Polycystic ovarian syndrome (PCOS) is characterized by elevated androgens such as testosterone. Clinical studies suggest that ketogenic diets lower the levels of androgens. The ketone 3-hydroxybutyrate (3-OHB) may play an important role in these effects and the main purpose of this study is to investigate whether a 3-OHB supplement acutely improves the hormonal and metabolic status in women with PCOS.
Polycystic ovary syndrome (PCOS) affects 5-18% of women and is characterized by the presence of two of three of the Rotterdam criteria: Hyperandrogenism (clinical or biochemical), irregular menstrual cycles, and polycystic ovary morphology, after exclusion of other conditions that mimic PCOS. PCOS is associated with elevated levels of luteinizing hormone (LH) and unaltered levels of the follicle stimulating hormone (FSH), which leads to the characteristic hyperandrogenism (high levels of testosterone), oligo- or anovulation, and a large number of premature follicles in the ovarian. Insulin resistance causes hyperinsulinemia that decreases sex hormone binding globulin (SHBG) levels and stimulates androgen production (e.g., elevated concentrations of testosterone). Ketogenic diets are characterized by a diet low in carbohydrates, and has shown beneficial effects on weight and hormonal status in women with PCOS. Whether these improvements are mediated by ketones (e.g., 3-hydroxybutyrate, 3-OHB) or other effects related to this diet is unknown. The main purpose of this study is to investigate whether a 3-OHB supplement acutely improves the hormonal and metabolic status in women with PCOS.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
DOUBLE
Enrollment
20
60 ml (30 g) of 3-OHB
60 ml water (added bitter taste)
Department of Diabetes and Hormone Diseases (DoH)
Aarhus N, Denmark
Plasma concentration of testosterone
Paired t-test
Time frame: 10 hours after first intervention
plasma SHBG
Time frame: 10 hours after first intervention
plasma 3-OHB
Time frame: 10 hours after first intervention
plasma glucose
Time frame: 10 hours after first intervention
serum insulin
Time frame: 10 hours after first intervention
plasma C-peptide
Time frame: 10 hours after first intervention
plasma free fatty acids
Time frame: 10 hours after first intervention
plasma triglycerides
Time frame: 10 hours after first intervention
plasma cholesterol
Time frame: 10 hours after first intervention
C reactive protein
Time frame: 10 hours after first intervention
plasma cytokines (such as Tumor Necrotic Factor alpha, Interleukin 6, Lipopolysaccharide -binding protein, soluble CD163)
Time frame: 10 hours after first intervention
plasma prolactin
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Time frame: 10 hours after first intervention
Plasma FSH
Time frame: 10 hours after first intervention
Plasma LH
Time frame: 10 hours after first intervention
plasma free testosterone
Time frame: 10 hours after first intervention
plasma estradiol
Time frame: 10 hours after first intervention
plasma keto-testosterone
Time frame: 10 hours after first intervention
Homeostatic Model Assessment for Insulin Resistance
Time frame: 10 hours after first intervention