation of plasma chitotriosidase activity. A novel hallmark of Gaucher disease. J Clin Invest 93:1288–1292PubMedCrossRef
25.
Boot RG, Renkema GH, Strijland A, van Zonneveld AJ, Aerts JM (1995) Cloning of a cDNA encoding chitotriosidase, a human chitinase produced by macrophages. J Biol Chem 270:26252–26256PubMedCrossRef
26.
27.
The Rotterdam ESHRE/ASRM-Sponsored PCOS Conference Workshop Group (2004) Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 81:19–25
28.
Ferriman D, Gallwey JD (1961) Clinical assessment of body hair growth in women. J Clin Endocrinol Metab 21:1440–1447PubMedCrossRef
29.
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC (1985) Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28:412–419PubMedCrossRef
30.
Legro RS, Castracane VD, Kauffman RP (2004) Detecting insulin resistance in polycystic ovary syndrome: purposes and pitfalls. Obstet Gynecol Surv 59:141–154PubMedCrossRef
31.
Escobar-Morreale HF, San Millán JL (2007) Abdominal adiposity and the polycystic ovary syndrome. Trends Endocrinol Metab 18:266–272PubMedCrossRef
32.
Lord J, Thomas R, Fox B, Acharya U, Wilkin T (2006) The central issue? Visceral fat is a good marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndrome. BJOG 113:817–824PubMedCrossRef
33.
Gesta S, Tseng YH, Kahn CR (2007) Developmental origin of fat: tracking obesity to its source. Cell 131:242–256PubMedCrossRef
34.
González F, Rote NS, Minium J, Weaver AM, Kirwan JP (2010) Elevated circulating levels of macrophage migration inhibitory factor in polycystic ovary syndrome. Cytokine 51:240–244PubMedCrossRef
35.
Gonzalez F, Thusu K, Abdel-Rahman E, Prabhala A, Tomani M, Dandona P (1999) Elevated serum levels of tumor necrosis factor alpha in normal-weight women with polycystic ovary syndrome. Metabolism 48:437–441PubMedCrossRef
36.
Escobar-Morreale HF, Luque-Ramırez M, Gonzalez F (2011) Circulating inflammatory markers in polycystic ovary syndrome: a systematic review and metaanalysis. Fertil Steril 95:1048–1058PubMedCrossRef
37.
González F, Rote NS, Minium J, Kirwan JP (2006) Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ovary syndrome. J Clin Endocrinol Metab 91:334–336
38.
González F, Rote NS, Minium J, Kirwan JP (2006) Increased activation of nuclear factor jB triggers inflammation and insulin resistance in polycystic ovary syndrome. J Clin Endocrinol Metab 91:1508–1512PubMedCrossRef
39.
Diamanti-Kandarakis E, Paterakis T, Alexandraki K, Piperi C, Aessopus A, Katsikis I, Katsilambros N, Kraetsas G, Panidis D (2006) Indices of low- grade chronic inflammation in polycystic ovary syndrome and beneficial effect of metformin. Hum Reprod 21:1426–1431PubMedCrossRef
40.
Cortón M, Botella-Carretero JI, Benguría A, Villuendas G, Zaballos A, San Milla′n JL, Escobar-Morreale HF, Peral B (2007) Differential gene expression profile in omental adipose tissue in women with polycystic ovary syndrome. J Clin Endocrinol Metab 92(1):328–337PubMedCrossRef
41.
Möhlig M, Spranger J, Ristow M, Pfeiffer AF, Schill T, Schlösser HW, Moltz L, Brabant G, Schöfl C (2006) Predictors of abnormal glucose metabolism in women with polycystic ovary syndrome. Eur J Endocrinol 154:295–301PubMedCrossRef
Metadata
Title
A macrophage activation marker chitotriosidase in women with PCOS: does low-grade chronic inflammation in PCOS relate to PCOS itself or obesity?
Authors
Ibrahim Alanbay
Cihangir Mutlu Ercan
Mehmet Sakinci
Hakan Coksuer
Mustafa Ozturk
Serkan Tapan
Publication date
01-10-2012
Publisher
Springer-Verlag
Published in
Archives of Gynecology and Obstetrics / Issue 4/2012
Print ISSN: 0932-0067
Electronic ISSN: 1432-0711
DOI
https://doi.org/10.1007/s00404-012-2425-0

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