Polycystic ovary syndrome and Insulin Resistance
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Date
2020-03-12
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faculty of Basic Medical Science - Libyan International Medical University
Abstract
Polycystic ovary syndrome (PCOS) is an imbalance of the female sex hormones also
is one of the most common metabolic and reproductive disorders among women of
reproductive age, associated with menstrual dysfunction and androgen excess which
significantly impacts their quality of life. They may be at increased risk of multiple
morbidities including obesity, type2 diabetes mellitus, infertility and cardiovascular
disease. Insulin resistance (IR) is characterized by impaired glucose response to
specific amount of insulin. Increasing interest in research on the mechanisms and
significance of the relationship between insulin resistance and ovarian syndrome have
both increased rapidly over the past 10 years. This report will review all of the risk
factor and relationship between insulin resistance and ovarian syndrome but will focus
primarily on the polycystic ovary syndrome (PCOS), which is the most common
disorder in which these abnormalities occur together. It will also discuss the
pathogenesis of polycystic ovary syndrome and its relationship to insulin resistance
Description
Polycystic ovary syndrome (PCOS) is the most common, although the least
understood cause of androgenic excess in premenopausal women, initially described
1935 and is also known as Stein- Leventhal syndrome. It is a multisystem
endocrinopathy. Including menstrual dysfunction, infertility, obesity, acne, hirsutism,
acanthosis nigricans and metabolic disorder.
POCS effect 4-6% of women incidents is fast increasing due to change in lifestyle and
stress.
A large proportion of women with PCOS are suffering from insulin resistance, they
have abnormal insulin activity which lead to risk of diabetes. Insulin stimulated
glucose utilization are significantly decreased in PCOS. Hyperinsulinemia seems to
play a major role in the pathogenesis of hyperandrogenism of PCOS.
Hyperinsulinemia stimulates androgen secretion by the ovarian theca, excess growth
of basal cells of the skin resulting in acanthosis nigricans, and abnormal hepatic and
peripheral lipid metabolism. (1)
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