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Obesity and polycistyc ovary sindrome. (CROSBI ID 624248)

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Jandrić Balen, Marica Obesity and polycistyc ovary sindrome. // 6. hrvatski endokrinološki kongres s međunarodnim sudjelovanjem Poreč, Hrvatska, 09.10.2013-13.10.2013

Podaci o odgovornosti

Jandrić Balen, Marica

engleski

Obesity and polycistyc ovary sindrome.

Polycystic ovary syndrome (PCOS) is a complex endocrine, reproductive and metabolic disorder with insufficiently known etiology and pathogenesis. It manifests itself through a whole range of clinical characteristics and symptoms three of which are the most common : 1 Ovulation disorders ; 2 Increased production of androgens ; 3 Ultrasound-shown polycystic ovary appearance with frequent association with obesity and insulin resistance. Etiology is complex and multifactorial in which genetic factors are involved, stimulated by environmental factors. However, today we have evidence to suggest that adipose tissue plays a significant role in developing and maintaining the pathology of PCOS. Adipose tissue plays a key role in the regulation of appetite, body weight, metabolism and reproductive capacity. PCOS is the most common female endocrinopathy whose frequency ranges between 15-22 %, according to European criteria (Rotterdam criteria, 2003) while in adolescents it can get up to 25 %. It is associated with the characteristics of metabolic syndrome, and women with PCOS have a higher risk of obesity, insulin resistance, abnormal glucose tolerance, type 2 diabetes, dyslipidemia, and high blood pressure. Most women with PCOS (between 38% and 88%) are overweight or adipose. Adiposity per se probably contributes to hyperandrogenism characteristic, even in women with normal ovaries and also contributes to the development of insulin resistance which is considered to be in PCOS because of post-receptor disorders in the metabolism of insulin at the level of peripheral tissues. Studies have shown that about 50% of women with PCOS adipocytes and fibroblasts exhibit elevated serine phosphorylation and reduced tyrosine phosphorylation upon binding of insulin to its receptor, which causes the stopping of insulin signaling pathway with consequently reduced cell response to insulin simultaneously activating overproduction of androgens. There is increasing evidence that abnormal production of high-adipokines leptin and resistin and low adiponectin impact on changes in the activity of insulin and IGF, on steroidogenesis in the ovary, and thus on the control the menstrual cycle. Obesity in women with PCOS increases insulin resistance, hyperandrogenism and dyslipidemia. Loss in body weight form 5 –10 % leads to reduction of androgen and insulin levels, and to increased concentrations of a protein that binds sex hormones - SHBG (sex hormone binding protein), and the possibility of establishing a reproductive function with higher incidence of menstrual cycle and ovulation.

Obesity; polycistyc syndrome

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Podaci o prilogu

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Podaci o skupu

6. hrvatski endokrinološki kongres s međunarodnim sudjelovanjem

pozvano predavanje

09.10.2013-13.10.2013

Poreč, Hrvatska

Povezanost rada

Kliničke medicinske znanosti