5α-reductase activity in women with polycystic ovary syndrome: a systematic review and meta-analysis

Wu, Chuyan; Wei, Ke; Jiang, Zhongli

doi:10.1186/s12958-017-0242-9

Cited by 33 publications

(23 citation statements)

References 25 publications

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“…AUC glucose (Area under the curve of blood glucose) = 1/4 × FBG + 1/2 × PBG30′ + 3/4 × PBG60′ + PBG120′ 20 . The insulin resistance index is defined as the ratio of HOMA-IR (Homeostasis model assessment) 21 .…”

Section: Methodsmentioning

confidence: 99%

Exercise activates the PI3K-AKT signal pathway by decreasing the expression of 5α-reductase type 1 in PCOS rats

Jiang

Wei

et al. 2018

Sci Rep

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Hyperandrogenism and hyperinsulinemia are main clinical endocrine features of PCOS. Exercise can adjust the androgen level, as well as increase the sensitivity of insulin by activating PI3K-Akt insulin signaling pathways. 5αR1 has certain effects on insulin resistance and can synthesize dihydrotestosterone by metabolizing testosterone. So 5αR1 may be the target of androgen and insulin for exercise-induced regulation. To investigate the role of 5αR1 in the PI3K-Akt signaling pathway in skeletal muscle of PCOS rats activated by exercise, fifty-four female rats were randomly divided into the PCOS group (n = 42) and the control group(n = 12). After injection of testosterone propionate for 28 days, the remaining 36 rats in the PCOS group were randomly assigned to six groups: the sedentary group (PS, n = 6), sedentary and 5αRI (5α-reductase inhibitor) group (PS + RI, n = 6), sedentary and 5αR2I (5α-reductase type 2 selective inhibitor) group (PS + R2I, n = 6), exercise group (PE, n = 6), exercise and 5αRI group (PE + RI, n = 6), and exercise and 5αR2I group (PE + R2I, n = 6). The rats undergoing exercise were trained to swim for 14 days. Finasteride (5α-reductase type 2 selective inhibitor) and dutasteride (5α-reductase inhibitor) were administered once daily and were dosed based on weight. At the end, the expression of 5αR1 proteins, the phosphorylation level of PI3K and AKT, were determined by Western blot. The PCOS non-exercise group and the PE + RI group displayed significantly lower phosphorylation of Akt, PI3K p85 and GLUT4 expression, while in the PE + R2I group, the level of Akt phosphorylation and PI3K p85 expression was significantly higher than that of the PCOS non-exercise group and the PE + RI group. In summary, our study demonstrated that exercise can activate the PI3K/AKT signal pathway of PCOS rats by decreasing the expression of 5αR1.

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Section: Methodsmentioning

confidence: 99%

Exercise activates the PI3K-AKT signal pathway by decreasing the expression of 5α-reductase type 1 in PCOS rats

Jiang

Wei

et al. 2018

Sci Rep

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“…A meta-analysis by Wu et al demonstrates higher proportions of 5α-reductase metabolites in PCOS women compared to BMI matched controls. Moreover, subgroup analyses confirm the association of 5 α reductase with insulin resistance 41 . 5α-reductase indirectly modulates hyperandrogenism; however, the exact mechanism is unclear.…”

Section: Role Of Insulinmentioning

confidence: 73%

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2019

IJPSR

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Polycystic ovarian syndrome (PCOS) is a reproductive metabolic disorder affecting nearly 20% females, globally. Though Rotterdam consensus is widely used for assessment, it lacks definite diagnostic guidelines. Absence of PCOS guidelines for adolescent and post-menopausal women might be influencing the prevalence data. The prevalence varied with ethnicities and found high in urban than rural. Among women in reproductive age, the obese rural population also found vulnerable to PCOS, indicates the role of lifestyle factors in this syndrome. Erratic lifestyle predisposes to insulin resistance, or obesity leads to subsequent hyperinsulinemia and hyperandrogenemia. Also, genetic predisposition to hypothalamic pituitary gonadal (HPG) axis dysfunction and impaired ovarian steroidogenesis further influence the disorder. It dysregulates the oocyte maturation leading to polycystic ovaries, thereby, affects the normal ovarian functions. The environmental toxins which are endocrine disruptors further worsens the consequence of the disorder. Multiple factors make it difficult to decipher the independent pathway of pathogenesis. Apart from ovulatory and reproductive dysfunctions, PCOS have chronic metabolic consequences: cardiovascular disease (CVD), obesity, dyslipidemia, obstructive sleep apnoea, and non-fatty liver. These factors are interdependent and progressive. Since the studies have contradicting results; it's difficult to determine the impact of these consequences. Both non-obese and obese PCOS women found vulnerable to the same metabolic consequences. Hence, further long term, controlled studies are required to understand the exact pathogenesis and metabolic consequences both in obese and non-obese PCOS women. Moreover, both regional and multicentre cohort studies are required to understand the progression of disease in different ethnicities.

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“…A study in adult men showed that testosterone reduced the CRH-stimulated rise in serum cortisol, in spite of increased ACTH, suggestive of adrenal hyporesponsiveness (54). Evidence for an effect of androgens on glucocorticoid metabolism was provided by other studies (55,56,57). It has been demonstrated by multiple studies that women with polycystic ovary syndrome -a condition characterized by increased androgen production -had a higher 5α-reductase activity than BMI-matched controls (55).…”

Section: Discussionmentioning

confidence: 99%

Sexual dimorphism in cortisol metabolism throughout pubertal development: a longitudinal study

Keulen

Dolan

Voorn

et al. 2020

Endocrine Connections

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Objective Sex differences in disease susceptibility might be explained by sexual dimorphism in hypothalamic-pituitary-adrenal axis activity, which has been postulated to emerge during puberty. However, studies conducted thus far lacked an assessment of Tanner pubertal stage. This study aimed to assess the contribution of pubertal development to sexual dimorphism in cortisol production and metabolism. Methods Participants (n = 218) were enrolled from a population-based Netherlands Twin Register. At the ages of 9, 12 and 17 years, Tanner pubertal stage was assessed and early morning urine samples were collected. Cortisol metabolites were measured with GC-MS/MS and ratios were calculated, representing cortisol metabolism enzyme activities, such as A-ring reductases, 11β-HSDs and CYP3A4. Cortisol production and metabolism parameters were compared between sexes for pre-pubertal (Tanner stage 1), early pubertal (Tanner stage 2–3) and late-pubertal (Tanner stage 4–5) stages. Results Cortisol metabolite excretion rate decreased with pubertal maturation in both sexes, but did not significantly differ between sexes at any pubertal stage, although in girls a considerable decrease was observed between early and late-pubertal stage (P < 0.001). A-ring reductase activity was similar between sexes at pre- and early pubertal stages and was lower in girls than in boys at late-pubertal stage. Activities of 11β-HSDs were similar between sexes at pre-pubertal stage and favored cortisone in girls at early and late-pubertal stages. Cytochrome P450 3A4 activity did not differ between sexes. Conclusions Prepubertally, sexes were similar in cortisol parameters. During puberty, as compared to boys, in girls the activities of A-ring reductases declined and the balance between 11β-HSDs progressively favored cortisone. In addition, girls showed a considerable decrease in cortisol metabolite excretion rate between early and late-pubertal stages. Our findings suggest that the sexual dimorphism in cortisol may either be explained by rising concentrations of sex steroids or by puberty-induced changes in body composition.

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5α-reductase activity in women with polycystic ovary syndrome: a systematic review and meta-analysis

Cited by 33 publications

References 25 publications

Exercise activates the PI3K-AKT signal pathway by decreasing the expression of 5α-reductase type 1 in PCOS rats

Exercise activates the PI3K-AKT signal pathway by decreasing the expression of 5α-reductase type 1 in PCOS rats

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Sexual dimorphism in cortisol metabolism throughout pubertal development: a longitudinal study

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