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Obesity and androgen excess in women

Research group

Short description

Clinical evidence pinpoints excessive secretion of male sex hormones, androgens, as the underlying cause of polycystic ovary syndrome (PCOS), which affects more than 15 percent of the female population. PCOS is associated with an increased risk of developing abdominal obesity, diabetes and mood disorders. Women with PCOS have high androgen levels during pregnancy, and the role of male sex hormone exposure during fetal life in the development of PCOS has gained increasing attention. Our overall aim is to develop new strategies to treat PCOS and to prevent the development of PCOS in daughters of mothers with PCOS.

Background 

Clinically, the androgen excess in PCOS manifests as excessive body hair and acne, and anovulation manifests as irregular cycles and reduced fertility.

PCOS is also associated with insulin resistance/diabetes, and obesity worsens all symptoms. The mechanisms underlying the development of PCOS are poorly understood, but maternal obesity and androgen excess can impact fetal development and programming.

Women with PCOS have an increased risk for pregnancy complications as well as delivery complications, and frequently deliver babies born large or small for gestational age. Birth weight is a sensitive marker of the overall impact of the intrauterine environment on fetal development and predicts the risk to develop obesity, diabetes, cardiovascular disease in adult life.

The hypothesis that PCOS originates during fetal life is supported by the finding that daughters of women with PCOS are more likely to develop the condition. Women with PCOS display high androgens and low levels of the insulin-sensitizing hormone adiponectin during pregnancy. Low adiponectin levels increase the risk of develop gestational diabetes, suggesting low adiponectin levels leads to an impaired capacity to handle metabolic changes during pregnancy.

Our research

Adiponectin acts on the placenta during pregnancy and this fact allows for the interesting possibility that adiponectin can exert endocrine effects on the developing fetus and protect against the effects of obesity and androgen exposure on the offspring.

We work according to the hypothesis that elevated levels of adiponectin improves maternal metabolism and placenta function, and thereby protects against fetal overgrowth by preventing excess nutrient and androgen transport to the fetus, which in turn will prevent the development of PCOS and mood disorders in the offspring.