Wos Açık Erişimli Yayınlar

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Author: search.filters.author.Bozkirli, EmreSubject: search.filters.subject.Polycystic ovary syndrome

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    Insulin Resistance in Non-Obese Polycystic Ovary Syndrome Subjects and Relation with Family History of Diabetes Mellitus
    (2015) Bozkirli, Emre; Bakiner, Okan; Ertorer, Eda; Anaforoglu, Inan; Tutuncu, Neslihan Basil; Demirag, Nilgun Guvener
    Purpose: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women in reproductive age. Conflicting results are reported in the studies examining insulin resistance in lean PCOS subjects. We aimed to observe the controversial presence of insulin resistance in lean PCOS subjects with the gold standard method and assess the impacts of family history of type 2 diabetes mellitus (T2DM) on insulin resistance in these patients. Material and Method: Nineteen patients with PCOS and nine age-BMI matched control subjects were recruited into the study. Patients with PCOS were divided into two groups according to their FH of T2DM among their first degree relatives (FHneg vs FHpos). Insulin resistance was evaluated with homeostasis model assessment of insulin resistance (HOMA-IR) and hyperinsulinemic euglycemic clamp technique for all participants. Results: Mean M values were significantly higher in the control group when compared with PCOS patients (p=0.003). There was no statistically significant difference for HOMA-IR and M values when FHneg and FHpos patients were compared. Although HOMA-IR values were similar between all groups, M values were lower in FHneg and FHpos groups compared to the controls (p=0.02 and 0.004 respectively). Discussion: Lean PCOS patients have evident insulin resistance when compared to healthy subjects, and FH of T2DM seems to not affect insulin resistance. Even non-obese PCOS patients should be encouraged for healthy eating style and exercise to prevent the potential risks associated with insulin resistance. Furthermore these patients can see benefits from medical therapies which improve insulin sensitivity.
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    Body Mass Index below Obesity Threshold Implies Similar Cardiovascular Risk among Various Polycystic Ovary Syndrome Phenotypes
    (2016) Bagir, Gulay Simsek; Bakiner, Okan S.; Bozkirli, Emre; Cavlak, Gulhan; Serinoz, Hulya; Ertorer, M. Eda; 26335185
    Objective: The aim of this study was to determine the cardiometabolic risk factors in different polycystic ovary syndrome (PCOS) phenotypes. Subjects and Methods: This cross-sectional study was performed between 2010 and 2011. Eighty-nine patients with PCOS and 25 age- and weight-matched healthy controls were included in the study. Patients were grouped using the Rotterdam 2003 criteria as: group 1, oligomenorrhea and/or anovulation (ANOV) and hyperandrogenemia (HA) and/or hyperandrogenism (n = 23); group 2, ANOV and polycystic ovaries (PCO; n = 22); group 3, HA and PCO (n = 22); group 4, ANOV, HA and PCO (n = 22); group 5, controls (n = 25). Laboratory blood tests for diagnosis and cardiometabolic risk assessments were performed. Insulin resistance (IR) was calculated in all patients with the homeostasis model assessment of IR (HOMA-IR) formula. An euglycemic hyperinsulinemic clamp test was performed on 5 randomly selected cases in each subgroup, making 25 cases in total, and indicated as the 'M' value (mg/kg/min), which is the total body glucose disposal rate. Results: The mean BMl values of the groups were: group 1, 26.1 +/- 5.3; group 2, 27.9 +/- 5.2; group 3, 24.3 +/- 4.2; group 4, 27.9 +/- 7.5; group 5, 24.7 +/- 5.2 (p > 0.05). There were no differences in the lipid profile, plasma glucose, HOMA-IR, insulin and M values between the groups (p > 0.05). Phenotypes with oligomenorrhea/anovulation (groups 1, 2 and 4) were more obese than group 3 (p = 0.039). Conclusions: The cardiometabolic risk profile was similar among the PCOS subgroups. This finding could be attributed to the mean BMl values, which, being below 30, were not within the obesity range. Obesity appeared to be an important determinant of high cardiovascular risk in PCOS. (C) 2015 S. Karger AG, Basel